Non-Hodgkin's Lymphoma in a Patient with Probable Hereditary Nonpolyposis Colon Cancer

Hirano, Kouichi; Yamashita, Kaname; Yamashita, Naoyuki; Nakatsumi, Yasuto; Esumi, Hiroyasu; Kawashima, Atsuhiro; Ohta, Tokio; Mai, Masayoshi; Minamoto, Toshinari

doi:10.1007/s10350-004-6161-9

Cited by 17 publications

(16 citation statements)

References 39 publications

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“…This resembles the occurrence of cancer in the hematopoietic compartments of children carrying biallelic germline MSH2 mutations (7)(8)(9)(10). In addition, although hematologic malignancies are rarely found in association with hereditary nonpolyposis colorectal cancer, B-or T-cell lymphomas have been reported in hereditary nonpolyposis colorectal cancer patients with heterozygous mutations in MSH2 or MLH1 genes (11,12). MMR recognizes DNA mismatches containing oxidized bases.…”

Section: Introductionmentioning

confidence: 89%

Role of MUTYH and MSH2 in the Control of Oxidative DNA Damage, Genetic Instability, and Tumorigenesis

et al. 2009

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Section: Introductionmentioning

confidence: 89%

Role of MUTYH and MSH2 in the Control of Oxidative DNA Damage, Genetic Instability, and Tumorigenesis

et al. 2009

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“…It is probable that as mutation carriers advance in age (thanks to improved survival for colorectal tumours), new types of tumours will be found to be associated with MMR mutations. Some case reports have already been published [25,26].…”

Section: Screening For Other Tumoursmentioning

confidence: 95%

Surveillance in Lynch Syndrome

Mecklin∥

Järvinen

2005

Familial Cancer

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The major aim of surveillance in Lynch syndrome is to diagnose malignant or premalignant lesions at the asymptomatic stage by regular checkups, particularly in the large bowel. Therefore, screening for colorectal adenomas and carcinomas by regular colonoscopies is the main topic of the present review. However, it should be remembered, that primary prevention - whether through the use of chemoprevention or the promotion of a healthy life-style may form a significant part of such surveillance in the future. Observational studies indicate that the adenoma carcinoma sequence is the main pathway in the development of colorectal cancer in Lynch syndrome. A colonoscopy every 1-3 years starting at age 20 to 25 years and the removal of observed adenomas is recommended for individuals known to have Lynch syndrome associated mutations. The incidence of colorectal cancer in family branches screened this way is lower than that in past unscreened generations. The screening of other malignancies associated with Lynch syndrome is more complex. Screening for endometrial cancer has recommended previously, but no benefits have been shown in recent studies. The value of screening for other extracolonic cancers remains also uncertain.

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“…Mutations in MMR genes segregate with cancer predisposition syndromes in humans, 3 with a greatly increased risk of developing different tumors. [4][5][6][7] Loss of MMR is also associated with sporadic cancers, where the silencing of MLH1 gene, secondary to promoter methylation, represents the inactivating mutation. 8,9 An age-related accumulation of DNA damage, in part due to alterations of DNA repair mechanisms, including MMR, is well documented in somatic cells.…”

Section: Introductionmentioning

confidence: 98%

Microsatellite Instability and Compromized Mismatch Repair Gene Expression During In Vitro Passaging of Monoclonal Human T Lymphocytes

Neri¹,

Pawelec

Facchini

et al. 2007

Rejuvenation Research

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An age-related accumulation of DNA damage caused by increased insult and/or decreased repair, could contribute to impaired cellular function. DNA mismatch repair (MMR), the main postreplicative correction pathway, can be monitored by assessing microsatellite instability and has been reported to decrease with age. Here, we analyzed the involvement of the MMR system in the accumulation of genetic damage in a cultured monoclonal human T lymphocyte model. We correlated microsatellite instability (MSI) and MMR gene expression, and replicative senescence of CD4+ clones derived from young, old and centenarian individuals or from CD34+ precursors. Cells were analyzed for MSI at five loci (CD4, VWA, Fes, D2S123, and BAT26), for the methylation status of MLH1 and MSH2 gene promoters, and for the expression of the MMR genes MSH2, MSH6, MSH3, MLH1, PMS2, and PMS1. MSI increased with increasing culture passages, particularly in the CD34+ progenitor-derived clones, but also in those from adult T cells. MSI and MMR gene expression were found to correlate, mostly due to a reduced expression of the components of MutL heterodimers, pointing to a role of MMR in the acquisition of DNA damage with in vitro aging.

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Non-Hodgkin's Lymphoma in a Patient with Probable Hereditary Nonpolyposis Colon Cancer

Cited by 17 publications

References 39 publications

Role of MUTYH and MSH2 in the Control of Oxidative DNA Damage, Genetic Instability, and Tumorigenesis

Role of MUTYH and MSH2 in the Control of Oxidative DNA Damage, Genetic Instability, and Tumorigenesis

Surveillance in Lynch Syndrome

Microsatellite Instability and Compromized Mismatch Repair Gene Expression During In Vitro Passaging of Monoclonal Human T Lymphocytes

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