Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0596263 (carcinogenesis)
 64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of our study was to investigate the expression of prostate stem cell antigen (PSCA), piwi-like 1 (PIWIL1) and T-box 2 (TBX2) and its correlation with HPV16 infection in cervical squamous cell carcinoma (CSCC). HPV16 was detected by amplifying the HPV16 E7 gene by the polymerase chain reaction (PCR) method, and the expression of PSCA, PIWIL1, TBX2 and HPV16 E7 in 59 CSCCs and matched adjacent normal cervix (MANC) was examined by the streptavidin-peroxidase (SP) method. Fifty-two CSCCs and MANC specimens that were positive for the E7 gene and the E7 protein were identified as infected with HPV16 and included in present study. The rate of infection with HPV16 in CSCC was 52% (27/52), but that in matched adjacent normal cervix (MANC) samples was 4% (2/52). Infection with HPV16 was found to be statistically more frequent in CSCC (P = 0.000). The expression rates of PSCA, PIWIL1 and TBX2 in MANC were 6% (3/52), 8% (4/52) and 2% (1/52), respectively, but those in CSCC were 62% (32/52), 75% (39/52) and 52% (27/52), respectively. Higher expression rates of PSCA, PIWIL1 and TBX2 were observed in CSCC than in MANC (P = 0.000). HPV16 had a statistical positive correlation with PSCA, PIWIL1 and TBX2 in CSCC (P < 0.05). The increased expression of PSCA, PIWIL1 and TBX2 had no correlation with the patient's age or histological grade P > 0.05). The elevated expression of PSCA and PIWIL1 was associated with invasion of CSCC (P < 0.05). Up-regulated expression of TBX2 had a positive association with lymph node metastasis (P = 0.014). These findings demonstrate for the first time the expression of PSCA, PIWIL1 and TBX2 in CSCC. Their correlation with HPV16 might provide new basic information for investigating the molecular mechanism of HPV and help us to deepen our understanding of the interaction between HPV16 and host cells the carcinogenesis of CSCC.
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PMID:Expression of PSCA, PIWIL1 and TBX2 and its correlation with HPV16 infection in formalin-fixed, paraffin-embedded cervical squamous cell carcinoma specimens. 2022 17

Infection-associated chronic inflammation plays an important role in tumorigenesis, and macrophages are a key player in both inflammation and tumorigenesis. Tumor-associated macrophages accelerate tumorigenesis through the enhancement of angiogenesis, remodeling and the suppression of antitumor immunity. Helicobacter pylori infection induces inflammatory responses, which are closely associated with gastric cancer development. Recent studies using mouse models indicate that activated macrophages in the infected and inflamed gastric mucosa express TNF-alpha, which stimulates the surrounding epithelial cells to promote Wnt signaling activity. Such a promotion of Wnt signaling activity beyond the threshold for tumorigenesis may, therefore contribute to gastric cancer development. Accordingly, it is possible that the TNF-alpha-induced promotion of Wnt signaling is a novel protumorigenic mechanism of inflammation in gastric carcinogenesis.
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PMID:Inflammation, tumor necrosis factor and Wnt promotion in gastric cancer development. 2037 66

Colonization of the human stomach with Helicobacter pylori induces chronic gastritis and is associated with the development of gastric and duodenal ulcers, gastric carcinoma, and gastric mucosa-associated lymphoid tissue lymphoma. Infection with an H. pylori strain containing the cytotoxin-associated (cagA) gene (a marker for a pathogenicity island) may increase the risk of atrophic gastritis and gastric cancer. The exact role of H. pylori in gastric carcinogenesis is still being investigated. Hence, we assessed whether H. pylori infection is associated with the development of gastric adenocarcinoma in northern Iran. Gastric biopsy specimens from 168 patients suffering from gastric adenocarcinoma, gastric ulcer, and non-ulcer dyspepsia were analyzed by means of the polymerase chain reaction. H. pylori was detected in the gastric mucosa of 34 (75.5%) gastric adenocarcinoma, 56 (88.8%) gastric ulcer, and 36 (60%) non-ulcer dyspepsia. In patients with gastric adenocarcinoma, the cagA was less commonly found than those in noncancer patients (4/34 vs. 58/92, p < 0.05). Our work suggests that although H. pylori infection is significantly associated with gastric adenocarcinoma in northern Iran, the cagA is not the dominant virulence in development of gastric adenocarcinoma.
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PMID:The relationship between Helicobacter pylori infection and gastric adenocarcinoma in Northern Iran. 2037 33

In addition to the classic risk factors of oral cancer, namely alcohol and tobacco, other factors both infectious and environmental are thought to be associated with the development of oral malignancy. Infections in the oral cavity may be an important preventable cause of cancer. Poor oral hygiene, periodontal disease, chronic candidiasis, human papilloma virus (HPV) and herpesvirus infections link statistically with cancer but the mechanisms involved are largely unknown. Infections may trigger cell proliferation, inhibit apoptosis, interfere with cellular signaling mechanisms and up-regulate tumor promoters. In addition, several oral micro-organisms metabolize alcohol to carcinogenic acetaldehyde thus explaining the association between poor oral hygiene, alcohol consumption and carcinogenesis. With regards to dietary factors the Mediterranean-type fruit and vegetable rich diet has been shown to reduce the risk of oral cancer but the evidence is weak, the effect of individual food components and trace elements on carcinogenesis remains unclear at present.
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PMID:Infectious and dietary risk factors of oral cancer. 2038 9

Human papillomaviruses are small DNA viruses that cause hyperproliferative lesions of the mucosa and skin. Some HPV types, collectively known as high-risk types, are etiologically associated to cervical cancer and other anogenital malignancies. Infection by these HPV types has been associated to genomic instability, a hallmark of most human malignancies. High-risk HPV types express two oncoproteins, E6 and E7, which target specific cellular factors to promote cell proliferation. Furthermore, these proteins induce structural and numerical chromosome alterations and modulate cellular response to DNA damage. These observations are discussed in the context of cervical carcinogenesis.
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PMID:HPV-mediated genome instability: at the roots of cervical carcinogenesis. 2038 33

Oesophageal squamous cell carcinoma (OSCC) remains a public health problem in many countries, especially in emerging and developing countries. Epidemiology of OSCC is characterized by marked differences in prevalence between countries/regions/ethnical groups. The highest incidence in the world is reached by populations living in specific areas of northwestern Xinjiang, China where age-adjusted mortality may reach 150 of 100 000. In fact, there are also marked differences among the various geographical areas and the various ethnic groups within the region, which suggests specific risk factors. Behavioural factors include those factors which are common to all 'high-risk populations', such as tobacco smoking and alcohol drinking. However, the very unusual sex ratio (1.2 : 1.0) and young age range of OSCC occurrence suggests the involvement of additional early risk factors shared by males and females, and which are different from those studied in other 'high-risk' areas of the world, including China, such as LinXian area. These include drinking very hot and salted tea, boiled with milk; a diet rich in meat, especially salted, dry and/or smoked meat, and dairy products; and a diet poor in fresh fruit and vegetables. The combination of hot drinks (such as milk, tea and soups) and high-degree spirit drinks, and hard food (bread, meat and cheese), together with poor oral hygiene and tooth loss, is likely to add mechanical injury of the oesophagus to other factors linked to climate characteristics of the area (drought) and dietary habits, which promote a sodium and nitrosamine-rich diet. Association of early and severe hypertension in the same populations at high risk of OSCC might likely raise more attention. Human papilloma virus (HPV) infection, and especially HPV 16/18 E6/E7, with gene mutations and association with p53 overexpression, may contribute to the extremely high incidence of OSCC observed in Xinjiang, and could be accessible to prevention. Infection may especially be a crucial additional factor in the Uygur population in which not only HPV infection but also infection with other oncogenic viruses, such as HHV8, are highly prevalent. Genetic polymorphism might interact with viruses and/or viral products to promote carcinogenesis. These observations in northwestern China suggest that usually neglected factors, such as sodium excess and viral infection, could be taken into more account when studying OSCC risk factors in other parts of the world, especially Europe.
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PMID:Northwestern China: a place to learn more on oesophageal cancer. Part one: behavioural and environmental risk factors. 2052 May 61

Infection with the high-risk HPV types 16 and 18 is the major cause of cervical cancer and plays a role in the development of certain head and neck and skin cancers. We have previously demonstrated that the Early Protein 2 of the Cottontail Rabbit papillomavirus (CRPV), required for skin carcinogenesis in a rabbit model, is able to induce the expression of a matrix metalloproteinase (MMP-9); a protease known to play a key role in invasion and metastasis. However, as of now we do not understand the underlying mechanism of activation nor relevance for the human system. Here, we report that high-risk human papillomavirus HPV16 E2 similar to our previously reported results on CRPV E2 activates the human MMP-9 promoter predominantly via the MEK1-ERK1/2-AP-1-signaling pathway. In addition this activation is associated with a nuclear sub-localisation of HPV16-E2 suggesting a nuclear protein-protein or protein-DNA interaction of E2 as the underlying mechanism of activation.
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PMID:Influence of HPV16 E2 and its localisation on the expression of matrix metalloproteinase-9. 2059 61

Adult T-cell leukemia (ATL) is a T-cell malignancy associated with human T-cell leukemia virus type 1 (HTLV-1). Mutations of tumor suppressor genes have been described in ATL. Although Tax, a product of HTLV-1, is associated with cellular genetic aberrations, the mechanisms of such association are not fully clear. Activation-induced cytidine deaminase (AID) is involved in somatic DNA alterations of the immunoglobulin gene for amplification of immune diversity. However, inappropriate expression of AID acts as a genomic mutator that contributes to tumorigenesis. To gain insight into the molecular mechanism underlying the emergence of somatic mutations in various genes during leukemogenesis, we examined the expression of AID. HTLV-1-infected T-cell lines and ATL cells expressed high levels of AID compared with uninfected T-cell lines and normal peripheral blood mononuclear cells (PBMCs). Immunohistochemistry showed AID-positive ATL cells in lymph nodes and skin lesions. Infection of a human T-cell line and normal PBMCs with HTLV-1 induced AID expression. Tax transcriptionally activated AID gene through both the nuclear factor-kappaB subunit p50 and cyclic adenosine 3',5'-monophosphate response element-binding protein signaling pathways. p50, which lacks a transactivation domain, interacted with the transcriptional coactivator Bcl-3 in HTLV-1-infected T cells. Thus, activation of p50/Bcl-3 complexes in T cells in response to Tax might explain the constitutive expression of AID in HTLV-1-infected T cells. The constitutive expression of AID in ATL cells can be speculated to result from mutations induced by the Tax-activated AID and/or other Tax-associated mutagenic mechanisms during the pre-leukemic stage, which cause functional modification within the AID promoter or in any of its cellular regulatory activator proteins.
Carcinogenesis 2011 Jan
PMID:Activation of AID by human T-cell leukemia virus Tax oncoprotein and the possible role of its constitutive expression in ATL genesis. 2097 84

A better understanding of the immune processes in the pathogenesis and progression of prostate cancer (CaP) may point the way towards improved treatment modalities. The challenge is to amplify immune responses to combat tumour escape mechanisms. Infection and inflammation may have a role in prostate carcinogenesis, including the newly discovered xenotropic murine leukaemia virus (XMRV). These inflammatory states damage defence mechanisms and induce a high proliferative state favouring further mutation and impaired immune surveillance. With this knowledge we are able to explore the use of immunotherapy to rejuvenate the immune system in combating CaP. Recently Sipuleucel-T, an immunotherapeutic agent for metastatic androgen independent CaP, has resulted in improved survival and might be the first immunotherapeutic agent to obtain approval for CaP treatment. This short review will focus on the growing body of evidence suggesting an immunity-based link between CaP and inflammation and infection.
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PMID:Prostate cancer immunology - an update for Urologists. 2107 May 75

The purpose of our study was to assess the prevalence and prognostic significance of HPV infection as well as K-ras codon 12 point mutations in lung cancer. Patients diagnosed with lung carcinoma between 1988 and 1992 (N=99) were selected. HPV detection and typing was performed by PCR from paraffin-embedded tissues, while mutations in codon 12 of K-ras gene were detected using the restriction fragment length polymorphism (RFLP) analysis. The prevalence of HPV infection was 15%, while K-ras codon 12 point mutations were found in 18% of the specimens examined. In 50% of the HPV-positive cases, K-ras gene mutation coexisted. HPV 18 was the most frequent type. No correlation was found between K-ras mutation and HPV infection with sex, age and clinical outcome of the patient, or the histological type and the differentiation grade of the tumor. An association was found between K-ms codon 12 point mutations and the stage of the tumor, occurring more frequently at stage III (p=0.037). Infection with potentially oncogenic HPV types could co-operate with K-ras gene activation in the progression of the disease, since K-ras activation by point mutations seems to be a late event in lung carcinogenesis.
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PMID:Detection of human papilloma virus (HPV) and K-ras mutations in human lung carcinomas. 2154 68


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