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. 2025 Jul 1;13(7):e70591. doi: 10.1002/ccr3.70591

Acute Myeloid Leukemia With Extramedullary Infiltration‐Gastric Myeloid Sarcoma: A Case Report and Literature Review

Cong Ding 1,2, Jianfeng Yang 1,2, Chang Shao 3, Bin Yang 4, Qiang Liu 1,2, Yishen Mao 1,2, Qi Ding 1,2, Jing Yang 1,2,✉
PMCID: PMC12213607  PMID: 40607281

ABSTRACT

Gastric myeloid sarcoma (MS) is a rare disease with numerous endoscopic manifestations and is typically diagnosed on the basis of immunohistochemistry. However, the epidemiology, treatment, and prognosis of gastric MS remain controversial. The goal of this study is to preliminarily analyze these controversial aspects of gastric MS.

Keywords: acute myeloid leukemia, case report, diagnosis, myeloid sarcoma, treatment

1. Introduction

Myeloid sarcoma (MS) is a solid tumor formed by extramedullary infiltration of hematopoietic blasts and recognized as a distinct entity under acute myeloid leukemia (AML) and related myeloid neoplasms in the 2008 World Health Organization classification [1]. MS is often closely related to AML and occurs in approximately 2%–9% of AMLs [2]. The incidence of MS in children (30%) is higher than in adults (2%–5%) [3]. The diagnosis of MS is based mainly on histopathology and immunohistochemical staining analysis [4, 5]. The commonest sites of clinical manifestation of MS are skin, bone, spine, and lymph nodes [6]. Gastrointestinal involvement is rare, and the endoscopic manifestations have not been systematically described [7, 8].

Here, we report one case of MS diagnosed by endoscopy and review and comprehensively analyze the endoscopic manifestations, histopathology and immunohistochemical characteristics of 34 cases of gastric MS (Table 1) to provide insights for clinical diagnosis and treatment [4, 5, 6, 7, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36].

TABLE 1.

Characteristics of reported cases of gastric MS.

Case Study Age Gender Hematological disease and condition Esophagogastroduodenoscopy Histologic evaluation Immunohistochemistry (+) Treatment Prognosis (months)
Location Lesion no. Shape Surface form
1 Nidal 2024 20 Male No Cardia, fundus, body Multiple Large mass Nodule Atypical cells CD34, CD43, CD33 RC + C NM
2 Xiang 2023 64 Female No Body Single Large mass Nodule, ulcer Neoplastic cells CD34, CD43, lysozyme, CD56, CD4 RC + C NM
3 Lu 2022 33 Female No Antrum Multiple Polypoid mass Ulcer Inflammation CD34, MPO, CD117, CD56 C Dead (6)
4 Patricia 2021 19 Female No Body Diffuse Thickened folds Normal Blast‐like cells CD34, MPO, CD117 C Dead (1)
5 Sugeeth 2019 55 Male No Cardia, body Diffuse Thickened folds Normal Blast‐like cells MPO, CD43, CD33 C Alive (3)
6 Tursi 2018 26 Male No NM NM NM NM Immature myeloid cells CD34, MPO, LAC, CD15 C NM
7 Xiao 2016 38 Male No Body Multiple Polypoid mass Congestion Atypical cells CD34, MPO, CD117, CD43, CD68, CD99 C Alive (3)
8 Pankit 2014 52 Female No Fundus Single Large mass Normal Atypical cells CD34, CD117, CD43, CD33, CD68, CD4, CD45, CD163, CD45 C + R Dead (several)
9 Enrico 2008 40 Male No Fundus, body Diffuse Thickened folds Normal Neoplastic cells CD34, MPO, CD117, CKIT C + RC + HSCT Dead (several)
10 Yutaka 2020 38 Male No Fundus Single Large mass Nodule, ulcer Blast‐like cells MPO, CKIT C + HSCT Alive (36)
11 Abdullah 2023 68 Female AML remission Body Single Large mass Nodule, ulcer Blast‐like cells CD34, CD117, CD43, CD33 C Dead
12 Chana 2021 59 Male AML remission Body Multiple Polypoid mass Normal Blast‐like cells NM C NM
13 Chia 2016 63 Female AML remission Fundus, body Multiple Polypoid mass Ulcer, congestion Atypical cells CD34, MPO, CD117 RC + R Alive
14 Akinori 2011 42 Female AML remission Body Single Large mass Ulcer Blast‐like cells CD34 C Alive (120)
15 Jalil 2011 34 Female AML remission Cardia Diffuse Large mass Normal Neoplastic cells MPO C + HSCT Dead (several)
16 Choi 2010 38 Female AML remission Body Diffuse Thickened folds Congestion Immature myeloid cells MPO, lysozyme, CD56, CD13 C Dead (3)
17 Abdullah 2020 68 Female AML remission Body Single Large mass Nodule, ulcer Blast‐like cells CD34, CD117, CD43, CD68 C Dead (5)
18 Amy 2021 69 Male MDS remission Fundus, antrum Diffuse Erythema Congestion Inflammation CD34, MPO, CD117 C NM
19 Mark 2014 56 Male MDS remission Body Single Large mass Ulcer Blast‐like cells CD34, CD117 C Dead (3)
20 Antonio 2010 18 Male CML remission Fundus, body Multiple Polypoid mass Ulcer Immature myeloid cells NM C Alive (42)
21 Yoko 2022 66 Male AML Body Diffuse Polypoid mass Ulcer Inflammation MPO C + R Alive
22 Pouyan 2021 60 Male AML Fundus, Cardia Single Large mass Ulcer Atypical cells MPO, CD43, CD68 NM NM
23 Sravanthi 2018 49 Male AML NM NM NM NM Blast‐like cells CD34, MPO, CD117, CD43 C + HSCT Alive (6)
24 Tom 2018 63 Male AML Body Single Large mass Normal Immature myeloid cells MPO C Alive
25 Annette 2016 73 Male AML Body Single Polypoid mass Normal Neoplastic cells CD34, CD33, CK18 NM NM
26 Jana 2013 71 Male AML Body Single Polypoid mass Congestion Blast‐like cells CD34, CD117 C Dead (6)
27 Sangeeta 2012 25 Male AML Body Diffuse Thickened folds Normal Neoplastic cells CD34, MPO, CKIT C Dead (0.3)
28 Gadage 2011 35 Male AML Body Multiple Polypoid mass Nodule Atypical cells CD43, CD68, CKIT, LCA C Dead (0.3)
29 Gadage 2011 25 Male AML Total Diffuse Thickened folds Normal Atypical cells CD34, MPO, LCA, CKIT NM Dead (0.5)
30 Anuradha 2011 25 Female AML Fundus, body Diffuse Large mass Nodule Atypical cells CD34, MPO, CD117 NM NM
31 Preasent 2024 49 Male AML Body Single Polypoid mass Normal Atypical cells CD34, MPO, CD117, CD43 ESD + C Alive (1)
32 Wang 2008 86 Female AML Body Multiple Polypoid mass Ulcer Blast‐like cells MPO C Alive (3)
33 Juan 2009 57 Male CML Pylorus Diffuse Large mass Normal Inflammation MPO, CD68, lysozyme NM Dead (0.5)
34 Hisaharu 2009 72 Male TE Body Multiple Polypoid mass Nodule Blast‐like cells CD34, CD117, CD13 NM Dead (5)
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Abbreviations: AML, acute myeloid leukemia; C, chemotherapy; CML, chronic myelomonocytic leukemia; ESD, endoscopic mucosal dissection; HSCT, hematopoietic stem cell transplantation; MDS, myelodysplastic syndrome; NM, no mention; R, radiation therapy; RC, resection; TE, thrombocythemia.

2. Case History/Examination

A 49‐year‐old male patient with fatigue, dysphagia, and weight loss for more than 4 months was admitted to the department of gastroenterology in our hospital. The patient indicated a decreased, and weight loss of approximately 5 kg (The patient's admission weight was 62.5 kg). There was no pressure or rebound pain on abdominal examination, and the lymph nodes of the whole body were not palpable or enlarged. The patient was previously healthy with no history of smoking or alcohol use and no family history of malignant tumors or genetic diseases. Routine blood test results (hemoglobin 130 g/L, platelet count 266 × 109/L, white blood cell counts 6.1 × 109/L), biochemistry results, carcinoma embryonic antigen (CEA) level, and carbohydrate antigen 199 (CA199) level were all within the normal range. Computerized tomography (CT) (Figure 1) of the abdomen revealed a polyp‐like bulge in the stomach wall. Endoscopy (Figure 2A,B) revealed a flat polypoid bulge of approximately 1.2 cm in size on the anterior wall of the upper part of the gastric body, and the surface glandular duct was dilated. Endoscopic diagnosis of fundic adenoma was possible, and endoscopic submucosal dissection (ESD) (Figure 2C) resection was then performed.

FIGURE 1.

FIGURE 1

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CT revealed a polyp‐like bulge in the stomach wall.

FIGURE 2.

FIGURE 2

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Endoscopic examination revealed a flat polypoid bulge on the anterior wall of the upper part of the gastric body, and ESD was performed. (A) White Light Imaging. (B) Blue Light Imaging. (C) ESD.

3. Investigations and Treatment

The pathological morphology (Figure 3A,B) of the ESD specimen revealed that the local glands were diffuse with the distribution of medium‐sized indifferent cells, not excluding neoplastic lesions, pending immunohistochemistry results. After 1 week, immunohistochemistry (Figure 3C–F) revealed MPO+, CD117+, CD43+, CD34+, CK−, CD20−, PAX‐5−, CD3−, CD5−, CD68−, and Ki‐67(+) 80%. The patient was diagnosed with gastric medullary sarcoma. Pathological sections confirmed negative margin and the lesion was completely removed (Figure 3A). The patient was transferred to the department of hematopathology for further treatment. Positron emission tomography‐computed tomography (PET‐CT) and bone marrow aspiration were further refined to fully evaluate the condition. PET‐CT revealed diffuse elevated glucose metabolism in multiple places with increased density in some bone medullary cavities, which is consistent with leukemia manifestations. The density of the spinal canal behind the 8–9 pyramidal tract of the thoracic vertebrae was slightly increased, and glucose metabolism was abnormally increased, which is considered to involve leukemia. After gastric ESD surgery, increased glucose metabolism was not observed in the surgical area. There was no obvious enlarged lymph node shadow in the neck or supraclavicular, intra‐abdominal, or bilateral inguinal region, and no abnormal aggregation of radioactive material was observed. The bone marrow aspirate specimen revealed that the hematopoietic tissue was actively proliferating, that the percentage of primitive granulocytes was greater than 90%, and that the percentage of precursor cells was substantially increased (80%), indicating a sheet‐like distribution, which was consistent with AML. Karyotype analysis of bone marrow cells: 46, XY, t (8;12) (q22; q22). Genetic testing for hematological tumors revealed the presence of the KIT D816V missense mutations, whereas NPM1, FLT3‐ITD, IDH1, IDH2, DNMT3A, ETV6, GATA1, KRAS and other genes of interest were not mutated. Fusion gene detection revealed the presence of the AML1‐ETO fusion gene, with an AML‐ETO/ABL ratio of 323.75%. The patient's final diagnosis was AML with extramedullary infiltration. The patient's gastric medullary sarcoma had been resected endoscopically, and the AML with extramedullary infiltration was treated with 3 cycles of chemotherapy with the “HA + Venetoclax” regimen (homotriglycerine: 4 mg once daily via intravenous drip on days 1–6; cytarabine: 100 mg twice daily via intravenous drip on days 1–5, and 1800 mg twice daily via intravenous drip on days 6–9; venetoclax: oral administration once daily, 100 mg on day 4, 200 mg on day 5, and 400 mg on days 6–11), along with two intrathecal injections (cytarabine 50 mg, methotrexate 15 mg, dexamethasone 5 mg) for central nervous system prophylaxis. Six months after disease onset, the patient received a peripheral blood stem cell transplant donated by their younger brother.

FIGURE 3.

FIGURE 3

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An ESD specimen obtained from the stomach revealed that the local glands were diffuse with the distribution of medium‐sized indifferent cells, and immunohistochemistry (200×) revealed MPO+, CD117+, CD34+, and CD43+. (A) Hematoxylin and eosin stain of the overall picture with the negative margins (Lesion: Between white arrows, cauterization margin: Red arrows). (B) Hematoxylin and eosin stain (200×). (C) MPO+. (D) CD117+. (E) CD34+. (F) CD43+.

4. Outcome and Follow‐Up

A follow‐up bone marrow aspiration 2 months posttransplant showed no abnormalities, indicating complete remission. Gastroscopy was performed again, which showed the ESD scar on the anterior wall of the upper part of the gastric body and no new growth or ulcer in the stomach (Figure 4). Subsequent follow‐ups were conducted at a local hospital.

FIGURE 4.

FIGURE 4

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The repeated gastroscopy showed the ESD scar on the anterior wall of the upper part of the gastric body.

5. Discussion

MS is a solid tumor formed by the extramedullary aggregation of myeloid tumor cells, also known as granulocytic sarcoma or green tumor, because myeloperoxidase secreted by the tumor turns green when exposed to air. According to Pileri et al. [37], MS usually occurs in the skin (28.2%), lymph nodes (16.3%), testes (6.5%), small intestine (6.5%), bone (3.25%), and central nervous system (3.25%). MS of the gastrointestinal tract is more common in the small intestine, and gastric MS is rare [38, 39].

When there is concomitant infiltration of the bone marrow with MS in an extramedullary site, the MS is called synchronous; when there is a lack of BM infiltration at diagnosis, the MS is called asynchronous or isolated. Larger studies have reported synchronous and isolated MS at diagnosis at rates ranging from 0.2% to 2.8% and from 0.6% to 0.8%, respectively [4, 40, 41, 42, 43]. Patients with isolated medullary sarcoma or MS with no previous history of hematologic disease are prone to misdiagnosis. In this case, the gastric MS endoscopically presented as flat polypoid elevation and was misdiagnosed as gastric adenoma carcinoma. Gastric MS can occur independently without bone marrow involvement, and this is referred to as isolated gastric MS (29.4%). Concomitant hematologic cancers, such as AML (55.9%), chronic myelomonocytic leukemia (CML, 5.9%), myelodysplastic syndrome (MDS, 5.9%), and thrombocythemia (TE, 2.9%), have also been observed. Gastric MS can occur during remission (29.4%) or in active (42.2%) hematologic malignancies, consistent with previous reports of MS [44]. Gastric MS is closely related to AML (64.7%). It has been reported that the vast majority of primary MSs progress, if left untreated, to AML within an average of 1 year [39].

MS can occur at all ages, and the incidence of MS in children is significantly higher than that in adults (30% vs. 2%–5%) [45]. Our study revealed that gastric MS was more common in males (64.7%), with an average age of onset of 49 years. Patients with gastric MS often present with epigastric pain, dysphagia, fatigue, and weight loss, which lack specificity. Gastric MS can appear in different parts of the stomach, and the most common locations are the corpus (75%), fundus (25%), cardia (15.6%), and duodenum (18.8%). Lesions can be single (37.5%), multiple (28.1%), or even diffuse (34.4%), so PET‐CT is often recommended for MS patients to clarify the extent of the lesions, especially for patients who require local surgery or radiotherapy.

Gastric MS is rare, so there are no previous studies that systematically describe the endoscopic manifestations of gastric MS. In this study, the endoscopic features of gastric MS were reviewed in 32 patients, and this review indicated that these patients often had large masses (40.6%), polypoid bulges (37.5%) or thickened folds (18.8%), and a few could manifest as mucosal erythema‐like changes (3.1%). Ulcers (40.6%), nodular hyperplasia (25%), or hyperemia (15.6%) are often present on the surface of the lesion, but they may also be unremarkable (37.5%). Endoscopic findings lack specificity, making the diagnosis of sarcoma difficult. Medium‐sized, indifferent cells were common in the histopathological analysis, and 61.7% of them were morphologically diagnosed as neoplastic lesions; however, only 11.8% were considered myeloid tumors, and the accuracy of histopathological diagnosis was relatively insufficient. The confirmative diagnosis of MS is based on immunohistochemical staining. CD34 and CD117 are expressed mainly in hematopoietic stem cells and hematopoietic progenitor cells. CD33 is a bone marrow cell differentiation antigen that is present mainly during the early stages of bone marrow cell differentiation; MPO, CD43, and lysozyme antigen positivity indicate myeloid differentiation characteristics. CD68 and CD4 are antigens of monocyte differentiation, and CD3, CD5, CD8, CD10, and Pax‐5 negativity can help exclude T‐cell and B‐cell tumors. Previous studies have shown that the most common antigens in MS patients are MPO (83.8%–97%), CD34 (43.4%–47%), CD43 (97%), CD68 (93%–100%), CD117 (80.4%), and lysozyme (89%–93%) [37, 46, 47]. In this study, the common antigen types of gastric MS were CD34 (68.8%), MPO (65.6%), CD117 (46.9%), CD43 (34.4%), CD33 (18.8%), and CD68 (15.6%).

Owing to the rarity of MS and the diversity of organs involved, there is no unified treatment plan for MS. AML‐based chemotherapy regimens are currently accepted as the standard of care for MS, and studies have shown that early systematic chemotherapy can delay the progression of isolated MS to AML [48]. We finally selected “homotriglycerine + cytarabine + venetoclax” for the patient. We do not select idarubicin as anthracycline was not covered by the national medical insurance policy for the first treatment of AML. We chose Venetoclax because the patient was diagnosed with AML with gastric MS who had a high risk of central nervous system invasion, while venetoclax could reduce this risk [49, 50]. What's more venetoclax treatment does not affect transplantation, and venetoclax combined with HA can enhance the efficacy.

There is still no consensus on whether MS patients should be treated with CNS prophylaxis, on the specific treatment course that should be used, and on how to prevent spread of the disease to the CNS [51]. Central nervous system prophylaxis imparts strong toxicity and side effects. The decision to carry out CNS prophylaxis should be based on the risk of CNS involvement. Studies have shown that patients with extramedullary involvement at the time of diagnosis have greater CNS involvement than those without extramedullary involvement [50, 52, 53]. Relevant studies have shown that young age (< 64 years), multi‐system involvement, a high level of LDH, and the FLT3‐ITD mutation indicate a high risk of CNS involvement [54, 55, 56]. We performed CNS prophylaxis for the patient who had high risk of CNS involvement, because he was diagnosed with AML with extramedullary infiltration, with KIT D816V missense mutations.

If the lesion has complications such as bleeding and obstruction, if the lesion is localized, or if the effect of chemotherapy with isolated MS is poor, surgical resection or local radiotherapy can be considered [2, 5, 9, 10, 23]. The patient had AML1‐ETO fusion gene (AML‐ETO/ABL was 323.75%) and t (8; 21) with KIT D816V mutation, according to the 2023 NCCN guidelines for AML; these mutations indicate poor prognosis [57]. In addition, the patient had an extramedullary lesion, which also suggests a poor prognosis. It has been hypothesized that hematopoietic stem cell treatment (HSCT) should be always used at the first remission to overcome the potential poor prognosis of MS [40]. HSCT is also recommended for patients with MS with or without bone marrow involvement to prolong survival and improve outcomes [58].

6. Conclusions

Endoscopic manifestations of gastric MS lack specificity and are easily misdiagnosed, and the diagnosis is based mainly on immunohistochemical results. Chemotherapy is the first recommended regimen, and hematopoietic stem cell bone marrow transplantation is actively performed.

Author Contributions

Cong Ding: conceptualization, data curation, formal analysis, visualization, writing – original draft, writing – review and editing. Jianfeng Yang: investigation, validation, writing – original draft. Chang Shao: investigation, supervision. Bin Yang: methodology, supervision. Qiang Liu: resources, software. Yishen Mao: project administration, supervision. Qi Ding: resources, software. Jing Yang: conceptualization, writing – review and editing.

Ethics Statement

This study was conducted in accordance with the Declaration of Helsinki. Ethics approval was not required for this case report, as it does not involve experiments or clinical trials.

Consent

Written informed consent was obtained from the patient for publication of this case report and any accompanying images.

Conflicts of Interest

The authors declare no conflicts of interest.

Acknowledgments

The authors have nothing to report.

Ding C., Yang J., Shao C., et al., “Acute Myeloid Leukemia With Extramedullary Infiltration‐Gastric Myeloid Sarcoma: A Case Report and Literature Review,” Clinical Case Reports 13, no. 7 (2025): e70591, 10.1002/ccr3.70591.

Funding: The authors received no specific funding for this work.

Data Availability Statement

All data generated or analyzed during this study are included in this published article. Further inquiries can be directed to the corresponding authors.

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Data Availability Statement

All data generated or analyzed during this study are included in this published article. Further inquiries can be directed to the corresponding authors.

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