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Review
. 2024 Aug;38(4):783-811.
doi: 10.1016/j.hoc.2024.04.002. Epub 2024 May 17.

Gastrointestinal Cancer Precursor Conditions and Their Detection

Asaf Maoz  1 , Nicolette J Rodriguez  2 , Matthew B Yurgelun  3 , Sapna Syngal  4
Affiliations
Review

Gastrointestinal Cancer Precursor Conditions and Their Detection

Asaf Maoz et al. Hematol Oncol Clin North Am. 2024 Aug.

Abstract

Gastrointestinal cancers are a leading cause of cancer morbidity and mortality. Many gastrointestinal cancers develop from cancer precursor lesions, which are commonly found in individuals with hereditary cancer syndromes. Hereditary cancer syndromes have advanced our understanding of cancer development and progression and have facilitated the evaluation of cancer prevention and interception efforts. Common gastrointestinal hereditary cancer syndromes, including their organ-specific cancer risk and surveillance recommendations, are reviewed in this article. The management of common gastroesophageal, pancreatic, and colonic precursor lesions is also discussed, regardless of their genetic background. Further research is needed to advance chemoprevention and immunoprevention strategies.

Keywords: CDH1; Cancer detection; Cancer prevention; Hereditary pancreatic cancer; Lynch syndrome; Polyposis.

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Conflict of interest statement

Disclosure Maoz has no disclosures related to this article. N.J. Rodriguez has no disclosures related to this article. M.B. Yurgelun has has Research funding from Janssen; and Consulting/scientific advisory board roles at Nouscom. Syngal has no disclosures related to this article. This study was supported by The Pancreatic Cancer Action Network Catalyst Award (N. Rodriguez) and the K12TR004381 award (N. Rodriguez) through Harvard Catalyst | The Harvard Clinical and Translational Science Center (National Center for Advancing Translational Sciences, National Institutes of Health). The content is solely the responsibility of the authors and does not necessarily represent the official views of Harvard Catalyst, Harvard University, and its affiliated academic health care centers, or the National Institutes of Health. This study was also supported by the Whittaker Family Fund, the Scragg Family Fund, and the Hooley Fund-Lynch Syndrome.

Figures

Fig. 1.
Fig. 1.
LS colorectal cancer development and progression differs across MMR genes. Most LS-associated colorectal cancers are thought to arise via early acquisition of somatic MMRD, followed by progression to MMRD adenoma and carcinoma. In MLH1-LS, direct progression to carcinoma without an intermediate adenoma phase may occur. MMRD can also be acquired after an adenoma has developed. In a minority of cases, MMR-proficient adenomas may progress to MMR-proficient adenocarcinomas, particularly in MSH6-LS and PMS2-LS. Figure created with BioRender.com.
Fig. 2.
Fig. 2.
Recommendations for timing of surveillance colonoscopy after polypectomy of an adenoma or SSP. aHigh quality colonoscopy as defined by the 2020 US Multi-Society Task Force on Colorectal Cancer (Adapted with permission from Elsevier: Gupta S, Lieberman D, Anderson JC, et al. Recommendations for Follow-Up After Colonoscopy and Polypectomy: A Consensus Update by the US Multi-Society Task Force on Colorectal Cancer. Gastrointest Endosc. 2020;91(3):463-485.e5. https://doi.org/10.1016/j.gie.2020.01.014. Please refer to the US Multi-Society Task Force on Colorectal Cancer for additional recommendations on follow-up colonoscopy for hyperplastic polyps.)
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