Pathologic Features of Hereditary Non-Polyposis Colorectal Cancer

Messerini, Luca; Mori, Sabrina; Zampi, G

doi:10.1177/030089169608200204

Cited by 12 publications

(3 citation statements)

References 11 publications

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“…Histologic characteristics of Lynch syndrome-related colon cancers have been observed to be poorly differentiated, with tumor-infiltrating lymphocytes, mucin containing, and with signet ring or cribriform histology 22,23. There appears to be a survival advantage when matched stage for stage with non-Lynch syndrome colorectal cancers 24–26…”

Section: Clinical Spectrum Of Lynch Syndromementioning

confidence: 99%

The genetic basis of Lynch syndrome and its implications for clinical practice and risk management

Cohen¹,

Leininger²

2014

TACG

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Lynch syndrome is the most common cause of hereditary colon cancer, and accounts for as much as 3% of all colon and endometrial cancers. The identification and management of individuals with Lynch syndrome have evolved over the past 20 years, yet the syndrome remains vastly underdiagnosed. It is important for clinicians to recognize individuals and families who are at risk in order to be able to manage them appropriately and reduce their morbidity and mortality from this condition. This review will touch on the history of Lynch syndrome, the current knowledge of genotype–phenotype correlations, the cancers associated with Lynch syndrome, and management of individuals who are gene carriers.

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Section: Clinical Spectrum Of Lynch Syndromementioning

confidence: 99%

The genetic basis of Lynch syndrome and its implications for clinical practice and risk management

Cohen¹,

Leininger²

2014

TACG

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“…Microscopically, the tumours are characterised by a Crohn's-like lymphoid reaction, a mucinous component, and poor differentiation. [5][6][7][8][9][10] Studies on adenomas in HNPCC are less consistent. When calculating the average distribution of HNPCC adenomas in the literature, 45% (range 27-70%) were located in the proximal colon.…”

mentioning

confidence: 99%

Proximal adenomas in hereditary non-polyposis colorectal cancer are prone to rapid malignant transformation

Rijcken¹

2002

Gut

153

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Background: Hereditary non-polyposis colorectal cancer (HNPCC) is thought to arise from adenomas. HNPCC mostly occurs in the proximal colon. We investigated whether this proximal preponderance is due to a proximal preponderance of adenomas or (also) differences in transformation rates from adenomas to cancer between the distal and proximal colon. Methods: A total of 100 HNPCC adenomas were evaluated and compared with 152 sporadic adenomas for location, size, and dysplasia. Twenty five adenomas from patients with a known mismatch repair (MMR) gene mutation were stained for expression of MLH1 and MSH2. Results: HNPCC adenomas were more often located proximally (50% v 26%; p=0.018) and were smaller in comparison with sporadic adenomas. They were similarly dysplastic. However, all proximal HNPCC adenomas >5 mm were highly dysplastic compared with 17% of the larger proximal sporadic polyps (p<0.001). They were also more often highly dysplastic than larger distal HNPCC adenomas (p<0.001). Small HNPCC adenomas were, except for their location, not different from sporadic adenomas. Fifteen of the 25 "known mutation" adenomas showed loss of expression of either MLH1 or MSH2. The 10 adenomas with expression were all small with low grade dysplasia. Conclusion: HNPCC adenomas are located mainly in the proximal colon. The progression to high grade dysplasia is more common in proximal than distal HNPCC adenomas, indicating a faster transformation rate from early adenoma to cancer in the proximal colon. MMR gene malfunction probably does not initiate adenoma development but is present at a very early stage of tumorigenesis and heralds the development of high grade dysplasia.

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“…MMR-defi cient tumors have a recognizable cellular phenotype with poorly differentiated mucinous histopathology with a peritumoral lymphocytic infi ltration ( Messerini et al, 1996 ). MMR-defi cient tumors have a recognizable cellular phenotype with poorly differentiated mucinous histopathology with a peritumoral lymphocytic infi ltration ( Messerini et al, 1996 ).…”

Section: Genomic Model Of Crcmentioning

confidence: 99%