scholarly journals Molecular characteristics of poorly differentiated adenocarcinoma and signet-ring-cell carcinoma of colorectum

1999 ◽  
Vol 84 (1) ◽  
pp. 33-38 ◽  
Author(s):  
Yuichi Kawabata ◽  
Naohiro Tomita ◽  
Takushi Monden ◽  
Masayuki Ohue ◽  
Tadashi Ohnishi ◽  
...  
Keyword(s):  
Cell Carcinoma ◽  
Signet Ring Cell Carcinoma ◽  
Signet Ring Cell ◽  
Molecular Characteristics ◽  
Poorly Differentiated Adenocarcinoma ◽  
Signet Ring ◽  
Poorly Differentiated ◽  
Ring Cell

scholarly journals A Case of Poorly Differentiated Adenocarcinoma with Signet Ring Cell Carcinoma of the Duodenal Bulb: A Case Report

2017 ◽  
Vol 102 (3-4) ◽  
pp. 141-144 ◽  
Author(s):  
Kosuke Hirano ◽  
Yukinori Yamagata ◽  
Teppei Tatsuoka ◽  
Yawara Kubota ◽  
Kazuyuki Saito ◽  
...  
Keyword(s):  
Cell Carcinoma ◽  
Rare Case ◽  
Case Reports ◽  
Duodenal Bulb ◽  
Signet Ring Cell Carcinoma ◽  
Signet Ring Cell ◽  
Poorly Differentiated Adenocarcinoma ◽  
Signet Ring ◽  
Poorly Differentiated ◽  
Ring Cell

Duodenal cancers are rare. Histopathologically, most duodenal cancers are adenocarcinoma. Signet ring cell carcinoma (SRCC) is a rare tumor more commonly found in the stomach than at other sites in the digestive tract. SRCC is extremely uncommon in the duodenum, with most of these tumors occurring in the ampulla. Until now, there are few case reports of duodenal cancers with SRCC. To accumulate case reports, we report a rare case of nonampullary duodenal bulb SRCC. A 74-year-old man was admitted to our hospital with melena. Esophagogastroduodenoscopy (EGD) showed a duodenal bulb ulcer. He was treated with a proton pump inhibitor. However, 1 month later, he was readmitted to our hospital with epigastric pain and nausea. A second EGD examination showed an ulcer at the duodenal bulb. Biopsies taken from the ulcer showed SRCC. Distal gastrectomy and duodenal bulb resection were performed. Histologic examination of the specimen showed a type 4 lesion located from the duodenal bulb to the pyloric antrum. The tumor was composed of poorly differentiated adenocarcinoma (por) with SRCC. The distal margin of the duodenal bulb was invaded with tumor. Therefore, pancreatoduodenectomy was performed. One year after the initial operation, he is alive and had no relapse. We described a rare case of por with SRCC of the duodenal bulb. It is important to bear in mind that an ulcer following an abnormal clinical course should be biopsied, and we have to select a suitable operation in cases of duodenal bulb cancer.

Poorly Differentiated Adenocarcinoma with Signet-Ring Cell Carcinoma in a Hyperplastic Polyp of the Stomach: Report of a Case

Surgery Today ◽  
2007 ◽  
Vol 37 (10) ◽  
pp. 901-904 ◽  
Author(s):  
Hiroshi Hirano ◽  
Toshimi Yoshida ◽  
Hitoshi Yoshimura ◽  
Masato Fukuoka ◽  
Eriko Ohkubo ◽  
...  
Keyword(s):  
Cell Carcinoma ◽  
Hyperplastic Polyp ◽  
Signet Ring Cell Carcinoma ◽  
Signet Ring Cell ◽  
Poorly Differentiated Adenocarcinoma ◽  
Signet Ring ◽  
Poorly Differentiated ◽  
Ring Cell

Comprehensive molecular profiling of signet-ring-cell carcinoma (SRCC) from the stomach and colon.

2019 ◽  
Vol 37 (4_suppl) ◽  
pp. 63-63
Author(s):  
Alberto Puccini ◽  
Kelsey Poorman ◽  
Mohamed E. Salem ◽  
Richard M. Goldberg ◽  
Anthony Frank Shields ◽  
...  
Keyword(s):  
Cell Carcinoma ◽  
Tumor Location ◽  
Signet Ring Cell Carcinoma ◽  
Signet Ring Cell ◽  
Molecular Profile ◽  
Molecular Characteristics ◽  
Molecular Features ◽  
Signet Ring ◽  
Ring Cell ◽  
The Impact

63 Background: Signet ring cell carcinoma (SRCC) is a rare variant of adenocarcinoma, accounting for about 10% of gastric cancer (GC) and 1% of colorectal cancer (CRC). SRCC is associated with poor prognosis, however little is known about the underlying molecular characteristics. Herein, we aimed to characterize the molecular features of SRCCs, and to compare the molecular profile of SRCC to adenocarcinoma; further, we assessed the impact of tumor location on the molecular profile of SRCC. Methods: SRCCs were analyzed using NGS (MiSeq on 47 genes, NextSeq on 592 genes), immunohistochemistry, and in-situ hybridization. Tumor mutational burden (TMB) was calculated based on somatic nonsynonymous missense mutations, and microsatellite instability (MSI) was evaluated by NGS of known MSI loci. Chi-square and t-tests were used for comparative analyses. Results: A total of 8,500 CRC and 1,100 GC were screened for SRCC histology. Seventy-six SRCC were identified from the CRC cohort (<1%) and 98 from the GC cohort (9%). The most frequently mutated genes in CRC-SRCC were TP53 (47%), ARID1A (26%), APC (25%), KRAS (22%), RFN43 (16%), KMT2D (12%), KMT2C (11%), SMAD4 (10%) and BRAF (10%), while in GC-SRCC were TP53 (42%), ARID1A (27%), CDH1 (11%), BAP1 (7%), PIK3CA (7%), ERBB2 (5%). When compared to non-SRCC histology (N=3522), CRC-SRCC (N=37) showed more frequently mutation in BRCA1 (11% vs 1%, P < .001) and less mutation in APC (19% vs 78%, P < .001), KRAS (22% vs 51%, P = .001) and TP53 (47% vs 73%, P = .001). Among GC cohort, SRCC (N=54) had a higher frequency of mutations in CDH1, BAP1, and ERBB2, and higher rate of amplification MYB compared to non-SRCC (N=540), although none of these differences were statistically significance. When we compared GC-SRCC vs. CRC-SRCC, only the mutation rate in APC (0% vs 25%) and KRAS (2% vs 22%) genes were significantly different (P < .001). Conclusions: Our research is the first to comprehensively characterize the molecular features of SRCC. Our data suggest that SRCCs harbor similar molecular profile, regardless the tumor location. On the other hand, significant differences were observed between SRCCs and non-SRCC tumors, therefore tailored therapy should be provided to these patients.

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