Table 2.

Clinicopathological features of reported spontaneous CRLM regression

Author Year	Age	Sex	Background of patient	Primary CRC: location, surgical procedure, and histopathological findings	Timing of CRLM onset, number, location, size	Diagnostic methods for CRLM	Diagnostic methods for spontaneous regression of CRLM	Histopathological evaluation methods, histological features of regressed CRLM	IgG4-positive plasma cell infiltration and/or IPT-like histological changes	Hypotheses for spontaneous regression of CRLM	Follow up period
Rankin [8] 1965	44	M	Familial polyposis	1st: Lower rectum, proctosigmoidectomy and combined APR, Grade 4 differentiated tubular adenocarcinoma 2nd: Ascending colon, Right colon resection, well-differentiated tubular adenocarcinoma	Synchronous at 1st CRC, 4 lesions, Right lobe	Biopsy at 1st CRC surgery: poorly differentiated carcinoma	Perioperative findings at 2nd operation	Not confirmed histologically.	Not mentioned	Not mentioned	10 years Alive
Francis [9] 1997	69	M	Unremarkable	Rectosigmoid junction, HAR, Moderate to poorly differentiated tubular adenocarcinoma	Synchronous, Multiple, Both lobes, Greater than 7 cm	Tru-cut biopsy at CRC surgery: fibrous tissue infiltrated with irregular clumps of neoplasm consistent with metastatic adenocarcinoma	US and CT showed regression of CRLM.	Not confirmed histologically.	Not mentioned	Removal of a source of trophic agents to an immunological effect	11 years Alive
Ikuta [10] 2002	60	M	Unremarkable	Lower rectum, APR and partial hepatectomy, Adenosquamous carcinoma (pT3pN3pM1)	Metachronous (4 months post primary tumor surgery), Mulitple, almost completely occuped both lobes	Follow-up CT	Follow-up CT showed remarkable regression of CRLM in the both lobes, autopsy	Autopsy, Chronic inflammation and coagulative necrosis with a few nodules of residual tumor.	Not mentioned	The biology of adenosquamous carcinoma or vascular obstruction due to enlarged hilar lymph nodes.	18 months Died due to peritoneal carcinomatosis.
Matsuki [11] 2018	72	F	Underwent PPPD for pancreatic head IPMN	Ascending colon, RHC, Moderately differentiated tubular adenocarcinoma (pT2pN1cM0)	Metachronous (5 months post primary tumor surgery), solitary, S3, 13 mm	CT, EOB-MRI, abdominal US	S3 segmentectomy	S3 Segmentectomy, Necrotic columnar epithelial cells surrounded by histiocytes, inflammatory cells and fibrosis.	Not mentioned	Host immune response to chronic biliary infection at the hepaticojejunostomy site after PPPD.	13 months Alive
Subasinghe [12] 2022	53	M	Unremarkable	Ascending colon, Lap-eRHC, Moderately differentiated tubular adenocarcinoma (pT2pN0cM0)	Metachronous (12 months post primary tumor surgery), solitary, S8, 21 mm	CT, EOB-MRI	S8 partial hepatectomy	S8 partial hepatectomy, Necrotic columnar epithelial cells surrounded by chronic inflammation and fibrosis.	Not mentioned	Infarct-like necrosis without chemotherapy, possibly induced by an immune-mediated injury following liver biopsy	12 months Alive
Zwart [13] 2023	59	F	Underment left lung transplantion for COPD, recurrent pulmonary infections under immunosuppression	Cecum, Biopsy, Mucinous adenocarcinoma	Synchronous, multiple, both lobes	CT, PET-CT, biopsy: adenocarcinoma (MLH1, PMS2, MSH6 loss; dMMR, BRAF V600E mutated, RAS wild type)	Follow-up CT showed remarkable regression of CRLM in the both lobes.	Autopsy, More than 40 CRLM lesions regressed completely, but the primary mucinous adenocarcinoma of the cecum did not.	Not mentioned	Withdrawal of immunosuppression activated anergic T cells, inducing regression of dMMR CRLM via anti-tumor immunity	7 months Died due to resrictive allograft syndrome
Our case	71	M	IgG4-RD	Rectum, Lap-Hartman’s operation, Moderately differentiated tubular adenocarcinoma (pT3pN0cM0)	Metachronous (8 months post primary tumor surgery), 2 lesions, S5 and S7, 6 mm and 11 mm	CT, EOB-MRI, PET-CT, enhance abdominal US	S5, S7 partial hepatectomy	S5, S7 partial hepatectomy, Necrotic CRLM surrounded by hepatic IPT, lymphoplasmacytic type	Marked IgG4-positive plasma cell infiltration with lymphoplasmacytic-type hepatic IPT-like changes	Intrahepatic presentation of CRLM antigens triggered an immune response, leading to tumor necrosis via IgG4-positive plasma cells, fibrosis, cytokines, and vascular damage.	20 months Alive

CRC, colorectal cancer; CRLM, colorectal liver metastasis; APR, abdominoperineal resection; HAR, high anterior resection; RHC, right hemicolectomy; Lap-eRHC, laparoscopic extended right hemicolectomy; PPPD, pylorus-preserving pancreaticoduodenectomy; IPMN, intraductal papillary mucinous neoplasm; COPD, chronic obstructive pulmonary disease; dMMR, deficient mismatch repair; IgG4-RD, immunoglobulin G4–related disease, IPT, inflammatory pseudotumor.