EPCAM deletions, Lynch syndrome, and cancer risk

The Lancet Oncology

Volumn 12, Issue 1, 2011, Pages 5-6

  Lynch, Henry T ^a   Lynch, Jane F ^a   Snyder, Carrie L ^a   Riegert Johnson, Douglas ^b  

^a CREIGHTON UNIVERSITY SCHOOL OF MEDICINE   (United States)

^b MAYO CLINIC   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

EPITHELIAL CELL ADHESION MOLECULE; PROTEIN MLH1; PROTEIN MSH2; PROTEIN MSH6;

CANCER RISK; CANCER SCREENING; COLORECTAL CANCER; ENDOMETRIUM CANCER; GENE DELETION; GENE EXPRESSION; GENE INACTIVATION; GENE MUTATION; GENETIC RISK; GENOTYPE PHENOTYPE CORRELATION; HEREDITARY NONPOLYPOSIS COLORECTAL CANCER; HUMAN; LETTER; MICROSATELLITE INSTABILITY; PRIORITY JOURNAL; PROMOTER REGION;

ANTIGENS, NEOPLASM; CELL ADHESION MOLECULES; COLORECTAL NEOPLASMS; COLORECTAL NEOPLASMS, HEREDITARY NONPOLYPOSIS; ENDOMETRIAL NEOPLASMS; FEMALE; GENE DELETION; HUMANS; MUTATION; MUTS HOMOLOG 2 PROTEIN; RISK;

EID: 78650713193     PISSN: 14702045     EISSN: None     Source Type: Journal    
DOI: 10.1016/S1470-2045(10)70291-6     Document Type: Letter

References (4)

1. Lindor NM, Rabe K, Petersen GM, et al. Lower cancer incidence in Amsterdam-I criteria families without mismatch repair deficiency: familial colorectal cancer type X. JAMA 2005, 293:1979-1985.
2. Kempers MJE, Kuiper RP, Ockeloen CW, et al. Risk of colorectal and endometrial cancers in EPCAM deletion-positive Lynch syndrome: a cohort study. Lancet Oncol 2011, 12:49-55.
3. Ligtenberg MJL, Kuiper RP, Chan TL, et al. Heritable somatic methylation and inactivation of MSH2 in families with Lynch syndrome due to deletion of the 3' exons of TACSTD1. Nat Genet 2009, 41:112-117.
4. Kovacs ME, Papp J, Szentirmay Z, Otto S, Olah E Deletions removing the last exon of TACSTD1 constitute a distinct class of mutations predisposing to Lynch syndrome. Hum Mutat 2009, 30:197-203.