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Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presence of human papilloma virus (HPV) has recently been demonstrated in colon tumors, but the incidence of HPV infection in normal colon mucosa or in benign or malignant neoplasms of the mucosa is unknown. We studied both neoplastic and normal human colon tissue for the presence of HPV antigen using immunohistochemical techniques. Ninety colon specimens were studied. Three consecutive series of normal colon mucosa (N = 30), single benign tubulovillous adenomas (N = 30), and invasive carcinomas (N = 30) were selected and confirmed histologically. Formalin-fixed paraffin-embedded samples of each tissue were prepared using immunohistochemical techniques and resultant slides were read blindly and graded simply as positive or negative for HPV antigen. The presence of HPV antigen varied dramatically between groups, with 97% of the invasive carcinomas, 60% of the benign tubulovillous adenomas, and 23% of the normal mucosa positive for HPV antigen. Groups were statistically significant using chi 2 analysis (P less than 0.001). We conclude that an association exists between the human colon neoplasia and the presence of HPV antigen. This may suggest an etiologic role of the virus in colon cancer.
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PMID:Immunohistochemical demonstration of human papilloma virus antigen in human colon neoplasms. 216 68

The Swedish Family-Cancer Database was used to analyze relationships between parents and offspring with in situ cancers and between in situ cancers in one generation and invasive cancer in the other generation. A total of 130,000 in situ cancers and close to 400,000 invasive cancers were included from 1959 to 1994. The data on family relationships and cancers came from registered sources and should be free from bias. The offsprings' familial relative risks (FRRs) were calculated for concordant and discordant parental cancer sites. The most common male in situ site was skin (both melanoma and precancerous epithelial lesion), whereas cervix, breast, and skin were common female sites. Increased FRRs were observed for concordant sites: colon, breast, cervix, skin (melanoma), and, in males, precancerous epithelial lesions. The findings were consistent when in situ cancer-in situ cancer and in situ cancer-invasive cancer relationships were explored. FRRs were higher for in situ colon cancer and melanoma than the respective estimates in invasive cancers, and for the remaining sites, they were equal or somewhat lower. At discordant sites, increased FRRs of in situ cancers were observed for female breast and melanoma and, at many sites, implicated in tobacco and human papilloma virus carcinogenesis, together with cervix. Family histories of in situ cancers deserve clinical attention.
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PMID:Familial risks in in situ cancers from the Family-Cancer Database. 979 30

It has been reported that the p53Arg homozygous genotype could be a potential genetic risk factor for cancer. In this study we investigated the proportion of p53 codon 72 genotypes in patients with colon cancer and compared to a control population. A region of the p53 gene containing the polymorphic site was amplified by PCR and the genotypes were determined by restriction enzyme digestion. No significant difference was found between genotype frequencies in the study groups. Infection with human papilloma virus was also investigated in the tumor samples. HPV 18 and HPV 33 infection was observed in a considerable number of the tumor samples. Incidence of HPV infection did not show a correlation with the genotypes. Thus the p53 genotypes do not seem to be associated with risk of colon cancer or HPV infection.
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PMID:P53 codon 72 genotypes in colon cancer. Association with human papillomavirus infection. 1145 82

The etiological role of human papilloma virus (HPV) in a number of squamous cell malignant tumours is well known. Squamous cell carcinoma of colon (SCC) is a rare disease with uncertain etiology. Our objective was to detect possible HPV infection in a colon SCC patient. The 94-year-old female patient was operated for an obstructive colon tumour. Histology confirmed SCC. Tumour tissue and the removed lymph nodes were examined with polymerase chain reaction and Southern blot hybridization techniques. From HPV types 16 and 18, which most commonly associated with malignant tumours, the presence of HPV type 16 could be confirmed in the primary tumour and in 4 out of the 9 surrounding lymph nodes (of which 2 were metastatic). HPV-16 infection was detected in a colon cancer patient with SCC histological type in the primary tumour and in surrounding lymph nodes. According to our knowledge, no similar study has been published yet.
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PMID:[Detection of human papilloma virus type 16 in squamous cell carcinoma of colon and its lymph node metastases]. 1879 6

According to the conflicting growth signal model, cells that are driven to proliferate by certain oncogenes undergo apoptosis but not growth arrest upon withdrawal of growth factors. However, we found that the majority of human cancer cell lines continued to proliferate and did not undergo apoptosis following serum withdrawal. As an exeption, wild-type (wt) p53-expressing HCT116 human colon cancer cells underwent apoptosis within 24-36 h of serum deprivation. p53 degradation in human papilloma virus EG-expressing HCT116 cells led to enhanced survival that was not due to growth arrest. These results are consistent with a role for p53 in starvation-induced death in HCT116 cells. However, other cell lines did not undergo apoptosis despite their expression of wt p53. Thus, H460 cells (wt p53) were resistant to starvation-induced death but introduction of the adenovirus EIA oncoprotein induced p53 and also increased sensitivity to serum withdrawal. p53 was not stabilized by E1A and resistance to starvation-induced cell death was observed in E6-expressing H460 cells. These results suggest that although p53 contributes to starvation-induced apoptosis in sensitive (HCT116 and E1A-expressing H460) cancer cell lines, most cancer cells survived despite the presence of wt p53. We conclude that naturally selected human cancer cell lines suppress apoptosis due to conflicting growth signals.
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PMID:Wild-type p53 is not sufficient for serum starvation-induced apoptosis in cancer cells but accelerates apoptosis in sensitive cells. 2152 17

The bromodomain protein, BRD4, has been identified recently as a therapeutic target in acute myeloid leukemia, multiple myeloma, Burkitt's lymphoma, NUT midline carcinoma, colon cancer, and inflammatory disease; its loss is a prognostic signature for metastatic breast cancer. BRD4 also contributes to regulation of both cell cycle and transcription of oncogenes, HIV, and human papilloma virus (HPV). Despite its role in a broad range of biological processes, the precise molecular mechanism of BRD4 function remains unknown. We report that BRD4 is an atypical kinase that binds to the carboxyl-terminal domain (CTD) of RNA polymerase II and directly phosphorylates its serine 2 (Ser2) sites both in vitro and in vivo under conditions where other CTD kinases are inactive. Phosphorylation of the CTD Ser2 is inhibited in vivo by a BRD4 inhibitor that blocks its binding to chromatin. Our finding that BRD4 is an RNA polymerase II CTD Ser2 kinase implicates it as a regulator of eukaryotic transcription.
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PMID:BRD4 is an atypical kinase that phosphorylates serine2 of the RNA polymerase II carboxy-terminal domain. 2250 28

Anal intraepithelial neoplasia (AIN) is a premalignant lesion of the anal mucosa that is a precursor to anal cancer. Although anal cancer is relatively uncommon, rates of this malignancy are steadily rising in the United States, and among certain high risk populations the incidence of anal cancer may exceed that of colon cancer. Risk factors for AIN and anal cancer consist of clinical factors and behaviors that are associated with the acquisition and persistence of human papilloma virus (HPV) infection. The strongest HPV-associated risk factors are HIV infection, receptive anal intercourse, and high risk sexual behavior. A history of HPV-mediated genital cancer, which suggests infection with an oncogenic HPV strain, is another risk factor for AIN/anal cancer. Because progression of AIN to anal cancer is known to occur in some individuals over several years, screening for AIN and early anal cancer, as well as treatment of advanced AIN lesions, is reasonable in certain high-risk populations. Although randomized controlled trials evaluating screening and treatment outcomes are lacking, experts support routine screening for AIN in high risk populations. Screening is performed using anal cytological exams, similar to those performed in cervical cancer screening programs, along with direct tissue evaluation and biopsy via high resolution anoscopy. AIN can be treated using topical therapies such as imiquimod, 5-flurouracil, and trichloroacetic acid, as well as ablative therapies such as electrocautery and laser therapy. Reductions in AIN and anal cancer rates have been shown in studies where high-risk populations were vaccinated against the oncogenic strains of HPV. Currently, the CDC recommends both high-risk and average-risk populations be vaccinated against HPV infection using the quadrivalent or nonavalent vaccines. It is important for clinicians to be familiar with AIN and the role of HPV vaccination, particularly in high risk populations.
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PMID:Anal intraepithelial neoplasia: A review of diagnosis and management. 2825 26

The generation of tumour-specific T cells is critically important for cancer immunotherapy. A major challenge in achieving a robust T-cell response is the spatiotemporal orchestration of antigen cross-presentation in antigen-presenting cells with innate stimulation. Here, we report a minimalist nanovaccine, comprising a simple physical mixture of an antigen and a synthetic polymeric nanoparticle, PC7A NP, which generates a strong cytotoxic T-cell response with low systemic cytokine expression. Mechanistically, the PC7A NP achieves efficient cytosolic delivery of tumour antigens to antigen-presenting cells in draining lymph nodes, leading to increased surface presentation while simultaneously activating type I interferon-stimulated genes. This effect is dependent on stimulator of interferon genes (STING), but not the Toll-like receptor or the mitochondrial antiviral-signalling protein (MAVS) pathway. The nanovaccine led to potent tumour growth inhibition in melanoma, colon cancer and human papilloma virus-E6/E7 tumour models. The combination of the PC7A nanovaccine and an anti-PD-1 antibody showed great synergy, with 100% survival over 60 days in a TC-1 tumour model. Rechallenging of these tumour-free animals with TC-1 cells led to complete inhibition of tumour growth, suggesting the generation of long-term antitumour memory. The STING-activating nanovaccine offers a simple, safe and robust strategy in boosting anti-tumour immunity for cancer immunotherapy.
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PMID:A STING-activating nanovaccine for cancer immunotherapy. 2843 62