Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04637 (p53)
 77,613 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to analysis the relationship between p53 codon 72 polymorphism with human papillomavirus (HPV) 16 and 18 E6 in Chinese cervical cancer. A total of 81 cervical squamous cancer (specimens of G1, G2, and G3 are 13, 24, and 44, respectively; and of stage IB, IIA, IIB, and IIIA are 15, 37, 24, and 5, respectively), 18 cervical adenocarcinoma, 88 cervical intraepithelial neoplasm (CIN) (specimens of CIN II and III are 30 and 58), and 60 normal cervical specimens were included in this study. Polymerase chain reaction was used to examine p53 genotypes and HPV 16 and 18 E6. The frequencies of p53 Arg homozygosity in cervical squamous cancer, cervical adenocarcinoma, and CIN (II-III) were 58.02%, 55.55%, and 59.09%, respectively, that was much higher than that of p53 Arg/Pro heterozygosity (30.86%, 27.78%, and 21.59%) and of p53 Pro homozygosity (11.12%, 16.67%, and 19.32%) in each groups and higher than the frequency of p53 Arg homozygosity in normal samples (23.33%). There is no statistic difference in the normal samples for the frequency of p53 Arg homozygosity, p53 Arg/Pro heterozygosity, and p53 Pro homozygosity (23.33%, 40.00%, and 36.67%, respectively). The frequency of p53 Arg homozygosity in high risk (HR)-HPV E6-positive cervical squamous cancer samples (64.06%) is much higher than that in (HR)-HPV E6-negative cervical squamous cancer samples (35.29%) and in HR-HPV E6-positive normal samples (33.33%). No difference of p53 codon 72 polymorphism was found according to FIGO staging and grades. In conclusion, based on the findings of this study, it is suggested that p53 Arg homozygosity could act as a potential risk factor for the tumorigenesis of the cervix. p53 codon 72 polymorphism has no relation with the FIGO staging and grades of cervical cancer. p53 Arg homozygosity and HR-HPV E6 positive simultaneously can predict the fate of cervical lesions.
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PMID:Analysis of p53 codon 72 polymorphism and its association with human papillomavirus 16 and 18 E6 in Chinese cervical lesions. 1717 38

Senescence and apoptosis are two key mechanisms that protect against cancer development. Many cell cycle regulators, such as p14(ARF), p15(INK4b) and p16(INK4a), are important in G1 cell cycle arrest and oncogene-induced senescence. The bcl-2 protein is one of the key components that control apoptosis, while the p53 protein plays key roles in both mechanisms. The genes of these key regulator proteins are often mutated or deleted in various malignancies. It is unknown how senescence and apoptosis are regulated in one of the most common tumors of the female genital tract, cervical squamous cell carcinoma (SCC). In this study the, expression of senescence, apoptosis and proliferation markers in normal cervical epithelium, cervical intraepithelial neoplasia (CIN) and SCC are characterized via immunohistochemical staining for p14(ARF), p15(INK4b), p16(INK4a), bcl-2, p53 and Ki-67 in tissue microarray blocks containing 20 samples each of normal cervix, moderate-to-severe cervical dysplasia (CIN II-III) and invasive SCC. Samples are derived from 60 total cases of cervical biopsies and cervical conizations. Results showed that the proliferation marker, Ki-67, is markedly increased, and the senescence markers, p15(INK4b), p16(INK4a) and p14(ARF) are overexpressed in both dysplasia and carcinoma. P53 immunostain is negative in all normal cervical tissue, and positive in dysplasia and carcinoma. Although the expression of bcl-2 is increased in dysplasia, this marker is negative in approximately half of SCC cases. These results suggest that some senescence pathways are activated and are still maintained in cervical dysplasia and carcinoma. However proliferation is increased and carcinogenesis is not thwarted, leading to eventual development of cervical cancer. Other mechanisms, such as those that account for the apparent overexpression of p53 and paradoxical loss of bcl-2 expression in some SCC cases, as well as additional senescence and apoptotic pathways, may play key roles carcinogenesis of cervical SCC.
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PMID:Senescence and apoptosis in carcinogenesis of cervical squamous carcinoma. 1763 54

The purpose of this study was to examine the implication of high-risk human papillomavirus (HPV) load in cervical intraepithelial neoplasia (CIN) and cancer, and to detect biomarkers in cervical disease. We conducted high-risk HPV DNA load and cervical cytology tests in 343 women, cervical tissue biopsy in 143 women, and immunohistochemistry for p16(INK4A), cyclin D1, p53, cyclooxygenase-2, Ki-67, GLUT1, hPygopus2, and beta-catenin. As a result, HPV load [relative light units (RLU) value] was correlated with the histological severity of cervical disease (p < 0.05). In the 'atypical squamous cells of undetermined significance' cytology group, 2.385 of HPV load seemed to be the cut-off value at which 'benign' or CIN I can be differentiated from 'CIN II or more severe' (AUC = 0.712), but not statistically significant. The relative risk (odds ratio) of p16(INK4A) and GLUT1 overexpression increased gradually according to the histological severity of cervical disease. The p16(INK4A) showed statistically significant odds ratios in CIN II, CIN III, and cancer; GLUT1, in CIN II and CIN III; hPygopus2, in CIN III; and beta-catenin, in CIN III and cancer. Conclusively, HPV load, p16(INK4A) , and GLUT1 can be instrumental in predicting the severity of HPV-related cervical disease. The beta-catenin/hPygopus2 signaling may be involved in proceeding to CIN III.
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PMID:High-risk human papillomavirus load and biomarkers in cervical intraepithelial neoplasia and cancer. 2402 Jul 24

The aim of the present study was to investigate human papillomavirus (HPV) infection and p16INK4A and p53 protein expression, to evaluate their roles in the pathological diagnosis and grading for cervical intraepithelial neoplasia (CIN). The detection of HPV DNA and p16INK4A and p53 protein expression were examined in a panel of clinical tissue samples using polymerase chain reaction or immunohistochemistry. In 104 cases, HPV16/18 DNA was identified in 49.0% and HPV6/11 DNA in 9.6% of cases. While in 203 cases, 74.4% positively expressed p16INK4A and 47.3% positively expressed p53. The expression of p16INK4A exhibited a significantly higher rate in the CIN I group than in the squamous metaplasia coupled with hyperplasia group (SMH; P<0.0001) and the CIN II-III group (P=0.005). A marked correlation was revealed between the band-like staining pattern of p16INK4A and HPV16/18 infection. On the contrary, p53 expression was not found to significantly correlate with CIN grade or the HPV16/18 infection status. These results suggested that p16INK4A expression correlates with a higher grade of CIN and may be used as a diagnostic marker to distinguish between CIN I and SMH, as well as between CIN I and CIN II-III.
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PMID:Detection and pathological value of papillomavirus DNA and p16INK4A and p53 protein expression in cervical intraepithelial neoplasia. 2452 81

Serum autoantibodies against tumor-associated antigens (TAAs) have received much attention as potential biomarkers for early detection of cancers, since they can be detected in the early stages of cancers. Autoantibodies against Cancer Antigen 15-3 (CA15-3), carcinoembryonic antigen (CEA), Cancer Antigen 19-9 (CA19-9), c-Myc, p53, heat shock protein (Hsp)27 and Hsp70 have been suggested as potential markers for detecting several types of cancer. In the present study, the seven types of antibody listed above were evaluated for detecting cervical lesions. Enzyme-linked immunosorbent assays (ELISAs) were used to measure IgG levels of the autoantibodies in women with normal cytology, cervical intraepithelial neoplasia (CIN) I, CIN II, CIN III and cervical cancer. The increases of anti-CA15-3 and anti-CEA IgG in cervical cancer were more pronounced than the increases of the other markers, and the level of anti-CA19-9 IgG in CIN III stage was higher than in normal CIN I, CIN II or cervical cancer. A combination of ELISAs detecting anti-CA15-3, anti-CEA and anti-CA19-9 IgGs was found to reliably discriminate CINs from normal and to strongly differentiate cancer from normal (90.3% of sensitivity and 82.1% of specificity). We suggest that the combination of three ELISA may be useful for detecting cervical lesions.
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PMID:Use of autoantibodies against tumor-associated antigens as serum biomarkers for primary screening of cervical cancer. 2928 61

There has been no attempt to apply protein-based markers of exfoliated cervical cells (ECCs) for primary screening of cervical cancer. In the present study, the levels of six tumor-associated protein [TAPs: Sialyl Lewis A (SLeA), Cancer Antigen 15-3 (CA 15-3), p53, heat shock protein (Hsp)70, Hsp27 and squamous cervical carcinoma antigen (SCCA)]and of two human papillomavirus (HPV) viral proteins (HPV16 E7 and HPV16 L1) of ECCs lysates were evaluated by enzyme-linked immunosorbent assays (ELISAs).The wells of 96-well plates were coated with the ECCs lysates from normal, cervical intraepithelial neoplasia (CIN) I, CIN II, CIN III and cancer groups, and candidate proteins were detected by relevant antibodies. SLeA level decreased with increasing severity of lesions, whereas the levels of other candidate proteins increased. SLeA, HPV16 L1 and p53 levels appeared more useful for detecting cervical lesions than the other candidates. The combination of ELISA-SLeA and ELISA-HPV16 L1 could efficiently detect cervical lesions from normal. The combination of ELISA-SLeA and ELISA-p53 could powerfully discriminate cancer from normal with 91.3% sensitivity and 96.7% specificity. The protein levels of ECCs have great potential as biomarkers for primary screening of cervical cancer.
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PMID:Use of protein-based biomarkers of exfoliated cervical cells for primary screening of cervical cancer. 2949 27


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