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At least 811 records · Page 45Linked to original sources
PubMed2003

Exclusion of Madh2, Madh4, and Madh7 as candidates for the modifier of Min 2 (Mom2) locus.

We recently identified the Modifier of Min 2 (Mom2) locus. Mom2 is a new modifier of intestinal tumorigenesis that resulted from a spontaneous mutation in a B6 Apc(Min)/+ mouse. The presence of one resistant Mom2(R) allele results in a significant reduction in small intestinal polyp number and colon polyp incidence in Apc(Min)/+ mice. Through linkage analysis, we previously localized Mom2 to a 14-cM region on mouse Chromosome (Chr) 18, distal to the Apc gene. This region is syntenic with human Chr 18q, which frequently undergoes loss of heterozygosity (LOH) in several human cancers, including colorectal cancer. Residing in this region are the Madh2 and Madh4 genes, which have both been implicated in human colorectal cancer. Based on meiotic recombinations within the Mom2 region in the derivation of our congenic animals, we have narrowed the location of the Mom2 locus and excluded Madh2, Madh4, and Madh7, as well as Mbd1, Mbd2, Dcc, and Tcf4, as candidates for the Mom2 gene.

Alleles↗
PubMed1986

Peutz-Jeghers syndrome: a clinical study of a large family in two generations.

A family group of 15 cases in two generations with Peutz-Jeghers syndrome has been studied and a review of the history and features of the syndrome is presented. This syndrome was detected in 10 of 15 family members in two generations. One family member underwent repeated surgery after small bowel obstruction was diagnosed. In addition, multiple polyps were removed from the rectum. Rectal bleeding dominated the clinical picture in two patients. Five of the family members had small bowel polyps, five of the siblings had polyps in the colon. Colonic polyp was also found in one patient who had a small bowel polyp. Four of the ten affected family members in two generations had mucocutaneous pigmentation. One of the siblings had died during the early postoperative period.

Adolescent↗
PubMed2000

Leptin promotes invasiveness of kidney and colonic epithelial cells via phosphoinositide 3-kinase-, rho-, and rac-dependent signaling pathways.

Leptin plays a key role regulating food intake, body weight and fat mass. These critical parameters are associated with an increased risk for digestive and mammary gland cancer in the Western population. Here we determined whether leptin contributes to the invasive phenotype of colonic and kidney epithelial cells at various stages of the neoplastic progression. First, leptin potently (EC50 = 10-30 ng/ml) induces invasion of collagen gels by premalignant familial adenomatous colonic cells PC/AA/C1 and nontumorigenic MDCK kidney epithelial cells, their src-transformed counterparts, and the human adenocarcinoma colonic cells LoVo and HCT-8/S11. Leptin and its Ob-Rb receptors were consistently identified by RT-PCR and immunoblotting in these cell lines, as well as in human colonic epithelial crypts, polyps, colonic tumor resections, and adjacent mucosa. Leptin-induced invasion was effectively blocked by pharmacological inhibitors of several downstream signaling pathways involved in cell transformation, namely, JAK2 tyrosine kinase (AG490), phosphoinositide PI3'-kinase (wortmannin and LY294002), mTOR kinase (rapamycin), and protein kinases C (GF109203X, Gö6976). Accordingly, leptin induces transient elevation of the PI3'-kinase lipid products in JAK2 immunoprecipitates prepared from parental MDCK cells. The leptin effect on invasion was potentiated by the activated form of the small GTPase RhoA and was abrogated by dominant negative mutants of RhoA, Rac1, and the p110alpha of PI3'-K. Our data indicate that leptin may exert a local and beneficial effect on migration of normal colonic epithelial cells and reparation of the inflamed or wounded digestive mucosa. We also emphasize a new role for leptin, linking the nutritional and body fat status to digestive cancer susceptibility by stimulating the invasive capacity of colonic epithelial cells at early stages of neoplasia. This finding has potential clinical implications for colon cancer progression and management of obesity.

Animals↗
PubMed2006

Muir-Torre syndrome: a case of this uncommon entity.

A 69-year-old Hispanic woman presented for the evaluation of nodules on the head and back. In the past, she had been treated for basal cell carcinoma (BCC) of the face; the referring physician was concerned that the new lesions might also be BCC. The patient had an extensive past medical history. In addition to BCC, she had been treated for breast cancer, colon cancer, and cervical cancer prior to emigrating to the USA. Her colonic malignancy had been localized proximal to the splenic flexure. She also had a history of colonic polyps and distal colonic villous adenoma. She denied ever being treated with radiation. Further details of her medical history and cancer staging were not available. Her family history was significant for a sister with colon cancer and transitional cell carcinoma of the urinary bladder. In addition, she had a great aunt with oral cancer and a great uncle with lung cancer. Neither the patient or her relatives had any history of tobacco use. On physical examination, in addition to scars from a radical mastectomy and midline abdominal laparotomy, four skin lesions were noted: two on the scalp, one on the tragus, and one on the mid-back. The first lesion on the vertex of the scalp was a yellow-brown waxy papule measuring 0.6 x 0.5 cm. This lesion was similar to that on the mid-back, except in size. The lesion on the back measured 1.2 x 1.0 cm. The second lesion on the frontal scalp measured 0.8 x 0.6 cm and was red-brown with a pearly appearance and some central hyperkeratosis. The tragus lesion was similar in appearance to that on the frontal scalp. Shave biopsies of all lesions were obtained. The lesions on the scalp and mid-back revealed lobules of sebaceous cells in the dermis with a minority of surrounding basaloid cells, consistent with a diagnosis of sebaceous adenoma (Fig. 1). Although the lesion on the frontal scalp also showed sebaceous differentiation, there were a greater number of basaloid cells, some with hyperchromatic nuclei and mitotic figures; this was consistent with a diagnosis of sebaceous epithelioma (Fig. 2). The final lesion (tragus) was histologically consistent with a keratotic BCC. No further treatment was required for these benign sebaceous tumors, but their presence defined our patient's condition as Muir-Torre syndrome. Mohs' micrographic surgery was performed on the tragus BCC and the margins were tumor free in one stage. The patient returned 1 year later with a lesion anterior to the left axilla which was biopsied to rule out BCC (Fig. 3). Histologically, this lesion was also consistent with sebaceous epithelioma.

Adenoma↗
PubMed2001

A de novo deletion of chromosome 5q causing familial adenomatous polyposis, dysmorphic features, and mild mental retardation.

Familial adenomatous polyposis (FAP) is an autosomal dominant disorder that typically presents with colorectal cancer secondary to extensive adenomatous polyps of the colon. The molecular basis and clinical phenotype of FAP are well known. Recurrent episodes of severe abdominal pain and a positive fecal occult blood test in an 18-yr-old boy with mild mental retardation and slight dysmorphic features of the face, head, and skeletal system led to the diagnosis of FAP. The clinical workup revealed the presence of over 100 sessile colonic polyps but no polyp formation in the upper GI tract, no cancer development, nor other FAP-associated lesions. To find out whether there is an association between mental retardation and FAP we performed a chromosome analysis including comparative genomic hybridization and an indirect genotype analysis with polymorphic markers from the APC gene region. Cytogenetic analysis showed an interstitial deletion of chromosomal region 5q that was confined to the region 5q21-q22 by comparative genomic hybridization. The deletion, spanning about 10 centimorgans, encompassed the complete APC gene and can be considered as causative for FAP. Moreover, molecular genetic analysis with polymorphic markers flanking the APC gene demonstrated a de novo deletion on the paternal chromosome. Cytogenetically detectable deletions on chromosome 5 including the APC gene generally lead to an associated gene deletion syndrome. Individuals who present with mild mental retardation and dysmorphic features should therefore be investigated for chromosomal deletions. If the deletion encompasses the APC gene, these patients are at high risk of developing FAP and associated complications.

Abnormalities, Multiple↗
PubMed1986

Incidence of methanogenic bacteria in a sigmoidoscopy population: an association of methanogenic bacteria and diverticulosis.

This study determined the incidence and concentration of methane-producing bacteria in tap water enema samples of 130 individuals taken before sigmoidoscopy. The number of subjects classified in five major colonic groups were as follows: normal colon 36, diverticulosis 57, inflammatory bowel disease 11, colon polyps 34, and colon cancer 11. Some patients were placed in more than one category. Ninety four of the subjects or 72% had methanogenic bacteria ranging in concentration from 6 to about 3 X 10(10)/g dry weight of faeces. The predominant methanogen in all groups was Methanobrevibacter smithii. Chi-square analysis showed that the incidence of methanogens in concentrations of 10(7)/g dry weight of faeces or greater in patients with diverticulosis (58%) was significantly greater than in normal patients (25%). High methanogen concentrations are associated with excretion of methane in the breath.

Adult↗