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)

Mutations in the p53 gene stimulate cell division. In our study we assessed the prognostic value of mutant p53 overexpression in cervical cancer stage FIGO III detected by immunohistochemistry. In 43 tissue specimens were detected p53 overexpression in 20 cases. Mean survival time was 36.4 (SE +/- 7.66) months in the p53 protein positive group. The group without p53 overexpression showed a mean survival time of 28.6 (SE +/- 3.85) months. p53 protein overexpression had no prognostic value in patients with stage III cervical cancer.
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PMID:Mutant p53 product in patients with stage III cervical cancer. 129 70

The present study evaluates the prognostic value of mutant p53 protein overexpression in 109 surgically treated cervical cancer stages IB to IIB. Squamous cell carcinoma stages IB, IIA, and IIB were present in 52, 13, and 44 cases, respectively. We performed immunohistochemistry using a monoclonal antibody against the p53 suppressor gene product (clone BP53-12). Data were analyzed for the end points of disease-free survival and overall survival. In 109 tissue specimens we detected 22 cases of p53 expression. Six of 22 patients with p53 expression and 21 of 87 patients without p53 expression showed tumor recurrences. p53 expression showed no significant correlation to age, tumor stage or lymph node involvement. In the univariate analysis p53 expression showed no prognostic value for disease-free (P = 0.5) and overall survival (P = 0.6). Multivariate analysis showed a significant prognostic value for established prognostic parameters while p53 expression had no prognostic value for recurrence-free (P = 0.6) and overall survival (P = 0.5). In contrast to other malignancies mutant p53 overexpression showed no relation to prognosis in surgically treated cervical cancer stage IB to IIB.
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PMID:Mutant p53 in patients with invasive cervical cancer stages IB to IIB. 772 36

Cervical cancer is driven by persistent infection of human papillomavirus (HPV), which is influenced by HPV type and intratypic variants, yet the impact of HPV type and intratypic variants on patient outcomes is far less understood. Here, we examined the association of cervical cancer stage and survival with HPV type, clade, lineage, and intratypic variants within the HPV E6 locus. Of 1,028 HPV-positive cases recruited through the CerGE study, 301 were in-situ and 727 were invasive cervical cancer (ICC), with an average post-diagnosis follow-up of 4.8 years. HPV sequencing was performed using tumor-isolated DNA to assign HPV type, HPV 16 lineage, clade, and intratypic variants within the HPV 16 E6 locus, of which nonsynonomous variants were functionally annotated by molecular modeling. HPV 18-related types were more prevalent in ICC compared to in-situ disease and associated with significantly worse recurrence-free survival (RFS) compared to HPV 16-related types. The HPV 16 Asian American lineage D3 and Asian lineage A4 associated more frequently with ICC than with in situ disease and women with an intratypic HPV 16 lineage B exhibited a trend toward worse RFS than those with A, C, or D lineages. Participants with intratypic E6 variants predicted to stabilize the E6-E6AP-p53 complex had worse RFS. Variants within the highly immunogenic HPV 16 E6 region (E14-I34) were enriched in ICC compared to in-situ lesions but were not associated with survival. Collectively, our results suggest that cervical cancer outcome is associated with HPV variants that affect virus-host interactions.
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PMID:Genetic variations in human papillomavirus and cervical cancer outcomes. 3051 67