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. 2022 Dec 26;14(12):e32970. doi: 10.7759/cureus.32970

The Spontaneous Regression of Primary Gastrointestinal Malignancies: An Observational Review

Carlos D Minacapelli 1,, Philip Leuszkiewicz 2, Ankoor Patel 3, Carolyn Catalano 1, George Abdelsayed 1, Alexander Lalos 1, Vinod Rustgi 1
Editors: Alexander Muacevic, John R Adler
PMCID: PMC9879583  PMID: 36712716

Abstract

The spontaneous regression or remission (SR) of cancer, often described as the partial or complete disappearance of a malignant tumor in the absence of all medical treatment and therapy, is a well-documented phenomenon. With efforts ongoing to establish cancer treatments that limit undesirable outcomes and adverse effects, these uncommon occurrences of SR carry significant implications for novel therapies and warrant further investigation. While several case studies have reported instances of SR in gastrointestinal (GI) malignancies, a comprehensive review of previous manifestations of SR in the GI tract remains lacking. The inclusion criteria for the rare phenomenon are also in need of an appropriate update that takes recent scientific advancements and emerging new medical technologies into account. Our analysis of 390 cases of SR in the GI tract focuses primarily on neoplasms of the hepatobiliary system and proposes an updated version of the older inclusion criteria for spontaneous regression.

Keywords: hepatobiliary system, neoplasms, oncology, gastroenterology, hepatology, gastrointestinal cancers, hepatocellular carcinoma, spontaneous remission, spontaneous regression

Introduction and background

In 2021 alone, 372,470 new cases of primary gastrointestinal (GI) cancer were reported worldwide, and approximately 124,348 deaths occurred as a result, comprising 19.6% and 20.4% of total new cancer cases and deaths, respectively [1]. Nonetheless, with the introduction of various novel diagnostic, therapeutic, and antineoplastic modalities, the mortality rates of GI cancers have declined significantly over the past several years [2]. These new modalities have led to a greater understanding of the pathogenesis of cancer and of achieving remission. Spontaneous regression (SR) is defined as the complete or partial disappearance of a primary and/or disseminated lesion of a histologically diagnosed metastatic disease in the absence of any medical treatment or therapy known to have antitumor effects. Spontaneous regression has been found to occur throughout the entire body, including the GI tract [3]. But it is not equivalent to a cure, as cancer may reappear or spread elsewhere in the body. The frequency of spontaneous regression varies based on the type of cancer, as it is most commonly reported in renal cell carcinoma, melanoma, and neuroblastoma [3-5]. Occurring at a rate of about one out of every 60,000 to 100,000 cases of all cancers, these extremely rare occurrences of SR have the potential to serve as an instructive in vivo model of biological tumor regulation and control [6].

A number of putative mechanisms have been proposed for the observed spontaneous disappearance of malignancies, including inflammation, apoptosis, ischemia, and immunological responses [7]. Other mechanisms proposed to cause SR include epigenetic modifications, hormonal responses, oncogenes, tumor suppressors, cytokines and growth factors, and psychological mechanisms. Unfortunately, several of these postulated mechanisms are based on association and speculation alone, with the exact mechanistic modalities surrounding the SR of GI cancer yet to be elucidated. Regardless, an immunological anti-tumoral response of a patient’s body to specific malignancies is among the most prevalently described mechanistic hypotheses for the observed spontaneous disappearance of neoplasms. Since the very inception of the term, spontaneous regression has historically been speculated to be a dynamic interplay of immunological anti-tumor responses. In 1956, Everson and Cole defined the criterion for SR as the partial or complete disappearance of a malignant tumor in the absence of all treatment or in the presence of therapy that is considered inadequate to exert a significant influence on neoplastic disease. At that time, they theorized that the phenomenon must be an opportunistic by-product of an activated immune response. Cases of SR linked to infections have significantly influenced the discovery of several different anticancer therapies that facilitate the targeting of cancer cells by the host’s immune system. For example, immune checkpoint inhibitors have revolutionized modern cancer treatment by targeting inhibitory receptors (e.g., PD-1, CTLA-4, LAG-3), ligands (e.g., PD-L1) expressed on T cells, antigen-presenting cells, and tumor cells, which result in an anti-tumor response by stimulating the host immune system.

Focusing chiefly on malignancies of primary GI origin, this observational review of the literature hopes to bring further attention to the phenomenon of SR while also identifying some potential mechanisms that have been purported to contribute to this largely unreported phenomenon. Secondarily, this comprehensive review aims to introduce a revised and up-to-date version of the older inclusion criteria for SR throughout the body. This updated criterion has been modified in a way that takes into account recent scientific advancements and emerging new medical technologies, with the intent that it will also be easy to follow for physicians and clinical researchers alike. Finally, this study seeks to broaden the scope of how SR is perceived by clinicians and members of the medical community by encouraging a holistic view of the exceptionally rare phenomenon as a dynamic interplay of various modalities.

Review

Materials and methods: 

Search Strategy 

A literature search across five databases (PubMed, Medline, Google Scholar, Semantic Scholar, and Jstage) was performed employing the following main keywords: gastrointestinal cancer, spontaneous regression, spontaneous remission, spontaneous necrosis, and abscopal effect. A full list of searched keywords is included in Appendix A. The clinical characteristics of each occurrence of SR within the GI pathway and the related long-term outcomes were then extracted. Articles were excluded if any systemic treatment was used or if any treatment directed at the lesion was utilized before the documented regression. All diseases were limited to the GI tract, spanning the oral cavity, esophagus, stomach, liver, bile duct, gallbladder, pancreas, mesenteries, peritoneum, small intestine, colon, and rectum. A manual search of each work’s citations was performed, utilizing additional published works listed in the supplementary materials or reference sections of each of the aforementioned studies. No restriction was applied to the date of publication, the form of publication, or the primary language of the publication.

Inclusion Criteria

Only publications that described the true SR of a histologically confirmed GI cancer were included following the inclusion criteria depicted in Figure 1. These criteria are based on the original criteria proposed by Cole, modified to emphasize histological diagnosis, and adapted to fit multiple clinical scenarios (2). These criteria are summarized as follows: (1) Partial or complete disappearance of the primary tumor or secondary metastasis was radiographically or pathologically demonstrated in the absence of systemic therapy; (2) localized therapy to the lesion prior to the observed shrinkage was excluded; and (3) the malignant neoplasm was histologically proven at some point during this course. Patients with primary neoplasms histologically determined to have originated from outside the GI pathway but demonstrating SR were excluded, even if they demonstrated SR of a secondary metastasis within the GI tract. Patients demonstrating regression of an extra-digestive lesion, histologically determined to have arisen in the GI tract, were included regardless of whether the primary GI lesion had also regressed.

Figure 1. Clinician guidelines or criteria for reporting spontaneous regression.

Figure 1

From a clinician’s initial encounter with a patient with a suspected cancerous lesion to the demonstration of tumor shrinkage or disappearance, potential clinical manifestations of spontaneous regression are schematically investigated and shown. Original figure by the authors.

Data Extraction and Analysis

The following information was extracted and recorded from each article: patient age and sex, location and histological typing of the primary tumor, the site of regression, the period of regression or remission, and the etiological mechanism of regression proposed by the author. The demonstrated recurrence of cancer was also noted in some patients. Limited to each author’s interpretation and the duration of follow-up included in each study, the period of remission was defined as one of the following, whichever was found to be the longest: (1) the total period of time during which the tumor demonstrated a shrinkage in size, beginning with the date when the tumor’s size was found to be at its maximum to the date when the tumor’s size was found to be at its minimum, (2) The total period of time between the partial or complete disappearance of cancer and the most recent follow-up date in which the patient continued to show no signs of metastatic spread or recurrence of the malignancy; (3) the total period of time during which the tumor demonstrated a shrinkage in size prior to its resection, from the proposed date when the tumor’s size was found to be at its maximum size to the date of the resection. After the tumor was resected, the specimen was pathologically found to have shrunk or disappeared.

Results

Of the 390 cases of SR of GI malignancies reported meeting our criteria, a majority were noted in men (272 cases, 69.7%) compared to women (118 cases, 30.3%). The mean patient age was 63 years, with a majority of patients between 65 and 74 years of age (114 cases, 29.2%) or 55 and 64 years of age (95 cases, 24.4%). Overall, the literature search demonstrated a global incidence of SR, with cases spanning all six inhabited continents.

All reported cases detailing the SR of GI malignancies throughout the clinical literature are comprehensively reviewed in Appendix B, with pertinent findings summarized in Table 1. These reported cases of SR included various cases of carcinoma (289 cases, 74.1%), primary gastrointestinal and oral lymphomas (67 cases, 17.2%), and a few neuroendocrine tumors (12 cases, 3.1%), among other primary gastrointestinal cancers (22 cases, 5.6%). Hepatocellular carcinoma (HCC) represented almost half of all reported cases of SR in GI cancers (193 cases, 49.5%). Several rare forms of cancer, including extramedullary plasmacytoma (EMP), peritoneal alveolar soft-part sarcoma (ASPS), and gastric gastrinoma, were also observed to spontaneously regress. A complete list of reported histological manifestations of GI malignancies recorded to have undergone SR is in Figure 2.

Table 1. Baseline characteristics of spontaneous regression within the study sample.

Patient characteristics* Oral (n=46) Esophageal (n=11) Gastric (n=38) Peritoneal (n=3) Hepatobiliary (n=212) Pancreatic (n=10) Small bowel (n=10) Colorectal  (n=60) Total (n=390)
Age (Mean (SD)) 61.2 (17.4) 59.0 (16.2) 60.1 (19.0) 47.7 (15.9) 64.7 (13.5) 50.4 (18.2) 51 (16.2) 62.1 (15.0) 63.1 (14.7)
Age group (n (%))                  
<19 1 (2.2%) 0 1 (2.6%) 0 0 0 0 1 (1.7%) 3 (0.8%)
19-34 3 (6.5%) 1 (9.1%) 2 (5.3%) 0 6 (2.8%) 2 (20.0%) 1 (10.0%) 1 (1.7%) 16 (4.1%)
35-44 1 (2.2%) 1 (9.1%) 7 (18.4%) 2 (66.7%) 6 (2.8%) 1 (10.0%) 2 (20.0%) 7 (11.7%) 27 (6.9%)
45-54 11 (23.9%) 1 (9.1%) 2 (5.3%) 0 21 (9.9%) 1 (10.0%) 1 (10.0%) 7 (11.7%) 44 (11.3%)
55-64 8 (17.4%) 4 (36.4%) 10 (26.3%) 0 49 (23.1%) 2 (20.0%) 5 (50.0%) 17 (28.3%) 95 (24.4%)
65-74 9 (19.6%) 2 (18.2%) 5 (13.2%) 1 (33.3%) 82 (38.7%) 1 (10.0%) 1 (10.0%) 13 (21.7%) 114 (29.2%)
75-84 11 (23.9%) 2 (18.2%) 10 (26.3%) 0 43 (20.3% 1 (10.0%) 0 12 (20.0%) 79 (20.3%)
85+ 2 (4.3%) 0 1 (2.6%) 0 4 (1.9%) 0 0 2 (3.3%) 9 (2.3%)
Sex (n (%))                  
Male 25 (54.3%) 8 (72.7%) 23 (60.5%) 2 (66.7%) 168 (79.2%) 6 (60.0%) 5 (50.0%) 35 (58.3%) 272 (69.7%)
Female 21 (45.7%) 3 (27.3%) 15 (39.5%) 1 (33.3%) 44 (20.8%) 4 (40.0%) 5 (50.0%) 25 (41.7%) 118 (30.3%)
Site of Regression (n (%))                  
Primary tumor/Recurrence 41 (89.1%) 8 (72.7%) 35 (92.1%) 0 194 (91.5%) 10 (100.0%) 7 (70.0%) 48 (80.0%) 288 (73.8%)
Lung metastases 2 (4.3%) 3 (27.3%) 0 1 (33.3%) 28 (13.2%) 0 1 (10.0%) 2 (3.3%) 37 (9.5%)
Liver metastases 0 0 1 (2.6%) 1 (33.3%) 2 (0.9%) 2 (20.0%) 2 (20.0%) 10 (16.7%) 18 (4.6%)
Lymph metastases 5 (10.9%) 2 (18.2%) 1 (2.6%) 0 2 (0.9%) 0 3 (30.0%) 2 (3.3%) 15 (3.8%)
Other metastases 1 (2.2%) 1 (9.1%) 1 (2.6%) 1 (33.3%) 13 (6.1%) 0 1 (10.0%) 6 (10.0%) 24 (6.2%)
Extent of regression (n (%))                  
Complete 43 (93.5%) 9 (81.8%) 32 (84.2%) 2 (66.7%) 156 (73.6%) 8 (80.0%) 10 (100.0%) 57 (95.0%) 317 (81.3%)
Partial 3 (6.5%) 2 (18.2%) 6 (15.8%) 1 (33.3%) 56 (26.4%) 2 (20.0%) 0 3 (5.0%) 73 (18.7%)
Histological profile (n (%))                  
Carcinoma 11 (23.9%) 8 (72.7%) 8 (21.1%) 0 198 (93.4%) 9 (90.0%) 1 (10.0%) 54 (90.0%) 289 (74.1%)
Primary lymphoma 28 (60.9%) 1 (9.1%) 24 (63.2%) 0 4 (1.9%) 0 6 (60.0%) 4 (6.7%) 67 (17.2%)
NET 1 (2.2%) 0 6 (15.8%) 0 2 (0.9%) 1 (10.0%) 1 (10.0%) 1 (1.7%) 12 (3.1%)
Other 6 (13.0%) 2 (18.2%) 0 3 (100.0%) 8 (3.8%) 0 2 (20.0%) 1 (1.7%) 22 (5.6%)
Period of regression (n (%))                  
<1 month 4 (8.7%) 0 3 (7.9%) 0 6 (2.8%) 0 0 0 13 (3.3%)
1-1.5 months 3 (6.5%) 1 (9.1%) 5 (13.2%) 0 11 (5.2%) 1 (10.0%) 0 9 (15.0%) 30 (7.7%)
2-5 months 2 (4.3%) 2 (18.2%) 6 (15.8%) 1 (33.3%) 27 (12.7%) 0 3 (30.0%) 13 (21.7%) 54 (13.8%)
6-11 months 6 (13.0%) 3 (27.3%) 3 (7.9%) 0 16 (7.5%) 1 (10.0%) 3 (30.0%) 1 (1.7%) 33 (8.5%)
12-23 months 6 (13.0%) 2 (18.2%) 5 (13.2%) 0 41 (19.3%) 2 (20.0%) 0 9 (15.0%) 65 (16.7%)
24-35 months 6 (13.0%) 1 (9.1%) 4 (10.5%) 1 (33.3%) 30 (14.2%) 1 (10.0%) 0 3 (5.0%) 46 (11.8%)
36-47 months 5 (10.9%) 0 2 (5.3%) 0 14 (6.6%) 1 (10.0%) 1 (10.0%) 5 (8.3%) 28 (7.2%)
48 months+ 8 (17.4%) 1 (9.1%) 8 (21.1%) 1 (33.3%) 33 (15.6%) 4 (40.0%) 2 (20.0%) 17 (28.3%) 74 (19.0%)
Unspecified 6 (13.0%) 1 (9.1%) 2 (5.3%) 0 34 (16.0%) 0 1 (10.0%) 3 (5.0%) 47 (12.1%)
Malignancy recurrence (n (%))                  
Reported 5 (10.9%) 0 1 (2.6%) 0 14 (6.6%) 1 (10.0%) 2 (20.0%) 1 (1.7%) 24 (6.2%)
Not reported 41 (89.1%) 11 (100.0%) 37 (97.4%) 3 (100.0%) 198 (93.4%) 9 (90.0%) 8 (80.0%) 59 (98.3%) 366 (93.8%)

Figure 2. Histological manifestations of gastrointestinal malignancies are recorded to have undergone spontaneous regression throughout the clinical literature.

Figure 2

Biopsy-confirmed cancers of the gastrointestinal pathway, including various carcinomas, gastroenteropancreatic neuroendocrine tumors (GEP-NETs), and primary oral and gastrointestinal lymphomas, have been shown to demonstrate spontaneous regression. These cases have been observed throughout the entirety of the alimentary canal, spanning all of the organs of digestion. Cases of each distinct histological denomination were enumerated and systematically organized by the anatomical distribution of the primary lesion. Original figure by the authors.

The vast majority of cases of partial or complete regression occurred within the primary tumor (288 cases, 73.8%); nonetheless, multiple cases demonstrated regression of liver metastases (18 cases, 4.6%), lung metastases (37 cases, 9.5%), lymph metastases (15 cases, 3.8%), or other metastases (24 cases, 6.2%). The period of regression (as defined above) varied greatly in these cases, with some cases reporting just a few days of regression and others expressing several years of remission. Cancer recurrence was reported in 24 cases of SR, comprising 6.2% of total cases of SR in the GI pathway (noted with an asterisk "*" in Appendix B).

The authors proposed various putative mechanisms of SR, which are summarized in Table 2.

Table 2. Proposed mechanisms of spontaneous regression within the gastrointestinal pathway.

Proposed mechanism n (%)
Immunological 202 (51.8%)
Abscopal effect 10 (2.5%)
Endocrine factors 4 (1.0%)
Restored immunogenicity 18 (4.6%)
Eradication of oncogenic virus 7 (1.8%)
Fever/Infection 35 (9.0%)
Inflammatory response 14 (3.6%)
Transfusions 1 (0.3%)
Treatment of primary/Metastases 7 (1.8%)
Other/Not specified 106 (27.2%)
Ischemic 146 (37.4%)
Anti-angiogenic factors 3 (0.8%)
Vascular ischemia/ thrombosis 26 (6.7%)
Tumor ablation/Biopsy/Angiography 44 (11.3%)
Tumor hypoxia/ Hypoperfusion 30 (7.7%)
Tumor microenvironment disruption 3 (0.8%)
Unpredictable/Rapid growth 14 (3.6%)
Other/Not specified 26 (6.7%)
Idiopathic 92 (23.6%)
Apoptotic tumor cell death 6 (1.5%)
Dislodged 10 (2.6%)
Drugs 14 (3.6%)
Genetic 5 (1.3%)
Herbal medicines 20 (5.1%)
Metabolic/Nutritional 7 (1.8%)
Psychoneurological 5 (1.3%)
Withdrawal of carcinogenic agent 16 (4.1%)
Other 9 (2.3%)
Not specified 68 (17.4%)

The majority of the reviewed authors provided at least one conjectural mechanism (322 cases, 82.6%), with most citing immunological (202 cases, 51.8%), ischemic (146 cases, 37.4%), or idiopathic (92 cases, 23.6%) processes.

Discussion

This systematic review includes the presentation of 390 cases reported in 346 scientific papers, journals, case studies, and published books. These publications were generated over the past 95 years. Interestingly, 325 cases were published in the modern era, defined as cases published in the past 30 years. Following the review of these articles, multiple common factors were revealed, including a tendency for SR to occur in patients over the age of 55 (297 patients, 76.2%), patients of the male sex (272 patients, 69.7%), and patients with primary liver tumors (209 patients, 53.6%) or secondary liver metastases (18 patients, 4.6%). The clinical features and proposed mechanisms surrounding these cases of SR within the GI pathway, along with the location and duration of remission, are documented in Appendix B. Patients within this cohort of reported cases displayed varied periods of stability, ranging from just a few days of observed partial tumor regression to several years of cancer remission, up to 20 years cancer-free.

Mechanisms of Spontaneous Regression

Historically, SR has been speculated to occur in the setting of a prolonged febrile illness due to viral or bacterial infection; nonetheless, only a fraction of cases of SR (35 patients, or 5.1%) have been attributed to a hyperthermic state and infection [8]. In cases of SR occurring during times of acute febrile infections, immune cell infiltrations and signaling cascades are postulated to lead to tumor cell death and cancer tissue necrosis via the release of interleukins, tumor necrosis factors, and interferons (specifically IL-2, IL-6, and IL-8) [9-17]. Viral infections notably induce the production of interferons, which are capable of their own immunomodulatory effects involving macrophages, B-cells, and monocytes, alongside the induction of IL-2 receptors in some cancers [6-8]. Most recently, tumor regression has been reported after COVID-19 vaccination and infection with its wide-ranging pro-inflammatory effects on the host immune system [18-23].

Enhanced antitumoral immunogenicity is proposed to play a profound role in the involution of several GI cancers. In fact, examples displaying the correlation between SR and the elimination of immunodisruptive factors (e.g., medications, viral infection, checkpoint proteins) are perhaps the best evidence supporting the involvement of immunological mechanisms in the achieved SR of GI cancer [24,25]. Tumors have also occasionally been found to regress following systemic or localized treatment for some other disease process. For example, certain localized therapies have been observed to cause tumor regression of both the target lesion and any untreated tumors [26]. Described as the "abscopal effect," this phenomenon is purportedly mediated by a systemic anti-tumor response that follows after receiving radiation therapy for a metastatic lesion or an entirely separate neoplasm. Overall, more than half of the reported cases of SR within the GI tract have been attributed to immunological processes (202 cases, 51.8%), with authors also suggesting the involvement of endocrine factors (four cases, 1.0%) and inflammatory responses (14 cases, 3.6%).

Ischemic models of regression are also proposed to play a key role in the dynamic interplay of antitumoral mechanisms described in the SR of cancer. Tumor cells require an ample supply of blood, so limiting their blood supply and perfusion could intuitively starve the cells to death [27-29]. Consequently, systemic and tumoral hypoperfusion (30 cases, 7.7%), rapid and unpredictable growth (14 cases, 3.6%), anti-angiogenic factors (three cases, 0.8%), and vascular compromise (26 cases, 6.7%) are all theorized to lead to the SR of GI cancer [30-34]. For example, there are multiple cases of SR described as following profound systemic hypoperfusion associated with hemodialysis, surgical invasion, or GI hemorrhage [30-34]. Several reviewed cases of SR (44 patients, 11.3%) have been specifically attributed to diagnostic biopsy procedures alongside tumor ablation and angiographic techniques [3,7,35]. In addition to impairing the adequate delivery of essential nutrients and oxygenation to the remaining (AL3) malignant tissue, these procedures are known to set forth a landslide of tumor-derived antigens into circulation, thus acting as a therapeutic vaccine [4,36].

While endocrinologic mechanisms are largely considered to play a secondary role in the course of tumor regulation, notable hormonal changes are considered possible antecedents to SR [37]. In a case describing a presumed appendiceal neuroendocrine tumor (NET) during pregnancy, Sewpaul et al. observed rapid regression following the patient’s completion of her pregnancy, suggesting that the pregnancy did not worsen the course of the disease but instead may have contributed to tumor regression [38]. Additional influences on the endocrine system by psychological events, such as trauma and stress, suggest that a patient’s psychological status might also influence the course of tumor development. In a case study detailing the SR of one patient’s recurrent oral squamous cell carcinoma (OSCC), Oya et al. describe how the 73-year-old patient was unable to understand the state of his recurrent cancer following cerebral infarction and dementia and postulate how this "unconsciousness" functioned as a preferable psychological condition for tumoral regression [39].

Spontaneous Regression in Cancers of Specific Pathohistology

Hepatocellular carcinoma: While testicular germ cell tumors, neuroblastomas, and renal carcinomas are conventionally the most frequent types of histologically diagnosed tumors presenting this phenomenon, several recent studies report an increasing incidence of SR within the GI pathway, particularly in primary hepatic lesions [6,40]. Correspondingly, we found that HCC was by far the most frequently observed type of cancer within the GI pathway to have undergone SR, with 199 total cases reported in the literature from 1982 to 2021. The reviewed cases proposed several mechanisms surrounding the involution of HCC, primarily citing ischemic and immunological antitumoral models of regression.

To prevent a barrage of immune responses to innocuous materials while still enabling immunity to pathogens, the complex cellular, functional, and molecular modeling of the liver allows for a dynamic, multifaceted approach to immune surveillance that incorporates the tolerogenic organ’s inherently immunosuppressive microenvironment and its distinct hepatic regulatory pathways [41]. It is possible that any manipulation of this multipronged system, such as through the abatement of the tolerogenic characteristics of hepatic APCs or the enhancement of effector lymphocyte function, could potentially have the desired effect of increased anti-tumor activity and tumor regression [42].

Interestingly, several of the changes associated with the SR of the poorly prognosed tumor can also be observed following transarterial chemoembolization (TACE) treatment, thus suggesting that the SR of HCC should, to some degree, involve ischemic processes [43]. Regression of HCC has also been linked to rapid tumor infiltration, in which the notably hypervascular tumor grows more rapidly than its blood supply, leading to local or centralized ischemia, intratumoral bleeding, and hemorrhagic necrosis of the lesion [44]. These distinct immunologic and vascular attributes of the liver combine to form a tumoral environment wherein an intrahepatic malignancy is uniquely positioned to respond to immune and ischemic changes compared to tumors of other organs of the GI tract. Otherwise, abstinence from alcohol, persistent fever, withdrawal from androgens, blood transfusions, and the use of herbal medicines have also been described as leading to the SR of primary hepatic lesions.

Primary oral and gastrointestinal lymphoma: Cases detailing the SR of primary oral and GI lymphomas were observed to span the entirety of the alimentary canal, from several primary extranodal lymphomas of the oral cavity to four cases of rectal lymphoma that regressed spontaneously. Regarding the spontaneous regression of aggressive NHLs of the digestive tract, several cases have been reported demonstrating the spontaneous involution of lymphoma following improved immunological status, particularly in HIV-infected patients receiving antiretroviral therapy [27-32].

While SR is an exceptionally rare occurrence in aggressive lymphomas, such as DLBCL and ALCL, it can occur relatively frequently in low-grade lymphomas such as follicular lymphomas (FLs) and mucosa-associated lymphoid tissue (MALT) lymphomas. Generally, well- or moderately-differentiated forms of cancer are considered low immunogenic tumors due to their limited mutational load and concomitant limited neoantigen expression. In a retrospective analysis of 209 cases of NHL from 1965 until 1978, Gattiker et al. reported the occurrence of SR in 18 out of 140 (12.9%) cases of nodular type malignant lymphoma and 2 out of 69 (2.9%) cases of diffuse type malignant lymphoma [45]. The relationship between gastric mucosa-associated lymphoid tissue (MALT) lymphoma and H. pylori is very well established, and low-grade gastric MALT lymphomas are known to regress following the bacteria’s eradication [46]. This reversible reactivity of low-grade MALT lymphomas to H. pylori infection is a clearly documented phenomenon; hence, cases detailing the regression of low-grade MALT lymphomas involving H. pylori eradication through the use of eradication therapy were excluded from the scope of this careful review.

Pancreatic ductal adenocarcinoma: With only a few cases reported in the literature, pancreatic tumors are seldom known to undergo SR, leaving clinicians skeptical of this lethal tumor’s ability to truly demonstrate involution when left untreated. Despite numerous molecular and immunological approaches, pancreatic cancer is typically poorly responsive to existing chemotherapeutic and immunological antineoplastic agents. This lack of response to immunotherapies is largely due to cancer’s low mutational burden and tendency to favor an immunosuppressive microenvironment characterized by self-isolating dense desmoplastic tissue and an exceptionally low number of infiltrating T cells [47,48]. In a recently published article investigating the possibility of misdiagnosis leading to a presumptive finding of SR in pancreatic cancer, Herreros-Villaneuva et al. emphasized how different types of pancreatic carcinomas must be cautiously distinguished from otherwise benign tumors, insulinomas, and immunoglobulin G4 (IgG4)-associated autoimmune pancreatitis during the process of recording SR [49]. Regardless, four additional cases of pancreatic ductal adenocarcinoma (PDAC) have since been published, citing various multifactorial models of SR, including acute pancreatitis and bacterial or fungal infection in the vicinity of the pancreatic tumor, leading to improved immunogenic tumor presentation [48,50-52].

Colorectal cancer: Like pancreatic cancer, colorectal cancer has long been considered poorly immunogenic, largely based on indirect data from epidemiological studies on the lack of SR in colorectal cancer [53,54]. This lack of immunogenicity in this cancer can be attributed to the failure of tumor-infiltrating lymphocytes to demonstrate substantial lytic activity against cancer cells, as demonstrated in in vitro models [55,56]. While colorectal cancer constitutes more than 15% of all malignancies, it represents less than 2% of all tumors to demonstrate SR [57]. Still, several other rare forms of GI cancer, including Merkel cell-like small cell carcinoma of the parotid gland and multiple gastroenteropancreatic neuroendocrine tumors (GEP-NETs) of the stomach, bile duct, and pancreas, were observed to spontaneously regress.

Strengths and Limitations

While prior retrospective analyses have investigated the incidence of SR for specific cancers and its occurrence within the individual organs of digestion, an observational study of this scope, broadly examining all prior cases of SR throughout the entire GI pathway, has never been published to date. This first-of-its-kind study systematically and thoroughly extracts and organizes information from an array of 390 individual cases of SR within the GI pathway. Although the majority of reports were restricted to the English literature, cases in other languages, including Spanish, Chinese, German, and Japanese, are included in this broad review in order to better demonstrate the global incidence of the otherwise rare phenomenon. Putative mechanisms for SR, including immunological, ischemic, and idiopathic modalities, are also explored and discussed in a detailed manner with the hopes of aiding in an understanding of SR as a dynamic interplay of complex and interconnected antitumoral responses.

In general, SR remains a poorly understood and somewhat vaguely defined phenomenon. Our review has multiple limitations. Recognizing true SR as a host response to specific tumors may continue to be obscured by bias in how the regression is reported. In addition to the possible underreporting of cases of SR by certain physicians, there is also a significant amount of variability in how SR is defined. Distinguishing SR from abscopal effects and tumor regression instigated by eradication therapy remains highly subjective and may result in the misreporting of true spontaneous antitumoral host responses to specific cancers. Overall, the literature is quite heterogeneous, and not every case study reported the duration of follow-up or the duration of remission in a similar manner as would be expected in a retrospective review of this kind.

Conclusions

SR is an extremely rare occurrence. Nonetheless, certain recurrent patterns in cases of SR, as demonstrated in this review, deserve ample consideration. To better study SR in the future, there must be an emphasis on standardizing how SR is reported. A well-defined registry would also be helpful. Ultimately, this broadly encompassing yet focused assessment is meant to bring attention to the phenomenon of SR and perhaps aid in the investigative efforts in the burgeoning field of immunotherapies.

Acknowledgments

Authors' contributions: Conceived and designed the analysis: CDM, PL, CC, VR. Collected the data: CDM, PL, CC. Contributed data or analysis tools: CDM, PL, CC, AP. Performed the analysis: CDM, PL, AP, GA, AL. Wrote the manuscript: CDM, PL, AP, CC, GA, AL, VR. Approved final manuscript version: CDM, PL, AP, CC, GA, AL, VR.

Appendices

Appendix A

Table 3. Keywords included in search criteria.

Each word from cohort P was cross-searched with a word or phrase from cohorts 1 or 2a and 2b. Phrases from cohort 1 were searched individually after being paired with a word from cohort P. Phrases searched with words from Cohort 2a were matched with a single word from cohort 2b (if applicable), and this pairing was used across the five databases.

Cohort P Cohort 1 Cohort 2a Cohort 2b
Abscopal effect Alveolar soft-part sarcoma Anus (anal) Adenocarcinoma
Spontaneous necrosis Cholangiocarcinoma Bile duct (biliary/hepatobiliary) Anaplastic lymphoma
Spontaneous regression Epithelioid hemangioendothelioma Cecum (Ileocecal) Cancer
Spontaneous remission Extramedullary plasmacytoma Colon (colorectal) Carcinoid
  Gastrinoma Duodenum (duodenal) Carcinoma
  Insulinoma Esophagus (esophageal) Diffuse large B-cell lymphoma
  Islet cell cancer Gallbladder Follicular lymphoma
  Malignant myoepithelioma Gastroesophageal junction Hodgkin lymphoma
  Malignant peritoneal mesothelioma Gastrointestinal Leiomyosarcoma
  Mucoepidermoid carcinoma Ileum (ileal) Lymphoblastic lymphoma
  Pseudomyxoma peritonei Jejunum (jejunal) Lymphoma
    Liver (hepatic/hepatocellular) Malignant melanoma
    Mesentery (mesenteric) MALT lymphoma
    Omentum (omental) Natural killer lymphoma
    Oral cavity (oral) Neuroendocrine tumor
    Pancreas (pancreatic) Plasmablastic lymphoma
    Peritoneum (peritoneal) T-cell lymphoma
    Rectum (rectal)  
    Salivary gland (adenoid)  
    Small bowel/intestine (enteric)  
    Tongue  

Appendix B 

Table 4. Clinical features of cases demonstrating the spontaneous regression of gastrointestinal cancers.

    Ref Age/ Sex Location Pathologic Histology Site of regression Period of Remission Proposed mechanism
Oral cancer 1 Roxburgh (1935) 60s/F Tongue OSCC Primary tumor 7 years Partial Resection
2 Grillet et al (1984) 26/M Parotid gland ACC Lung metastases 7 years Diet
3 Grillet et al (1984) 53/M Submandibular gland ACC Lung & nasolabial metastases 3 years Not reported
4 Grem et al (1986) 54/F Vallecula DLBCL Primary tumor 4 years Immunological; viral/bacterial infection; Biopsy
5 Poppema et al (1988) 12/M Oropharynx LBL Primary tumor & cervical lymph node 3 years Immunological (cytotoxic)
6 Savarrio  et al (1999) 77/M Soft palate ALCL Primary tumor 1 year* Immunological; Biopsy
7 King et al (2001) 52/M Parotid gland MM Primary tumor & regional lymph nodes 6 weeks Immunological
8 Notani et al (2002) 77/M Tongue ALCL (TCL) Primary & multiple oral recurrences multiple Not reported
9 Koga et al (2003) 78/F Maxillary mingiva DLBCL Primary tumor 3 years Biopsy
10 Yamamato et al (2003) 80/F Maxilla DLBCL Primary tumor 1.5 years Biopsy
11 Yokoyama et al (2003) 46/F Hard palate MALT Lymphoma Primary tumor 2.5 years Biopsy
12 Heibel H et al (2004) 70/M Mandible DLBCL Primary tumor 1.5 years Biopsy
13 Lester et al (2004) 50/M Palate PBL Primary tumor 4 months* Restoration of immune function (HAART)
14 Sakuma et al (2006) 70/F Palatine salivary gland MALT Lymphoma Primary tumor 3 years Biopsy; Localized infection
15 Armstrong et al (2007) 35/M Maxilla PBL Primary tumor (partial) 2 weeks Restoration of immune function (antiretroviral)
16 Kurita et al (2007) 67/M Tongue OSCC Cervical lymph node metastases 10 months Enhanced Apoptosis
17 Oya andikemura K (2007) 73/M Tongue OSCC Primary tumor 3.5 years Psychoneurological ("unconsciousness to cancer" S/P cerebral infarct & dementia); Immunological
18 Rujirojindakul et al (2007) 26/M Submandibular gland LBL Primary tumor multiple* Not reported
19 Daly et al  (2008) 56/M Maxillary gingiva TCL Primary tumor 4 years Biopsy
20 Mulder et al (2009) 78/M Parotid gland Merkel cell-like SmCC Primary tumor 5 months* T-cell mediated response triggered by trauma; Apoptosis
21 Brachet et al (2011) 58/F Hard palate DLBCL Primary tumor 15 days* Biopsy
22 Corti et al (2011) 55/F Oral PBL Primary tumor 10 months Restoration of immune function (antiretroviral cART)
23 Tamás et al (2011) 66/F Vallecula/tongue DLBCL Primary tumor 7 years Not reported
24 Fitzpatrick et al (2012) 88/F Labial mucosa ALCL (TCL) Primary tumor 2 weeks Biopsy
25 García-Noblejas et al (2013) 78/F Buccal mucosa PBL Buccal & cervical lymph node lesions 2 years Restoration of immune function (removal of methotrexate)
26 Choi et al (2014) 52/F Buccal mucosa OSCC Cervical lymph node metastases Not reported Tumor Microenvironment modification
27 Sousa et al (2014) 62/M Mouth floor OSCC Primary tumor 3 months Biopsy; Immunological
28 Cuenca-Jimenez et al (2015) 65/M Parotid gland OSCC Primary tumor Not reported Not reported
29 Igawa et al (2015) 80/M Maxillary gingiva PBL Primary tumor 8 months Genetic (immunosenescence)
30 Kaibuchi et al (2015) 87/M Gingiva DLBCL Primary tumor 2.5 years Biopsy
31 Gonzalez-Perez et al (2016) 75/M Mandibular gingiva EMP Primary tumor 1.5 years Immunological (cytokines. Growth factors); Biopsy
32 Wagner et al (2016) 33/F Mandibular gingiva PBL Primary tumor 1.5 months Restoration of immune function (HAART)
33 Daroit et al (2017) 66/F Maxilla PBL Primary tumor 1 year Restoration of immune function (HAART)
34 Kitamura et al (2017) 61/M Maxillary gingiva PBL Primary tumor 2 years Restoration of immune function (antiretroviral)
35 Rajan & Samant et al (2017) 49/F Hard palate MM Primary tumor Not reported Immunological
36 Yao et al (2017) 80/M Maxillary gingiva PBL Primary tumor Not reported Traumatic factors (Biopsy)
37 Miyagawa et al (2018) 46/M Upper lip ALCL Primary tumor 1 year Biopsy
38 Gamarra et al (2018) 50/F Maxilla MEC Primary tumor (partial) 10 years Not reported
39 Ono et al (2019) 69/M Mandibular gingiva PBL Primary tumor 2 years Not reported
40 Curioni et al (2020) 51/F Submandibular gland SGAC Primary tumor 7 years Metabolic derangement (hypoglycemia); Immunological
41 Oliveira et al (2020) 52/F Hard palate MM Primary tumor 6 years Inflammatory; Immunological
42 Peeters et al (2020) 59/M Buccal/Masticator space FL Primary tumor 6 months Biopsy
43 Aoki et al (2021) 84/M Maxillary gingiva DLBCL Primary tumor 2 years Biopsy
44 Lau et al (2021) 66/F Oropharyngeal tonsil OSCC Primary tumor 7 months Biopsy (Anti-tumoral T-cell response); Hyperthermal state (COVID-19 vaccine)
45 Ueno et al (2021) 83/F Mandibular gingiva MM Primary tumor (partial) 26 days Not reported
46 Sousa et al (2022) 61/F Parotid gland MME Primary tumor 9 months Inflammatory response (COVID-19 vaccine)
Esophageal cancer 47 Rees et al (1983) 49/M Lower esophagus EAC Lung metastases 1 year Abscopal effect
48 Oshwada et al (1990) 78/M Thoracic esophagus ESCC Primary tumor (partial) & pulmonary metastases 7 months Change in T-cell subsets; surgical trauma
49 Vergeau et al (1991) 36/M Mid esophagus ESCC Primary tumor (partial) 1 year Leukocyte infiltration; Inflammation
50 Hahm et al (1993) 30/M Thoracic esophagus PEL Primary tumor Not reported H2-blocker (Cimetidine)
51 Saruki et al (1994) 82/F Thoracic esophagus ESCC Primary tumor 2 years Infection (Pneumonia)
52 Takemura et al (1999) 63/F Thoracic esophagus ELMS Pleural & splenic metastases 10 months Removal of Primary
53 Chang (2000) 57/M Lower esophagus ESCC Primary tumor 9 years Infection (Pneumonia); Inflammation
54 Kubota et al (2003) 73/M Thoracic esophagus SCEC Primary tumor 1 month Infection (Hepatitis C)
55 Hornby et al (2015) 57/M GEJ MM Primary tumor 2 months Immunological; Occult Primary
56 Mitchell et al (2021) 58/F GEJ GEJAC Local & supraclavicular lymph metastases 6 months Not Reported
57 Kahn et al (2021) 66/M Lower esophagus ESCC Primary tumor 3 months Immunological (T-cell response)
Stomach cancer 58 Takeuchi et al (1971) 39/M Corpus-antrum PGL (RCS) Primary tumor (partial) 2 months Not reported
59 Nakano et al (1972) 55/F Corpus PGL (RCS) Primary tumor (partial) 3 weeks "malignant cycle" of early gastric cancer
60 Rosenberg et al (1972) 51/M Lesser curvature GAC Liver metastases 12 years Fever
61 Ohashi et al (1973) 42/M Corpus-antrum PGL (RCS) Primary tumor (partial) 1 month "malignant cycle" of early gastric cancer
62 Tietjen et al (1974) 60/F Gastric antrum duodenum PGL (RCS) Primary tumor 5 years "malignant cycle" of early gastric cancer
63 Yamazaki et al (1974) 39/M Pyloric antrum PGL (RCS) Primary tumor (partial) 20 days Not reported
64 Kimura et al (1987) 85/F Residual stomach GAC Primary tumor Not reported Not reported
65 Strauchen et al (1987) 73/M Pyloric antrum PGL (DLBCL) Primary tumor 3 weeks H2-receptor antagonist
66 Strauchen et al (1987) 84/M Pyloric antrum PGL (DLBCL) Primary tumor 1 month H2-receptor antagonist
67 Harvey et al (1988) 78/F Gastric body/fundus GEP-NET (ECL-cell Carcinoid) Multifocal gastric lesions (majority) 10 years Not reported
68 Harvey et al (1988) 55/M Stomach GEP-NET (ECL-cell Carcinoid) Multifocal gastric lesions 5 years Not reported
69 Sawant et al (1989) 40/F Unspecified stomach GEP-NET (Carcinoid) Primary tumor 1 year Biopsy
70 Shigematsu et al (1989) 40/F Pyloric antrum PGL (DLBCL) Primary tumor (partial) 2 months Not reported
71 Shigematsu et al (1989) 73/M Pyloric antrum PGL (DLBCL) Primary tumor 2 months Not reported
72 Rebollo et al (1990) 77/M Gastric body/fundus GAC Primary tumor 8 months Infection (abdominal wall abscess)
73 Yoshimine et al (1991) 69/F Gastric angulus PGL Primary tumor 2.5 months Dislodged (ulceration)
74 Hayakawa et al (1992) 62/F Lesser curvature PGL (DLBCL) Primary tumor 1 year Necrosis & Detachment
75 Takehara et al (1992) 44/M Gastric angulus/Antrum PGL Primary tumor (partial) 1 month H2-blocker
76 Matsusaki et al (1996) 64/F Pyloric antrum PGL (DLBCL) Primary tumor 1 month Not reported
77 Ogawa et al (1998) 63/F Gastric corpus PGL (DLBCL) Primary tumor 13 months H Pylori eradication
78 Bariol et al (2001) 24/M Gastric antrum PGL (TCL) Primary tumor 2 years H Pylori eradication
79 Salam et al (2001) 73/F Greater curvature PGL (DLBCL) Primary tumor 2.5 years H Pylori eradication
80 Pentimone et al (2002) 84/M Residual stomach PGL (MALT) Recurrences 15/5 years Not reported
81 Chung et al (2003) 48/M Lesser curvature GAC Primary tumor 4 years Ischemia (angiography)
82 Watanabe et al (2003) 22/M Gastric body & Antrum PGL (TCL) Primary tumor 1 month Infection (Severe EBV viremia in CAEBV)
83 Watari et al (2005) 60/F Gastric angulus/Antrum PGL (DLBCL) Primary tumor 1 year H2-blocker; H. pylori eradication
84 Watari et al (2005) 61/M Gastric angulus PGL (DLBCL) Primary tumor 6 months H2-blocker; H. pylori eradication
85 Ohno et al (2006) 14/M Lower gastric corpus PGL (MALT) Primary tumor 10 years Immunological (Cessation of exposure to H pylori antigen)
86 Lee et al (2010) 84/M Cardia & Lower body GAC Primary tumor 1 year Not reported
87 Ip et al (2011) 77/M Gastric cardia GEP-NET (LCNEC) Primary tumor 3 months Infection (cytomegalovirus); Cross-autoimmune reaction against neuronal cells
88 Yang et al (2012) 77/M Gastric body GAC Primary tumor & recurrences Multiple Not reported
89 Rojas-Hernandez et al (2014) 57/M Greater curvature PGL (DLBCL) Primary tumor 2 years Immunological (B-cell stimulation by HCV)
90 Shibata et al (2016) 75/M Gastric antrum GEP-NET Peripancreatic lymph metastases 6 months* EUS-FNA; Bacterial infection
91 Sugiyama et al (2018) 62/F Gastric body PGL (DLBCL) Primary tumor 10 years Not reported
92 Bonilla et al (2019) 78/F Gastric antrum GAC Retroperitoneal adenopathies 3 months Abscopal effect
93 Hatsuse et al (2019) 82/F Unspecified stomach PGL (DLBCL) Primary tumor 2 years Not reported
94 Okamoto et al (2021) 37/M Gastric antrum GEP-NET (Gastrinoma) Primary tumor 3 years Biopsy; Resection of omental metastases
95 Zafar et al (2021) 74/M Lesser curvature GAC Primary tumor 6 years Not reported
Primary peritoneal cancer 96 Schwartz et al (1991) 39/M Peritoneum, omentum MPM Local regression 8 years Fever; Rheumatoid factor
97 BaniHani et al (2009) 38/M Mesentery ASPS Abdominal mass, heart & lung metastases 5 months Immunological; Herbal medicine
98 Jagodic et al (2018) 66/F Retroperitoneal space RLMS Liver metastases 2 years Not reported (possible delayed response to ChT)
Hepatobiliary Cancer 99 Gottfried et al (1982) 65/M Diffuse hepatic HCC Primary tumor 4 years Abstinence from alcohol; A-P shunt; Portal vein thrombosis
100 Lam et al (1982) 50/M Unspecified liver HCC Primary tumor & lung metastases 13 years Chinese herbal medicine; Bronchopneumonia
101 McCaughan et al (1985) 28/M Right lobe HCC Primary tumor 6.5 years Androgen withdrawal
102 McCaughan et al (1985) 40/M Right lobe HCC Primary tumor 9 years Androgen withdrawal
103 Sato et al (1985) 78/M Right lobe HCC Primary tumor & bone metastases 5 years Ischemia (GI Bleeding)
104 Takayasu et al (1986) 38/M Unspecified liver HCC Primary tumor (partial) 2 months Subintintimal injury (angiography)
105 Takayasu et al (1986) 58/F Unspecified liver HCC Primary tumor 2.5 years Subintintimal injury (angiography)
106 Andreola et al (1987) 75/M S6/7 HCC Primary tumor 18 days Venous thrombosis
107 Saez-Royeula (1989) 66/M Unspecified liver HCC Primary tumor 2.5 years Not reported
108 Suzuki et al (1989) 65/M Posterior right lobe HCC Primary tumor 6 years Rapid growth
109 Ayres et al (1990) 63/F Diffuse hepatic HCC Primary tumor (partial) 1 year Not reported
110 Gaffey & Joyce (1990) 63/M Right lobe HCC Primary tumor (partial) 1.5 years Ischemia (GI Bleeding); Macrobiotic diet
111 Tocci, G et al (1990) 79/M Hepatic hilum HCC Primary tumor 3 months Ischemia (GI Bleeding)
112 Mochizuki et al (1991) 61/M Unspecified liver HCC Primary tumor (partial) 1.5 years Abscopal Effect
113 Yamamoto et al (1991) 58/M Unspecified liver HCC Primary tumor Not reported Ischemia (hemorrhage)
114 Yamamoto et al (1991) 68/F Unspecified liver HCC Primary tumor Not reported Not reported
115 Chien et al (1992) 65/M Right lobe HCC Primary tumor 2.5 years Herbal Remedies
116 Imaoka et al (1994) 65/M Left lateral lobe HCC Primary tumor Not reported Arterial thrombosis
117 McDermott & Khettry (1994) 23/F Left lobe Clear cell HCC Primary tumor (partial) 5 years Not reported
118 Grossmann et al (1995) 52/M Diffuse hepatic HCC Primary tumor (partial) 1 year Abstinence from alcohol
119 Herrera et al (1996) 76/M Unspecified liver HCC Primary tumor 1 year Not reported
120 Ozeki et al (1996) 69/F S3 HCC Primary tumor 1 year Herbal Remedies
121 Markovic et al (1996) 62/M S5/6 HCC Primary tumor 8 years Fever; Ischemia (hemorrhage S/P biopsy); Biological effects by cytokines
122 Yoshimitsu et al (1996) 34/M Intrahepatic (left lobe) CCA Primary tumor 4 months* Fibrous component
123 Iwasaki et al (1997) 72/F Posterior/lateral HCC Primary tumor (partial) 1.5 years Tumor's rapid growth
124 Van Halteren et al (1997) 72/F Right lobe HCC Primary tumor 2 years Ischemia & infarction due to Cirrhosis
125 Kaczynski et al (1998) 73/M Central part/Hilum HCC Primary tumor 3 years Not reported
126 Ohba et al (1998) 76/M S5 HCC Primary tumor (partial) 2 years Abscopal Effect
127 Magalotli et al (1998) 66/M Unspecified liver HCC Primary tumor 4 years* Not reported
128 Megalotli et al (1998) 75/F Unspecified liver HCC Primary tumor (partial) 3 years* Not reported
129 Sanz et al (1998) 66/M Right lobe HCC Primary tumor 1 year Immunological
130 Stoelben et al (1998) 56/M S6 HCC Primary tumor 2 years Immunological (Resection of tumor); Infection (abscess)
131 Stoelben et al (1998) 74/M S6 HCC Primary tumor 3.5 years Immunological (resection of tumor); Infection (abscess)
132 Takeuchi et al (1998) 53/M S8 HCC Primary tumor Not reported Ischemia (thrombus)
133 Itoh et al (1999) 58/M S5 HCC Primary tumor 13 days Tumor Hypoxia (Thick capsule)
134 Toyoda et al (1999) 82/M Right lobe HCC Primary regression (Primary & Lung metastases) 1.5 years Transition from necrosis to fibrosis
135 Izuishi et al (2000) 50/M S2/3 HCC Primary tumor 5 years Ischemia; Immunological; Angiography
136 Jang et al (2000) 54/F Right lobe HCC Primary tumor 4 years Not reported
137 Lee et al (2000) 44/M S4/8 HCC Partial regression (Primary) 1 year* Infection; Abstinence from alcohol
138 Lee et al (2000) 63/M Right lobe HCC Partial regression (Primary) 3 years Infection; Arterial thrombosis/intimal injury (angiography)
139 Takeda et al (2000) 68/M S4/5/6/7/8 HCC Primary tumor 1 year Herbal Remedies
140 Terasaki et al (2000) 72/F S5 HCC Primary tumor, peritoneal & splenic metastases 2 years Apoptosis
141 Uenishi et al (2000) 65/M Right lobe HCC Primary tumor (partial) 1 year Abstinence from alcohol; A-P shunt; Portal vein thrombosis
142 Ikeda et al (2001) 75/M S7 HCC Primary tumor (partial) 6 years Not reported
143 Jung et al (2001) 58/M Right lobe HCC Primary tumor (partial) & lung metastases 1.5 years* Herbal Remedies; cessation of smoking;
144 Kawai et al (2001) 58/M S6 HCC Primary tumor 1 month Ischemia; Immunological; Angiography
145 Matsuo et al (2001) 72/M S5 HCC Primary tumor (partial) 1 year Immunological; Hypoxia; Inflammatory cell infiltration
146 Nakai et al (2001) 76/M Residual liver HCC Primary tumor 2 years Immunological (NK cell response)
147 Sakurai et al (2001) 65/M Gallbladder fundus GBAC Primary tumor Not reported Ischemia; Inflammation; Pancreaticobiliary maljunction
148 Serrano et al (2001) 71/M Left lobe HCC Primary tumor 3 years Growth factors; Ischemia (hepatic artery)
149 Abiru et al (2002) 70/M Unspecified liver HCC Primary tumor, lung & bone metastases 2 years Immunological (IL-18)
150 Abiru et al (2002) 65/F Unspecified liver HCC Primary tumor, lung & lymph metastases 4 months Immunological (IL-18)
151 Abiru et al (2002) 65/M Unspecified liver HCC Primary tumor, lung & bone metastases 1 year Immunological (IL-18)
152 Lee et al (2002) 70/M S2/3 HCC Primary tumor 24 days Occlusion of feeding artery
153 Misawa et al (2002) 62/M Anterior segment HCC Primary tumor 1 year Biological effects by A-P shunt
154 Morimoto et al (2002) 73/M S2/3 HCC Primary tumor 1 year Arterial thrombosis
155 Zimmermann et al (2002) 56/M S6 Medullary-like HCC Primary tumor 2 years Immunological (Cytotoxic pathway); Apoptosis
156 Iiai et al (2003) 69/M S6/7 HCC Primary tumor 4 years Portal vein thrombosis; cessation of smoking
157 Jozuka et al (2003) 52/M Hepatic surface HCC Primary tumor 2.5 years Psychoneurological; Antidepressants; Immunological
158 Li et al (2003) 53/M S6 HCC Primary tumor Not reported Biological effects by cytokines
159 Ohta et al (2003) 74/M S2/3 HCC Primary tumor 1 year Immunological; hypoxia (arterial sclerosis)
160 Blondon et al (2004) 64/M Diffuse hepatic HCC Local regression 9 months Infection (peritonitis); Ischemia (Intraperitoneal bleed)
161 Blondon et al (2004) 70/F Diffuse hepatic HCC Local regression 3 years Infection (peritonitis); Ischemia (Intraperitoneal bleed); tamoxifen
162 Cheng et al (2004) 74/M Medial left lobe HCC Primary tumor 6 years Herbal remedies
163 Erturk et al (2004) 69/M Left lobe HCC Primary tumor 3 years Blood transfusion
164 Feo et al (2004) 71/F S3/5 HCC Primary tumor (partial) 1.5 years Ischemia
165 Kato et al (2004) 72/M Right lobe HCC Primary tumor (partial) 2 years Not reported
166 Kato et al (2004) 77/M Right lobe HCC Primary tumor & lung metastases 1 year Abstinence from smoking
167 Lin et al (2004) 42/M S8 HCC Primary tumor (partial) 2 years Herbal remedies
168 Nakajima et al (2004) 80/M S4/6 HCC Partial regression (Primary) 6 months Ischemia; Intratumoral bleeding/hemorrhagic necrosis
169 Jeon et al (2005) 72/M Right lobe Clear Cell HCC Primary tumor (partial) & chest wall metastases 9 months Metabolic derangement (hypoglycemia & HLD)
170 Moon et al (2005) 72/M S6 HCC Primary tumor 2 years Alcohol cessation
171 Nam et al (2005) 65/M Right lobe HCC Liver & bone metastases (partial) 1 year Abscopal Effect
172 Nouso et al (2005) 85/M S5/6/7/8 HCC Primary tumor (partial) 2 years Ischemia; Vitamin K administration
173 Ohtani et al (2005) 69/M S4 HCC Primary tumor (partial) 3 years Tumor Hypoxia (Thick capsule)
174 Randolph et al (2005) 56/M Left lateral lobe HCC Primary tumor 1.5 years Alcohol cessation, ischemia (obstruction of portal vein thrombosis); Infection (Pneumonia)
175 Rizell et al (2005) 58/M Central liver HCC Primary tumor (partial) 1.5 years Sirolimus (Immunosuppressive)
176 Yano et al (2005) 71/F S8 HCC Primary tumor (partial) 2 years Hypoxia (artery rupture)
177 Otrock et al (2006) 75/F Diffuse hepatic HEHE Primary tumor 3.5 years Not reported
178 Kojima et al (2006) 79/M S8 HCC Lung metastases 6 months Steroids, Hormones, or Herbal Remedies
179 Kondo et al (2006) 67/M S4 HCC Primary tumor (partial) 2 months Immunological
180 Kondo et al (2006) 67/M S5/3 HCC Primary tumor & lung metastases 4 years CAM's; Immunological
181 Kondo et al (2006) 70/M Right lobe HCC Primary tumor (partial) 5 years Bleeding (esophageal varicies); Immunological
182 Kondo et al (2006) 75/M S7 HCC Lung metastases (partial) 2 years Immunological
183 Shibuya et al (2006) 71/M S5 HCC Primary tumor 2 months Ischemia; Immunological; Angiography
184 Heianna et al (2007) 70/F Unspecified liver HCC Lung metastases 5 years Immunological (Host cytokines); Systemic inflammatory (TACE of primary)
185 Matsunaga et al (2007) 71/F Left lateral lobe Sarcomatoid HCC Peritoneal metastases 4 months* Ischemia (rapid growth)
186 Meza-Junco et al (2007) 56/F S5 HCC Primary tumor 2 years Hypoxia (Thick capsule)
187 Peddu et al (2007) 57/M S4 HCC Primary tumor 2 months Auto-infarction
188 Vardhana et al (2007) ?/M S2/3/4 HCC Primary tumor 8 months Immunological
189 Arakawa et al (2008) 78/F S2/3 HCC Primary tumor 2.5 years Immunological; Portal vein thrombosis
190 Hori et al (2008) 71/M Gallbladder GBAC Primary tumor Not reported Increased intraluminal pressure (PBM); Pancreatic enzymes
191 Sibartie et al (2008) 76/M S5 HCC Primary tumor (partial) 2 years Ischemia (disturbance of blood flow)
192 Del Poggio et al (2009) 77/F S6 HCC Primary tumor (partial) 1.5 years Immunological (tumor antigens)
193 Hsu et al (2009) 66/M S7/8 HCC Primary tumor (partial) 1.5 years Hypoxia; Immunological; Silymarin; Portal vein thrombosis
194 Kanzaki et al (2009) 52/M S8 HCC Primary tumor 8 months Tumor Hypoxia (thick capsule)
195 Nishijima et al (2009) 86/F S7 HCC Primary tumor (partial) 4 months Tumor infarction
196 Oquiñena et al (2009) 54/M S6 HCC Primary tumor 2 years Vascular ischemia; Immunological
197 Oquiñena et al (2009) 61/M S1 HCC Primary tumor 1.5 years Vascular ischemia; Immunological
198 Oquiñena et al (2009) 60/M Right lobe HCC Primary tumor 3 years Vascular ischemia; Immunological
199 Park et al (2009) 57/M S5/6/7/8 HCC Primary tumor (partial) 5 years Infiltrating lymphocytes
200 Harada et al (2010) 70/M S7 HCC Primary tumor 2 years Ischemia; Herbal remedies
201 Hong et al (2010) 67/M Resection margin HCC Primary tumor & lung metastases 1 year TACE of Primary
202 Kai et al (2010) 58/F S6/7 HCC Primary tumor 1 month intimal injury (angiography)
203 Kai et al (2010) 49/M S6 HCC Primary tumor 3 weeks intimal injury (angiography)
204 Satou et al (2010) 83/M Right lobe HCC Primary tumor Not reported NSAIDS (Ketoprofen)
205 Storey et al (2010) 52/M S5/6 HCC Primary tumor 3 years Cessation of alcohol
206 Alqutub et al (2011) 65/M Right lobe HCC Primary tumor 2 years Ischemia (Rapid growth; Intratumoral hemorrhage)
207 Arora et al (2011) 54/M Right lobe HCC Primary tumor 2 years Immunological; Necrosis
208 Fukushima et al (2011) 69/M Right lobe HCC Lung metastases 7 years Immunological (TACE of Primary)
209 Maejima et al (2011) 68/M S3/5 HCC Primary tumor 3 months Ischemia; Immunological
210 Okano et al (2011) 68/M Right lobe HCC Tumor recurrence 2 years PVT; Ischemia (rapid growth)
211 Okuma et al (2011) 63/M Right lobe HCC Lung metastases 3 years Abscopal Effect
212 Bastawrous et al (2012) 63/M Right lobe HCC Primary tumor (partial) Not reported Ischemia
213 Harimoto et al (2012) 73/M S6/7 HCC Primary tumor & lung metastases 1 year Ischemia (hypotension during dialysis)
214 Komatzu et al (2012) 65/M Right lobe HCC Primary tumor & recurrences 6 months (x3) Not reported
215 Nakayama et al (2012) 92/F Right lobe HCC Primary tumor Not reported Ischemia (rapid growth); Immunological
216 Takeura et al (2012) 69/F Unspecified liver HCC Primary tumor & bone metastases 10 months Inflammatory (trauma)
217 Takeura et al (2012) 84/F Unspecified liver HCC Primary tumor & peritoneal carcinomatosis 1.5 years Inflammatory (trauma)
218 Yamamoto et al (2012) 60/M S4-8 HCC Primary tumor 3 weeks Immunological; Diabetes Control
219 Yokoyama et al (2012) 80/M S4 HCC Primary tumor 1 month Immune; Ischemia (thrombus)
220 Katayama et al (2013) 74/M S5/6 HCC Primary tumor 1 month Tumor Hypoxia (thick capsule)
221 Okano et al (2013) 77/M S4/6/7/8 HCC Primary tumor (partial) 1 year Ischemia (Disruption of feeding artery); Abstinence from alcohol
222 Sasaki et al (2013) 79/M S2 HCC Primary tumor 2 months Not reported
223 Tomishige et al (2013) 76/F S6 HCC Primary tumor Not reported Not reported
224 Ueda et al (2013) 63/F S7 HCC Primary tumor Not reported Ischemia (Hypotension during dialysis)
225 Bhardwaj et al (2014) 74/M Left lobe HCC Primary tumor Not reported Not reported
226 Chiesara et al (2014) 65/M S6 HCC Primary tumor (partial) 2 years Herbal remedies; Ischemia; Inflammatory Processes
227 Inoue et al (2014) 57/M S5 HCC Primary tumor Not reported Drugs (Inhibition of angiogenesis by rifampicin & minocycline)
228 Lim et al (2014) 64/M Right lobe HCC Primary tumor 6 months Immunological; Herbal medicine
229 Miyake et al (2014) 79/M S6/8 HCC Primary tumor 1 month Tumor Hypoxia (thick capsule)
230 Saito et al (2014) 74/M S8 HCC Primary tumor (partial) 2 months Immunological; Cessation of drinking & smoking
231 Tomino et al (2014) 77/M S1 HCC Primary tumor 1 month Hypoxia; Fever; Biopsy
232 Tsai et al (2014) 74/M Left lobe HCC Primary tumor 4 years Not reported
233 Zhao et al (2014) 22/F Diffuse hepatic HEHE Primary tumor (partial) 3 years Not reported
234 Parks et al (2015) 69/M S8 HCC Recurrent Hepatic Lesions 6 months* Immunological (Vitiligo autoimmunity)
235 Parks et al (2015) 63/M S7 cHCC-CC Retroperitoneal lymph metastases 2 months Immunological
236 Parks et al (2015) 67/M Left lobe HCC Primary tumor 5 months Immunological
237 Kim et al (2015) 57/M S6 HCC Primary tumor Not reported Immunological; Ischemia
238 Kohda et al (2015) 80/M S1 HCC Primary tumor Not reported Ischemia (rapid growth)
239 Kuwano et al (2015) 84/M S4 HCC Primary tumor Not reported Ischemia
240 Matsuoka et al (2015) 67/M S6 HCC Primary tumor 3 years Hypoxia; Hepatic arterial & portal vein thromboses
241 Okano et al (2015) 73/M S8 HCC Primary tumor 6 months Ischemia; Angiography
242 Sugamoto et al (2015) 77/F S3 HCC Primary tumor 9 months Immunological (weight loss)
243 Takeda et al (2015) 68/M S4 HCC Primary tumor (partial) 1 year Hypoxia; Vessel thrombosis
244 Tazawa et al (2015) 77/M S7 HCC Primary tumor 3 months Ischemia (postoperative hypotension)
245 Verla-Tebit et al (2015) 53/M Right lobe HCC Primary tumor & lung metastases (partial) 1.5 years Anti-hepaciviral medication for Hepatitis C (sorafenib & ribavirin)
246 Wang et al (2015) 50/M S7/8 HCC Primary tumor Not reported Immunological
247 Yang et al (2015) 59/M S6 HCC Primary tumor 6 months Seroconversion of HBV
248 Yoo et al (2015) 62/M S5 HCC Primary tumor (partial) 2 years Immunological; Hypoxia/Ischemia
249 Gunasekaran et al (2016) 49/M Left lobe HCC Pulmonary metastases 5 months Consumption of Guaynabo fruit extract
250 Heron et al (2016) 61/F S7 HCC Primary tumor 1 year Withdrawal of azathioprine in Crohn's Disease; Biopsy
251 Jianxin et al (2016) 64/M S6 HCC Tumor recurrence and omental metastases 2.5 years Immunological; Herbal medicine
252 Kumar et al (2016) 40/M S2/3/5 HCC Primary tumor 7 years Cessation of immunosuppressive therapy
253 Kumar et al (2016) 74/M Right HCC Primary tumor (partial) 8 months Cessation of immunosuppressive therapy
254 Luo et al (2016) 61/F S4 HCC Primary tumor 2.5 years Cirrhosis related hypoxia
255 Mahmood et al (2016) 59/M S4/8 HCC Primary tumor 4 months Anti-hepaciviral medication for Hepatitis C (sorafenib & ribavirin)
256 Ooka et al (2016) 63/M S7/8 HCC Primary tumor 6 months Ischemia (PVT)
257 Pectasides et al (2016) 53/M S4 HCC Primary (partial) & lung metastases (partial) 2 months Portal vein thrombosis; Immunological reaction
258 Sawatsubashi et al (2016) 59/M S5-8 HCC Primary tumor 1 month Tumor Hypoxia (thick capsule)
259 Sugiura et al (2016) 90/F S6 HCC Primary tumor Not reported Not reported
260 Alam et al (2017) 65/M S5/6 HCC Primary tumor (partial) 3 months Immunological
261 Iwatani et al (2017) 59/M S8 HCC Primary tumor Not reported Ischemia (Duodenal Ulcer)
262 Murata et al (2017) 67/M S1/8 HCC Primary tumor 2 months Ischemia
263 Noij et al (2017) 74/M Diffuse hepatic HCC Primary (partial) & lung metastases 6 months Not reported
264 Oyama et al (2017) 79/M Diffuse hepatic HCC Primary tumor Not reported Hypoxia
265 Oyama et al (2017) 78/F Left lobe HCC Primary tumor Not reported Inflammatory; Immunological; Infection (Bacterial)
266 Sakamaki et al (2017) 78/M S8 HCC Primary tumor & lymph metastases 3 months Immunological; hemodialysis
267 Sano et al (2017) 30/F Common bile duct NET Primary tumor Not Reported Biopsy; Central necrosis
268 Yamaguchi et al (2017) 63/M Right lobe HCC Primary tumor Not reported Not reported
269 Yamaguchi et al (2017) 67/M S5 HCC Primary tumor Not reported Not reported
270 Yamaguchi et al (2017) 84/F S7 HCC Primary tumor Not reported Not reported
271 Yamaguchi et al (2017) 60/M S8/S1 HCC Primary tumor Not reported Not reported
272 El-Badrawy et al (2018) 45/F Porta hepatis DLBCL Primary tumor 18 days Biopsy (Aspiration); Regional immune reaction
273 Goto et al (2018) 64/M S6/7 HCC Primary tumor 1 month Portal vein thrombosis; Immunological
274 Koya et al (2018) 83/M S2/3/4 HCC Primary tumor 1 year PVT
275 Lee et al (2018) 67/M Diffuse hepatic HCC Primary tumor 1 year Infection (diabetic foot); Ischemia (obstruction of portal vein thrombosis)
276 Taniai et al (2018) 74/M S7 HCC Primary tumor 2 years Not Reported
277 Taniguchi et al (2018) 70/M S3 HCC Primary tumor Not reported Ischemia (dialysis); Drugs (Elythrocin Steroids)
278 Alhatem et al (2019) 60/M Right lobe DLBCL Primary tumor 4 years Immunological (HIV, Hep C); Genetic
279 Chohan et al (2019) 79/F S6 HCC Primary (partial) & lung metastases 1.5 years* Ischemia; Immunological
280 Fujikawa et al (2019) 78/M S2/7 HCC Primary tumor Not reported Anemia (fracture)
281 Hirota et al (2019) 67/M S7 HCC Primary tumor Not reported Ischemia; Cessation of alcohol and smoking
282 Kim et al (2019) 70/M Bile duct CCA Liver Metastasis 3 months Abscopal effect; Post-radiotherapy antitumoral immunity
283 Kawaguchi et al (2019) 68/M S3 HCC Primary tumor 2.5 months Antiangiogenesis (SGLT2i)
284 Lee et al (2019) 78/F S5-8 HCC Primary tumor 1 month Immunological; Ischemia (rapid tumor growth or disruption of feeding artery)
285 Yoshida et al (2019) 71/F Right lobe Clear cell HCC Primary tumor 1 year Not reported
286 Arjunan et al (2020) 53/M Liver HCC Pulmonary, Omental, retroperitoneal metastases 5 years Immunological
287 Arjunan et al (2020) 48/M Left Lobe HCC Pulmonary metastases 13 years Immunological
288 Arjunan et al (2020) 62/M Liver HCC Systemic metastases 11 years Immunological
289 Arjunan et al (2020) 73/M Liver HCC Primary tumor 6 years Immunological
290 Costa-Santos et al (2020) 68/M S4 HCC Hepatic lesions 5 years Megestrol; Herbal remedies
291 Hokkoku et al (2020) 77/M S6 HCC Primary tumor Not reported Not reported
292 Muroya et al (2020) 78/M Right lobe HCC Lung metastases 1 year Hypoxia; Immunological; Dialysis
293 Nakamoto et al (2020) 74/M Right lobe HSTCL Hepatic, splenic, & osseous lesions 1.5 months Biopsy
294 Ohmatsu et al (2020) 77/M Right lobe HCC Lung metastases 1 month Abscopal Effect
295 Onishi et al (2020) 28/M Left lobe HEHE Primary lesion (partial) 6 years* Unpredictable growth (new lesions)
296 Onishi et al (2020) 44/M Unspecified liver HEHE Primary lesion (partial) 4 years* Unpredictable growth (new lesions)
297 Onishi et al (2020) 47/M Unspecified liver HEHE Primary lesion (partial) 12 years Calcification
298 Onishi et al (2020) 51/F S6 HEHE Primary lesion (partial) 11.5 years* Unpredictable growth (new lesions)
299 Onishi et al (2020) 61/F Unspecified liver HEHE Primary lesion (partial) 5.5 years* Unpredictable growth (new lesions)
300 Onishi et al (2020) 63/M Unspecified liver HEHE Primary lesion (partial) 6 years* Unpredictable growth (new lesions)
301 Raufi et al (2020) 63/M Porta hepatis PHNEC Pulmonary metastases 2 months Immunological
302 Sakamoto et al (2020) 62/M S3 HCC Primary tumor Not reported Ischemia
303 Sakamoto et al (2020) 75/F S4 HCC Primary tumor Not reported Tumor hypoxia  (bleeding from rectal varicose veins)
304 Sonbare et al (2020) 74/M S8 HCC Primary tumor 1 year Immunological; Ischemia
305 Franses et al (2021) 64/M S4 HCC Primary tumor 2 months Immunological
306 Kakuta et al (2021) 71/M Not reported HCC Lung metastases 3 months* TACE of Primary
307 Kimura et al (2021) 84/F S8 HCC Primary tumor (partial) Not reported Immunological
308 Liu et al (2021) 67/M Diffuse hepatic HCC Pulmonary metastases 5 months Immunological; Chinese herbal remedies
309 Obu et al (2021) 83/M S2 HCC Primary tumor 1 year Ischemia (rapid growth); Capsule formation; PVT
310 Tanaka et al (2021) 71/F Diffuse hepatic HHL Hepatic lesions 1 year Cessation of immunosuppressive therapy
Pancreatic cancer 311 Shapiro (1967) ?/F Unspecified pancreas PDAC Primary tumor 7.5 years Not reported
312 Lokich et al (1973) 42/M Pancreatic head PDAC Primary tumor 2 years* Not reported
313 Eidemiller et al (1971) ?/M Pancreatic head PDAC Primary tumor 6 years Not reported
314 Tchertkoff et al (1974) 21/M Pancreatic head PDAC Primary tumor 12 years Bacterial Infection
315 Cann et al (2003) 50/M Pancreatic body PDAC Primary tumor 6 months Acute febrile response; alternative therapies; Chinese herbs; High-dose Vitamin C
316 Chin et al (2017) 77/M Pancreatic head PDAC Primary tumor & liver metastases 1 year Leukocyte activation; Fever; Allergenic & hormonal influences
317 Sreevathsa et al (2018) 32/M Pancreatic body pNET (Carcinoid) Primary tumor 19 years Apoptosis (cytokines); VEGF blockade
318 Lemus et al (2019) 56/F Pancreatic body/tail PDAC Primary tumor & liver metastases 3 years Immunogenic; angiogenic effects on the tumor microenvironment.
319 Ibrahimi et al (2019) 59/F Residual pancreas PDAC Primary tumor (partial) 1 year Acute pancreatitis; Bacterial/fungal infection (abscess)
320 Kawaguchi et al (2021) 66/F Pancreatic tail PDAC Primary tumor (partial) 1 month Not reported
Small bowel cancer 321 Sroujieh et al (1988) 55/M Occult (Ileal lesion) MM Intestinal lesion (occult primary) 7 years Not Reported
322 Nagashima et al (1996) 58/M Duodenum MALT Lymphoma Primary tumor 1 year Eradication of H. Pylori
323 Rayson et al (1996) 45/F Ileum GEP-NET (Carcinoid) Liver metastases 5 months* Valvular surgery for carcinoid heart disease
324 Horiuhi et al (2003) 74/F Diffuse enteric NKTCL Upper Abdominal tumors (non-radiated) 1 year Abscopal Effect
325 Makino et al (2010) 38/M Terminal Ileum MALT Lymphoma Primary tumor & ileocecal lymphadenopathy 1 year Resolution of infection; Inflammatory
326 Hayashi et al (2013) 64/F Duodenum FL Primary tumor 5.5 years Eradication of H. Pylori
327 Tanaka et al (2014) 61/F Duodenum SBAC Primary tumor & liver metastases 4 months Methotrexate
328 Sasaki et al (2016) 60/M Ileum RL Primary tumor Not reported* Radiography Radiation
329 Hori et al (2017) 20/F Small intestine EAS Lung & mediastinal lymph metastases 2 months Immunological; Biopsy (transbronchial); Inflammatory
330 Tanaka et al (2019) 35/M Small intestine DLBCL Primary tumor & lymph metastases 3 years Immunological (PD-L1/PD-1 axis)
Colorectal cancer 331 Most (1927) 57/M Rectum CRAC Local recurrence 9 years Sepsis
332 Henry (1944) 60/M Rectum CRAC Primary tumor & liver metastases 11 years Not reported
333 Fergeson (1954) 45/M Descending colon CRAC Primary tumor with local extension 10 years Severe sepsis (abscess)
334 Dunphy (1956) 46/M Rectum CRAC Primary tumor & liver metastases 8 years Severe debilitation; Fecal diversion
335 Ellison (1956) 59/M Rectum CRAC Peritoneal carcinomatosis 3 years Persistent high fever (Pneumonia)
336 Fallis (1959) 42/M Transverse colon CRAC Primary tumor with local extension 18 years Severe sepsis (abscess); Fecal diversion; Religious rituals
337 Brown (1961) 54/F Sigmoid colon CRAC Primary tumor & liver metastases 3 years Not reported
338 Brunschwig et al (1963) 68/F Rectum CRAC Local recurrence 14 years Not reported
339 Mayo et al (1963) 63/F Descending colon CRAC Liver metastases 16 years Not reported
340 Fullerton & Hill (1963) 58/F Transverse colon Anaplastic CRAC Primary tumor 16 years Not reported
341 Rankin et al (1965) 44/M Rectum CRAC Liver metastases 9 years Not reported
342 Margolis & West (1967) 71/M Rectum CRAC Peritoneal carcinomatosis 1 year Fecal diversion
343 Synder et al (1968) 62/F Sigmoid colon CRAC Primary tumor with local extension 15 years Persistent high fever (wound infection); Immunologic; Genetic
344 Synder et al (1968) 60/M Cecum CRAC Peritoneal carcinomatosis 9 years Severe Sepsis (abscess w/ fecal fistula); Immunologic; Genetic
345 Weinstock (1977) 40/F Sigmoid colon CRAC Primary tumor with local extension & liver metastases 20 years Psychological
346 Meares (1979) 64/M Rectum CRAC Primary tumor 1 year Intensive meditation
347 Glasser et al (1979) 36/M Ascending colon CRAC Primary tumor & peritoneal carcinomatosis 28 years Genetic factors
348 Beechy et al (1986) 23/F Ascending colon CRAC Primary tumor with local extension, peritoneal, & liver metastases 4 years Not reported
349 Tominaga et al (1999) 44/F Transverse colon CRAC Primary tumor 3 years Dislodged
350 Wadsworth et al (1999) 67/M Rectum CRAC Pulmonary metastases 3 years Infection (Pneumonia)
351 Okamura et al (2000) 54/M Rectum MALT Lymphoma Primary tumor Not reported Not reported
352 Kamesui et al (2000) 66/F Ascending colon CRAC Primary tumor 1 year Dislodged
353 Takenaka et al (2000) 76/F Rectum MALT Lymphoma Primary tumor 1.5 years Not reported
354 Ikuta et al (2002) 60/M Rectum ASC Liver metastases 2 years Interruption of blood supply; growth factors
355 Abdelrazeq et al (2005) 51/M Rectum CRAC Local recurrence & peritoneal carcinomatosis 16 years Immunologic; Metabolic; Endocrine; Diversion of carcinogen
356 Itano et al (2006) 63/M Rectum MM Primary tumor 2 years Dislodged
357 Tomiki et al (2007) 80/F Rectum CRAC Primary tumor 5 years Dislodged
358 Kochi et al (2008) 80/M Transverse colon CRAC Primary tumor 3 years Dislodged
359 Bir et al (2009) 86/F Ascending colon CRAC Peritoneal lymph node metastases 2 years Immunologic
360 Sakamoto et al (2009) 80/M Rectum CRAC Primary tumor 3 months Immunological
361 Shimizu et al (2010) 80/M Transverse colon CRAC Primary tumor 5 years Physical stimulation (peristaltic movement; dislodged)
362 Sakuma et al (2011) 64/M Sigmoid colon CRAC Primary tumor 3 months* Not reported
363 Nakashima et al (2012) 76/F Ileocecal junction CRAC Primary tumor 2 months Dislodged
364 Flynn et al (2013) 36/M Descending colon/rectum DLBCL Primary tumor 6 months Cessation of immunosuppressive therapy (infliximab & azathioprine)
365 Flynn et al (2013) 52/M Sigmoid colon HL Primary tumor 1 year Cessation of immunosuppressive therapy (infliximab & azathioprine)
366 Nakamura et al (2013) 60/M Rectum CRAC Primary tumor 1.5 years Biopsy; Immunological
367 Sekiguchi et al (2013) 76/F Cecum CRAC Primary tumor 1.5 months Hyperimmunity & perioperative stress (lung surgery)
368 Kihara et al (2014) 64/M Transverse colon CRAC Primary tumor 1.5 months Immunological
369 Mitchell et al (2014) 75/F Cecum MC Regional lymph metastases 1 year Immunological
370 Sewpaul et al (2014) 35/F Appendix (presumed) GEP-NET (Carcinoid) Primary tumor 1 year Pregnancy
371 Kyoichi et al (2015) 65/M Transverse colon CRAC Primary tumor 1.5 months Drugs (Metformin); Immunological
372 Serizawa et al (2015) 75/M Transverse colon CRAC Primary tumor 2.5 months Immunological; Apoptosis
373 Ito et al (2016) 73/M Ascending colon CRAC Primary tumor 3.5 months Biopsy; mechanical stimulation (intestinal peristalsis)
374 Nemésio et al (2016) 51/F Splenic angle CRAC Liver metastases Not reported Removal of Primary; Tumor necrosis
375 Chida et al (2017) 80/M Transverse colon CRAC Primary tumor 1 month Immunological (CD4 +T-cells)
376 Matsuki et al (2016) 72/F Ascending colon CRAC Liver metastases 2 months Infection (Biliary S/P pancreaticoduodenectomy)
377 Chuang et al (2018) 74/F Occult CRAC Lung metastases 2 months Abscopal effect
378 Yoshida et al (2018) 73/M Transverse colon CRAC Primary tumor 2.5 months Not reported
379 Fukutomi et al (2019) 87/F Transverse colon CRAC Primary tumor 1 month Immunological (CD8+ T-cells)
380 Karakuchi et al (2019) 70/M Transverse colon CRAC Primary tumor 2 months Immunological; Biopsy
381 Kawakita et al (2019) 62/M Ascending colon CRAC Primary tumor 1 month Immunological (CD4 +T-cells)
382 Tanaka et al (2019) 63/F Sigmoid colon CRAC Primary tumor 2.5 months Injection for non-lifting sign; Ischemia (vasoconstriction S/P epinephrine)
383 Utsumi et al (2020) 78/M Ascending colon CRAC Primary tumor 1 month Immunological (dMMR)
384 Utsumi et al (2020) 66/M Ascending colon CRAC Primary tumor 1.5 months Immunological (dMMR)
385 Utsumi et al (2020) 73/M Ascending colon CRAC Primary tumor 1.5 years Immunological (dMMR)
386 Mehawej et al (2020) 18/F Occult CRAC Primary tumor Unknown Not reported
387 Nishiura et al (2020) 67/F Transverse colon CRAC Primary tumor 3 months Immunological
388 Yokota et al (2020) 76/F Transverse colon CRAC Primary tumor 2 months Immunological
389 Yokota et al (2020) 64/F Cecum CRAC Primary tumor 3 months Immunological
390 Yokota et al (2020) 64/M Transverse colon CRAC Primary tumor 1 month Immunological
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218 Yamamoto, S., Tokuhara, T., Nishikawa, M., Nishizawa, S., Nishioka, T., Nozawa, A., … Kubo, S. (2012). Spontaneous regression of hepatocellular carcinoma after improving diabetes mellitus: possibly responsible for immune system. Kanzo, 53(3), 164–174. 
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238 幸田昌樹, 杉浦 愛, 森 弘樹. 経過中に一時自然退縮を認めた肝細胞癌の1例. 浜松医療センター学術誌 2015; 9: 130-133
239 桑野哲史, 宮ケ原典, 多喜研太郎, 他. 自然退縮が疑われた肝腫瘤の1例. 診断と治療 2015; 103: 697-701
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242 菅本祐司, 太田拓実, 木村正幸, 他. 肥満患者の減量中に自然退縮した肝細胞癌の1例. 千葉医学 2015; 91: 59-63
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244 Tazawa, H., Fukuda, S., Fujisaki, S., Sakimoto, H., Eto, T., Moriya, T., … Nishida, T. (2015). Suggesting of spontaneous complete necrosis of hepatocellular carcinoma: Report of a case. Kanzo, 56(12), 645–654.
245 Verla-Tebit E, Rahma OE. Regression of hepatocellular carcinoma after treatment of hepatitis C: a case report. J Gastrointest Oncol. 2015 Jun;6(3):E52-4.
246 Wang Z, Ke ZF, Lu XF, Luo CJ, Liu YD, Lin ZW, Wang LT. The clue of a possible etiology about spontaneous regression of hepatocellular carcinoma: a perspective on pathology. Onco Targets Ther 2015; 8: 395-400
247 Yang SZ, Zhang W, Yuan WS, Dong JH. Recurrence of Hepatocellular Carcinoma With Epithelial-Mesenchymal Transition After Spontaneous Regression: A Case Report. Medicine (Baltimore) 2015;94:e1062.
248 Yoo YJ, Kim JH. [Spontaneous Complete Remission of Hepatocellular Carcinoma]. Korean J Gastroenterol. 2015 Dec;66(6):359-62. Korean. doi: 10.4166/kjg.2015.66.6.359. PMID: 27175457.
249 Gunasekaran SS, Emmadi R, Landers LA, Gaba RC. Regression of Hepatocellular Carcinoma Lung Metastases after Guyabano Fruit Extract Consumption. J Diet Suppl. 2016;13(3):237-44. doi: 10.3109/19390211.2015.1008613. Epub 2015 Feb 9. PMID: 25664807.
250 Heron V, Fortinsky KJ, Spiegle G, Hilzenrat N, Szilagyi A. Resected hepatocellular carcinoma in a patient with Crohn’s disease on azathioprine. Case Rep Gastroenterol 2016;10:50-6.
251 Jianxin C, Qingxia X, Junhui W, Qinhong Z. A Case of Recurrent Hepatocellular Carcinoma Acquiring Complete Remission of Target Lesion With Treatment With Traditional Chinese Medicine. Integr Cancer Ther. 2016 Epub ahead of print.
252 Kumar A, Le DT. Hepatocellular Carcinoma Regression After Cessation of Immunosuppressive Therapy. J Clin Oncol. 2016;34:e90–e92.
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254 Luo, S. C., Wu, C. C., Jheng, S. B., & Huang, Z. Y. (2016). Spontaneous remission of hepatocellular carcinoma without any treatment. Journal of Cancer Research and Practice, 3(4), 128-131.
255 Mahmood, Shafaq & Gul, Aleesha & Saif, Tayyaba. (2016). Regression of hepatocellular carcinoma after treatment with Sofosbuvir - A case report. JPMA. The Journal of the Pakistan Medical Association. 66. 1507-1509.
256 Ooka, Y., Chiba, T., Inoue, M., Wakamatsu, T., Saito, T., Sekimoto, T., … Yokosuka, O. (2016). A case of hepatocellular carcinoma with spontaneous regression of a tumor thrombus invading the main portal trunk. Kanzo, 57(4), 178–185. 
257 Pectasides E, Miksad R, Pyatibrat S, Srivastava A, Bullock A. Spontaneous regression of hepatocellular carcinoma with multiple lung metastases: A case report and review of the literature. Dig Dis Sci 2016;61:2749-54.
258 Sawatsubashi, Y., Abe, Y., Nishihara, K., Takesue, S., Nakashima, Y., & Nakano, T. (2016). A Spontaneous Complete Regression of Hepatocellular Carcinoma. The Japanese Journal of Gastroenterological Surgery, 49(6), 488–495. 
259 杉浦 玄.高齢女性に発症し自然退縮した肝細胞が んの 1 例.内科 2016;117:329―331
260 Alam MA, Das D. Spontaneous Regression of Hepatocellular Carcinoma-a Case Report. J Gastrointest Cancer. 2017;48:194–197.
261 Iwatani, Y., Kuroda, D., Abe, T., Kohama, T., Urade, T., Murata, K., … Oka, S. (2017). A case of complete spontaneous necrosis with residual intrahepatic metastasis of hepatocellular carcinoma. Kanzo, 58(3), 170–175.
262 Murata, R., Kamiyama, T., Kanno, H., Yokoo, H., Orimo, T., Wakayama, K., … Taketomi, A. (2017). Spontaneous Complete Regression of a Hepatocellular Carcinoma with Hepatic Vein Tumor Thrombosis. The Japanese Journal of Gastroenterological Surgery, 50(7), 535–543.
263 Noij DP, van Der Linden PW.Spontaneous regression of hepatocellular carcinoma in a Caucasian male patient: A case report and review of the literature. Mol Clin Oncol 2017;6:225-8.
264 大山 潤,山下 航,川田秀一,他.肝細胞癌の自 然退縮と考えられた 2 例.臨床放射線 2017;62: 469―473
265 大山 潤,山下 航,川田秀一,他.肝細胞癌の自 然退縮と考えられた 2 例.臨床放射線 2017;62: 469―474
266 Sakamaki A, Kamimura K, Abe S, et al. Spontaneous regression of hepatocellular carcinoma: A mini-review. World J Gastroenterol 2017; 23 (21): 3797― 3804
267 Sano I, Kuwatani M, Sugiura R, Kato S, Kawakubo K, Ueno T, Nakanishi Y, Mitsuhashi T, Hirata H, Haba S, Hirano S, Sakamoto N. Hepatobiliary and Pancreatic: A rare case of a well-differentiated neuroendocrine tumor in the bile duct with spontaneous regression diagnosed by EUS-FNA.
268 山口晃典,藪崎哲史,加藤扶美,他.肝細胞癌の自 然退縮と考えられた 4 症例.臨床放射線 2017;62: 781―789
269 山口晃典,藪崎哲史,加藤扶美,他.肝細胞癌の自 然退縮と考えられた 4 症例.臨床放射線 2017;62: 781―789
270 山口晃典,藪崎哲史,加藤扶美,他.肝細胞癌の自 然退縮と考えられた 4 症例.臨床放射線 2017;62: 781―789
271 山口晃典,藪崎哲史,加藤扶美,他.肝細胞癌の自 然退縮と考えられた 4 症例.臨床放射線 2017;62: 781―789
272 El-Badrawy A, Abd El-Wahab R, Emarah Z, Eisa N. Rapid Spontaneous Regression of Diffuse Large B-Cell Lymphoma after Fine Needle Aspiration Cytology: A Case Report. Clin Oncol. 2018; 3: 1455.
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275 Lee J, Lee N, Yoon K, et al. Cystic degeneration of hepatocellular carcinoma mimicking mucinous cystic neoplasm. Korean J Gastroenterol 2019; 73: 303―307
276 Taniai T, Shirai Y, Shiba H, Sakamoto T, Furukawa K, Yanaga K. Spontaneous pathological complete regression of hepatocellular carcinoma. Case Rep Gastroenterol 2018;12:653-9.
277 Taniguchi, M., Sakuma, Y., Koizumi, M., Sasanuma, H., Lefor, A. K., & Sata, N. (2018). Spontaneous Complete Necrosis of Hepatocellular Carcinoma—A Case Report—. Nihon Rinsho Geka Gakkai Zasshi (Journal of Japan Surgical Association), 79(9), 1922–1927.
278 Alhatem, A., Badeti, S., Liu, C., Liu, D., & Cai, D. (2019). Spontaneous Regression of Hepatic Diffuse Large B-cell Lymphoma in HIV and HCV Positive Patient: A Novel Case Study. Int J Cancer Clin Res, 6, 127.
279 M.B.Y. Chohan, N. Taylor, C. Coffin, K.W. Burak, O.F. Bathe, Spontaneous regression of hepatocellular carcinoma and review of reports in the published English literature, Case Rep. Med. 2019 (2019), 9756758.
280 Koichi Fujikawa, Ken Fujishiro, Harufumi Makino, et al. Spontaneous regression of multiple hepatocellular carcinoma and peritoneal disseminations. Rinsho Geka 2019; 74: 763-767
281 Masashi Hirota, Hiroki Murakami, Koichi Omoto, et al. A case of hepatocellular carcinoma with spontaneous regression caused by temperance and non-smoking. Surgery 2019; 81: 284-287
282 Kim, J.O.; Kim, C.A. Abscopal Resolution of a Hepatic Metastasis in a Patient with Metastatic Cholangiocarcinoma Following Radical Stereotactic Body Radiotherapy to a Synchronous Early Stage Non-small Cell Lung Cancer. Cureus 2019, 11, e4082.
283 Kawaguchi T, Nakano D, Okamura S, et al. Spontaneous regression of hepatocellular carcinoma with reduction in angiogenesis-related cytokines after treatment with sodium-glucose cotransporter 2 inhibitor in a cirrhotic patient with diabetes mellitus. Hepatology Research 2019; 49: 479―486
284 Lee J, Lee N, Yoon K, et al. Cystic degeneration of hepatocellular carcinoma mimicking mucinous cystic neoplasm. Korean J Gastroenterol 2019; 73: 303―307
285 Yoshida, T., Yoshida, S., Yamagishi, T., Yamane, H., Matsumoto, T., Kobayashi, A., … Tominaga, M. (2019). Clear Cell Type of Hepatocellular Carcinoma with a Slow Progression Accompanied by Natural Necrosis. The Japanese Journal of Gastroenterological Surgery, 52(9), 513–520. 
286 Arjunan, V., Hansen, A., Deutzmann, A., Sze, D. Y., & Dhanasekaran, R. (2021). Spontaneous Regression of Hepatocellular Carcinoma: When the Immune System Stands Up to Cancer. Hepatology (Baltimore, Md.), 73(4), 1611-1614.
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290 Costa-Santos, M. P., Gonçalves, A., Ferreira, A. O., & Nunes, J. (2020). Spontaneous regression of hepatocellular carcinoma: myth or reality? BMJ Case Reports CP, 13(2), e233509.
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298 Onishi, Y., Kusumoto, M., Motoi, N., Hiraoka, N., Sugawara, S., Itou, C., & Sone, M. (2021). Natural history of epithelioid hemangioendothelioma of the liver: CT findings of 15 cases. Academic Radiology, 28(6), 778-782.
299 Onishi, Y., Kusumoto, M., Motoi, N., Hiraoka, N., Sugawara, S., Itou, C., & Sone, M. (2021). Natural history of epithelioid hemangioendothelioma of the liver: CT findings of 15 cases. Academic Radiology, 28(6), 778-782.
300 Onishi, Y., Kusumoto, M., Motoi, N., Hiraoka, N., Sugawara, S., Itou, C., & Sone, M. (2021). Natural history of epithelioid hemangioendothelioma of the liver: CT findings of 15 cases. Academic Radiology, 28(6), 778-782.
301 Raufi, A. G., May, M., Greendyk, R. A., Iuga, A., Ahmed, F., Mansukhani, M., & Manji, G. A. (2020). Spontaneous Regression and Complete Response to Immune Checkpoint Blockade in a Case of High-Grade Neuroendocrine Carcinoma. JCO Precision Oncology, (4), 1006–1011.
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380 Karakuchi N, Shimomura M, Toyota K, Hinoi T, Yamamoto H, Sadamoto S, Mandai K, Egi H, Ohdan H, Takahashi T. Spontaneous regression of transverse colon cancer with high-frequency microsatellite instability: a case report and literature review. World J Surg Oncol. 2019 Jan 15;17(1):19.
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383 Utsumi T, Miyamoto S, Shimizu T, et al. Spontaneous regression of mismatch repair-deficient colorectal cancers: a case series. Dig Endosc 2020. Epub 2020/05/18.
384 Utsumi T, Miyamoto S, Shimizu T, et al. Spontaneous regression of mismatch repair-deficient colorectal cancers: a case series. Dig Endosc 2020. Epub 2020/05/18.
385 Utsumi T, Miyamoto S, Shimizu T, et al. Spontaneous regression of mismatch repair-deficient colorectal cancers: a case series. Dig Endosc 2020. Epub 2020/05/18.
386 Mehawej, J., El Helou, N., Pejovic, T., & Mhawech-Fauceglia, P. (2020). Metastatic colorectal carcinoma to one ovary with vanishing primary: A case report in an 18-year-old patient. Clin Obstet Gynecol, 6, 1-3.
387 Nishiura, B., Kumamoto, K., Akamoto, S., Asano, E., Ando, Y., Suto, H., ... & Suzuki, Y. (2020). Spontaneous regression of advanced transverse colon cancer with remaining lymph node metastasis. Surgical Case Reports, 6(1), 1-6.
388 Yokota, T., Saito, Y., Takamaru, H., Sekine, S., Nakajima, T., Yamada, M., ... & Matsuda, T. (2021). Spontaneous Regression of Mismatch Repair-Deficient Colon Cancer: A Case Series. Clinical Gastroenterology and Hepatology, 19(8), 1720-1722.
389 Yokota, T., Saito, Y., Takamaru, H., Sekine, S., Nakajima, T., Yamada, M., ... & Matsuda, T. (2021). Spontaneous Regression of Mismatch Repair-Deficient Colon Cancer: A Case Series. Clinical Gastroenterology and Hepatology, 19(8), 1720-1722.
390 Yokota, T., Saito, Y., Takamaru, H., Sekine, S., Nakajima, T., Yamada, M., ... & Matsuda, T. (2021). Spontaneous Regression of Mismatch Repair-Deficient Colon Cancer: A Case Series. Clinical Gastroenterology and Hepatology, 19(8), 1720-1722.

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