Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We tested the antiproliferative effects of Diheptyl Diselenide (DHDSe) on several different human cancer cell lines. Cells derived from human cancer (CG5), colon cancer (WIDR), laryngeal cancer (Hep-2), ovarian cancer (OV 166, OV 1225) and IM-9 lymphoblastoid cells were used. In all cell lines DHDSe inhibited cell growth in a dose dependent manner. At the highest concentration tested, an inhibition of cell proliferation ranging from 48% to 75% compared with control cells was observed. Our results show that DHDSe exerts a direct antiproliferative effect on human cancer cells in vitro and suggest that it may represent the parent compound of a new group of anticancer agents.
 ...
PMID:Growth inhibitory effect of diheptyl diselenide on various human cancer cell lines. 262 22

Hereditary nonpolyposis colorectal cancer (HNPCC) accounts for about 4% to 6% of the total colorectal cancer burden. It is subdivided into Lynch syndrome I and II. Lynch syndrome I is characterized by an autosomal dominant inheritance pattern for site-specific, early onset, adenocarcinoma of the colon, with proximal predominance and an excess of synchronous and metachronous colonic cancers. Lynch syndrome II (cancer family syndrome) shows these same colon cancer characteristics, but differs in that there is an excess proclivity of other forms of cancer, particularly of the endometrium and ovary. This article documents a family that shows features of Lynch syndrome II. Unique aspects pertain to a patient who is in the direct genetic lineage (whose five brothers manifested colonic cancer), but who developed carcinoma of the uterine cervix at age 34 and laryngeal cancer at 60. The pedigree also shows uterine cervical carcinoma among other patients at genetic risk. Her son, who is a nonsmoker and nondrinker, manifested laryngeal cancer at age 31. These observations appear to add new information about tumor heterogeneity in HNPCC.
 ...
PMID:Laryngeal carcinoma in a Lynch syndrome II kindred. 340 61

1. n-Butyrate, a short chain fatty acid produced by colonic fermentation, induces differentiation in human neoplastic cell lines, and reduces expression in vitro of a sialyltransferase that glycosylates N-linked glycoproteins in hepatoblastoma cells. Gangliosides are amphipathic, sialylated glycosphingolipids that undergo profound changes in many transformed cells and may protect neoplastic cells from host immune surveillance. Colonic mucosal cells are exposed to luminal short-chain fatty acid concentrations of up to 80 mmol/l, and there is some evidence that short-chain fatty acids may alter ganglioside expression in colon cancer cells. 2. Because of the importance of gangliosides in cancer pathogenesis, we investigated the effects of n-butyrate on ganglioside expression of colonic (human and murine) and non-colonic cancer cells. 3. Three separate colon cancer cell lines (LS174T, T84 and MCA-38), when butyrate treated, demonstrated striking amplification of specific individual gangliosides. However, the total lipid-bound sialic acid content of gangliosides of butyrate-treated LS174T cells diminished. In contrast to earlier reports, n-butyrate did not mediate expression of all gangliosides and specifically did not mediate expression of GM3. This effect persisted even after removal of butyrate. 4. In contrast, exposure of extracolonic cells to butyrate, including cervical cancer (HeLa) and laryngeal cancer (HEp-2) cell lines in this study and hepatoblastoma cells (Hep G2) in our previous work, caused no detectable changes in ganglioside expression. 5. In conclusion, our results indicate a relative tissue specificity of butyrate-mediated alterations in ganglioside expression that is not universal but is limited to specific gangliosides.
 ...
PMID:n-Butyrate mediation of ganglioside expression of human and murine cancer cells demonstrates relative cell specificity. 778 51

Operations were carried out on 94 patients with pulmonary metastases at the Cologna University Clinic from 01.01.1980 to 31.12.1991. The prevailing primary tumors which metastasized to the lungs were sarcomas (24.5%, 23 cases), carcinoma of the kidneys (22.3%, 21 cases), malignant melanomas (19.1%, 18 cases), carcinoma of the large intestine (15.9%, 15 cases), and carcinoma of the testes and ovaries (10.6%, 10 cases). Metastasis to the lung from an esophageal tumor was encountered in one case, from the contralateral lung in one case, from a malignant thymoma in one case, and from carcinoma of the larynx in one case. Metastases of carcinoma of the mouth floor were encountered in 3 cases. The metastases were removed by atypical wedge resection in 71 cases, by lobectomy in 22 cases, and by segmental resection in one case. Postoperative mortality was 1.1%. Average survival for all groups of patients was as follows: one year 60%, 3 years 40%, 5 years 38.3%.
 ...
PMID:[Surgery of lung metastasis]. 817 76

Occurrences of malignancy in 308 patients who were clinically free of cancer 60 months or more after surgical treatment of T1 N0 non-small-cell lung cancer are summarized. At last report, 210 patients remained alive with no evidence of malignant disease, 43 patients died of nonmalignant causes, and 55 patients had 59 occurrences of malignant disease. Late lung cancer recurrence was observed in 22 patients (concurrent with nasopharyngeal cancer in one patient and with laryngeal cancer in one patient). Metachronous second lung cancer was noted in 20 patients (including concurrent colon cancer in one patient and metastatic recurrence in one patient). Other nonpulmonary malignant tumors appeared in 13 patients. Including second lung cancer, 25 cancers of aerodigestive epithelium were observed in 23 patients. The malignancy-free survival advantage for patients with squamous cancer observed until 60 months after resection was not sustained at 60 months and beyond. At the time of last follow-up, 84 patients (27%) had died; 43 were free of malignancy, and 41 had malignancy (14 patients were alive with malignancy and 210 with no evidence of disease). These data reinforce two conclusions: (1) The probability of lung cancer recurrence or appearance of new lung cancer 5 years or more after successful operation in this select subpopulation of patients with lung cancer is of concern. (2) The malignancy-free survival advantage of patients with squamous cancer disappears after 5 years.
 ...
PMID:Malignant disease appearing late after operation for T1 N0 non-small-cell lung cancer. The Lung Cancer Study Group. 824 38

We have been investigating the mathematical nature of intercancer linkage that underlies the mutual regulation of cancer risks between any 2 tumors in their variations in time and space. Applications of both sequential regression test and topological manipulation of age-adjusted incidence rate (AAIR) data set enabled us to prepare the oncogene (Onc) activation profile and the tumor suppressor gene (TSG) inactivation profile for each tumor. The purpose of this study was to investigate the relation between the changes of 2 cancer gene profiles and the sex discrimination of cancer risk in 7 human neoplasias. Results obtained are as follows: i) The sex discrimination of cancer risk could better be defined by the use of log-transformed AAIR data rather than of untransformed AAIR data. ii) The sex discrimination of cancer risk, as calculated with the AAIR data of 47 population units of the world, is as follows: a) breast cancer (Br), M:F=1:120.2; b) thyroid cancer (Thy), M:F=1:2. 64; c) colon cancer (Co), M:F=1.18:1; d) liver cancer (Li), M:F=2. 63:1; e) lung cancer (Lu), M:F=3.66:1; f) esophageal cancer (Eso), M:F=3.68:1; g) laryngeal cancer (Lar), M:F=7.26:1. iii) Female-dominant cancers were associated with inversion (Br) or defectiveness (Thy) of male oncogene profile, whereas male-dominant cancers were associated with inversion (Lar) or defectiveness (Li, Lu and Eso) of female Onc profiles. Sex-indifferent cancer, Co, was distinguished from other tumors by the emergence of defectiveness in the TSG profiles of both sexes. TSG defectiveness was also detectable in female (Br, Thy) and bisexual (Lu) tumors. iv) The Onc vs TSG interaction, as assessed in terms of r value of the reciprocal regression analysis, was increasing in its positivity rate from the top of the female-dominant family (Br) through the sex-indifferent tumor (Co) to the bottom of the male-dominant family (Lar). In conclusion, the emergence of sex discrimination of cancer risk was positively correlated to the extent of integrity of oncogene activation in the dominant gender relative to the recessive gender. Findings with 6 sex-discriminant tumors are discussed in their relevancy to tumorigenesis from the point of view of endocrinological epidemiology.
 ...
PMID:Relation between the changes of oncogene versus tumor suppressor gene interaction and the transition of cancer risk from female dominance through no sex discrimination to male dominance, as investigated by the reciprocal regression analysis of 5 human neoplasias. 968 28

CDKN2A is thought to be the main candidate gene for melanoma susceptibility. Deletion or mutations in the CDKN2A gene may produce an imbalance between functional p16 and cyclin D, causing abnormal cell growth. We here describe a novel mutation consisting of a 1 bp deletion at nucleotide position 201 (codon 67) (CACGGcGCG) resulting in a truncated protein (stop codon 145). The patient, a female subject from a melanoma-prone family, presented at the age of 47 years with a superficial spreading melanoma of the trunk. Her father had colon cancer at the age of 43 years and melanoma at 63 years, her uncle suffered from gastric cancer, and her grandfather had laryngeal cancer.
 ...
PMID:CDKN2A novel mutation in a patient from a melanoma-prone family. 1159 80

During the last 2 decades, long-term survival after lung transplantation has significantly improved. However, among the complications related to the continuous administration of immunosuppressive drugs, malignancy plays an important role. We retrospectively revisited our series of patients to report our experience. From January 1991 we performed 134 lung transplantations in 128 recipients (mean age, 33.4 +/- 13.5 years). In all patients the first-line immunosuppressive regimen was based on a calcineurin inhibitor (cyclosporine or tacrolimus), an antimetabolic agent (azathioprine), and steroids. Five patients (4.2%) developed malignancy and the mean time of occurrence after the transplantation was 46.4+/-23 months. The mean age was 41 +/- 16 years (P = not significant [ns]). The tumors were as follows: laryngeal cancer (radiotherapy), colon cancer (surgery plus adjuvant chemotherapy), gastric cancer (surgery plus adjuvant chemotherapy), endobronchial non-Hodgkin lymphoma (NHL) (endoscopic resection plus chemoradiotherapy), and cutaneous and visceral Kaposi's sarcoma (KS) (chemotherapy). All patients have reduced the dose of immunosuppressive drugs; in 1 of them, tacrolimus was changed to rapamycin. Two patients died because of neoplastic dissemination, another 1 due to obliterans bronchiolitis. The 2 patients with NHL and KS are alive at 6 and 9 months, respectively, without signs of recurrence. Malignancies after lung transplantation represent an important problem. A multidisciplinary approach is mandatory to obtain satisfactory results in terms of improved quality of life and long-term survival.
 ...
PMID:Malignancies following lung transplantation. 1769 72

Mutations in the CHEK2 gene have been associated with increased risks of breast, prostate and colon cancer. In contrast, a previous report suggests that individuals with the I157T missense variant of the CHEK2 gene might be at decreased risk of lung cancer and upper aero-digestive cancers. To confirm this hypothesis, we genotyped 895 cases of lung cancer, 430 cases of laryngeal cancer and 6391 controls from Poland for four founder alleles in the CHEK2 gene, each of which has been associated with an increased risk of cancer at several sites. The presence of a CHEK2 mutation was protective against both lung cancer [odds ratio (OR) = 0.3; 95% confidence interval (CI) 0.2-0.5; P = 3 x 10(-8)] and laryngeal cancer (OR = 0.6; 95% CI 0.3-0.99; P = 0.05). The basis of the protective effect is unknown, but may relate to the reduced viability of lung cancer cells with a CHEK2 mutation. Lung cancers frequently possess other defects in genes in the DNA damage response pathway (e.g. p53 mutations) and have a high level of genotoxic DNA damage induced by tobacco smoke. We speculate that lung cancer cells with impaired CHEK2 function undergo increased rates of cell death.
 ...
PMID:Constitutional CHEK2 mutations are associated with a decreased risk of lung and laryngeal cancers. 1828 Dec 49

The NOD2 gene has been associated with susceptibility to Crohn's disease and individuals with Crohn's disease are at increased risk for cancer at a number of organ sites. We studied the association between the 3020insC allele of the NOD2 gene and cancer among 2604 cancer patients and 1910 controls from Poland. Patients were diagnosed with one of twelve types of cancer in the Szczecin region between 1994 and 2004. Significant associations were found for colon cancer (OR = 1.8; 95% CI 1.2 to 2.6), for lung cancer (OR = 1.7; 95% CI = 1.1 to 2.5) and for ovarian cancer (OR = 1.6; 95% CI 1.1 to 2.3). In addition, a significant association was found for early-onset laryngeal cancer (OR = 2.9; 95% CI 1.4 to 6.2) and for breast cancer in the presence of DCIS (OR = 2.1 95% CI = 1.2 to 3.6). The NOD2 3020insC allele is relatively common (in Poland 7.3% of individuals) and may be responsible for an important fraction of cancer cases. We estimate that the lifetime cancer risk among carriers of this allele is 30% higher than that of individuals with two wild-type alleles.
 ...
PMID:The 3020insC Allele of NOD2 Predisposes to Cancers of Multiple Organs. 2022 31


1 2 Next >>