Chromosome 18q allelic loss and prognosis in stage II and III colon cancer

Chromosome 18q deletion and Smad4 protein inactivation correlate with liver metastasis: a study matched for T- and N- classification

“…Moreover, they argued that stage II colorectal cancer patients without 18q allelic loss show similar prognosis to those with stage I patients. A study by Lanza et al (1998) also showed similar results in that patients with stage II disease whose tumour had no 18q allelic loss demonstrated a 5-year survival rate of 96%, while those with stage II disease and 18q allelic loss showed a 5-year survival rate of only 54%. Ogunbiyi et al (1998) reported that Chromosome 18q allelic loss was significantly associated with reduced disease-free and disease-specific survival in patients with stage II (P ¼ 0.05 and P ¼ 0.0156) and III disease (P ¼ 0.038 and P ¼ 0.032).…”

“…Loss of heterozygosity (LOH) is one of the major types of genetic inactivation, and the long arm of chromosome 18 is the most frequently deleted region in colorectal cancers. To date, many reports suggest that this deletion is a molecular predictor that affects survival (Fearon et al, 1990;Jen et al, 1994;Chung, 1998;Lanza et al, 1998;Ogunbiyi et al, 1998;Jernvall et al, 1999;McLeod and Murray, 1999;Sarli et al, 2004). We too reported that the allelic deletion of chromosome 18q was associated with poorer prognosis in stage III colon cancer after adjuvant chemotherapy (Watanabe et al, 2001.…”

Genetic alterations in poorly differentiated endocrine carcinomas of the gastrointestinal tract

“…Losses at 18q, possibly involving the tumor suppressor gene DCC, DPC4/Smad4, or Smad2, are considered a peculiar feature of the adenomacarcinoma sequence of colorectal malignancy. 14,38 Nonetheless, recent reports of frequent 18q LOH in midgut carcinoids indicate that a novel putative tumor suppressor gene (distinct from DCC or DPC4) that is located on 18q may play an important role in the pathogenesis of midgut endocrine tumors. 15,16 In an attempt to evaluate whether the pathogenesis of PDECs is more consistent with that of WDECs, as suggested by some studies, [5][6][7][8] or with that of classical nonendocrine adenocarcinomas (i.e., CRCs), as suggested by other reports, 3,4 we compared the gastric subset of PDECs with a series of gastric WDECs and also compared the colorectal subset of PDECs with a series of CRCs.…”

“…13 The aim of the current study was to investigate the pattern of genetic alterations in GI PDECs through loss-of-heterozygosity (LOH) and/or immunohistochemical (IHC) analysis of several gene loci that are thought to be involved in the pathogenesis of endocrine tumors of the gastrointestinal tract, nonendocrine epithelial tumors of the gastrointestinal tract, or SCLCs. The following genes and loci have been investigated: 1) FHIT, at 3p14.2; 2) 3p21.3, possibly corresponding to the tumor suppressor gene RASSF1A; 3) MEN1, at 11q13; 4) p53, at 17p13.1; 5) 18q23, a region frequently deleted in the progression of colorectal carcinomas (CRCs) 14 and in the induction of midgut carcinoids 15,16 ; 6) p16 INK4 , at 9p21; and 7) Rb, at 13q14.…”

Refined mapping of loss of heterozygosity on 1q31.1-32.1 in sporadic colorectal carcinoma

“…When this occurs at a tumor suppressor gene locus where one of the alleles is already abnormal, it can result in neoplastic transformation [5] . According to the previous study, in colorectal carcinomas, frequent allelic loss was identified in chromosome 5q (30%) [3,6] , 8p (40%) [3,7] , 17p (75%-80%) [3,8] , 18q (80%) [3,9] , and 22q (20%-30%) [3,10,11] . Moreover tumor suppressor genes APC, p53, and DCC were found, which were located on chromosome 5q, 17p, and 18q, respectively [12][13][14] .…”