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 p53 gene product has been detected frequently in various human malignancies. We have studied the expression of p53 protein in urothelial transitional cell cancers (TCCs) and examined its correlation with pathologic grade, stage(pT) and patient survival. Specimens from 69 surgically-resected TCCs (38 cases of urinary bladder cancer, 17 cases of ureteral cancer and 14 cases of renal pelvic cancer) were examined by immunohistochemical staining, using two anti-p53 monoclonal antibodies, PAb1801 and PAb240, and a polyclonal antibody, CM-1. Twenty-six TCCs (37.6%) were positively stained by at least one of the three antibodies. Statistical analysis showed a significant correlation between p53 expression and high pathologic grade (p < 0.05, p < 0.001) or progressive pathologic stage (p < 0.01). In addition, in 51 of the patients who were available for follow-up (23 cases of urinary bladder cancer, 13 cases of ureteral cancer, and 15 cases of renal pelvic cancer), the correlation between p53 protein expression and prognosis was examined. The survival of patients exhibiting positive p53 protein expression was significantly worse than those with p53-negative tumors (p < 0.05). These results suggest that an immunohistochemical test for p53 protein may be a useful method of evaluating the malignant potential of TCCs. Additionally, expression of p53 protein in TCCs is an indicator of a poor prognosis which should be considered in drawing up treatment strategies.
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PMID:Correlation of p53 protein expression in human urothelial transitional cell cancers with malignant potential and patient survival. 762 37

Expression of p53 protein, c-erbB-2 protein, neuron-specific enolase (NSE), Phe 5, chromogranin, laminin and collagen type IV was studied by immunohistochemistry in formalin-fixed and paraffin-embedded specimens from 20 patients with renal pelvic carcinoma. Positive membrane-bound c-erbB-2 staining was not found in any case. Two tumors stained for p53 protein. Focal immunoreactivity for laminin was present in 55% and for collagen type IV in 80%. 25% of the cases were NSE positive. None of the tumors stained for Phe 5 or chromogranin. The results were compared with the clinical outcome and the immunohistological findings of p53 protein and c-erbB-2 protein in 13 cases of bladder carcinoma in the same patient group. Four of the thirteen bladder cancer specimens, but only 2 of the 20 renal pelvic cancer specimens, expressed p53 protein. As for renal pelvic carcinoma, c-erbB-2 protein was not expressed in bladder carcinoma. We conclude that p53 gene abnormalities may be of importance in the development of carcinoma in the renal pelvis and urinary bladder, but c-erbB-2 protein expression does not play a major role.
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PMID:Transitional cell carcinoma of the renal pelvis and its expression of p53 protein, c-erbB-2 protein, neuron-specific enolase, Phe 5, chromogranin, laminin and collagen type IV. 771 33

Early detection of a mutated p53 gene is thought to provide useful information in a wide range of human tumors. The aim of this study was to identify the role of the p53 gene in transitional cell carcinoma of the urinary tract. From March 1992 to July 2003, 75 patients (54 men and 21 women) with a mean age of 66.85 years and pathologically diagnosed transitional cell carcinoma were enrolled in this study. Fifty-eight patients had bladder cancer, eight had ureteral cancer, and nine had renal-pelvic cancer. Rapid screening for mutation of the p53 gene was performed using polymerase chain reaction (PCR), single-strand conformation polymorphism (SSCP), and sequencing analysis. Primer sets were designed to amplify fragments within exons 4, 5, 6, 7, and 8 of the p53 gene. Pathology classified 37 tumors as low grade and 38 as high grade. Tumor stage was pT1 or less in 29 patients and at least pT2 in 46 patients. Of the 75 patients in this study, 47 (62.7%) had a p53 mutation. Of the patients with a p53 mutation, 33 (70.2%) had invasive tumors. Invasive tumors were associated with p53 mutation (p < 0.05). Noted in 20 patients (26.7%), exon 4 was the most common site of the mutation. Of the patients with exon 4 mutations, 15 (75%) had invasive tumors and nine (45%) had high-grade tumors. Additionally, among the 20 patients with a common polymorphism at codon 72, 16 (80%) had invasive tumors and 14 (70%) had high-grade tumors. In this study, 62.7% of patients with transitional cell carcinoma had a p53 mutation, suggesting that the p53 gene mutation may be used as a marker of transitional cell carcinoma. Invasive tumors are more likely to have a p53 gene mutation. A simple analysis of the p53 gene using PCR/SSCP is suitable for screening for p53 abnormalities in transitional cell carcinoma. The relationship between cancer risk and the codon 72 polymorphism of exon 4 needs further investigation.
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PMID:Mutation of the p53 tumor suppressor gene in transitional cell carcinoma of the urinary tract in Taiwan. 1582 90

The objective of this study was to evaluate the role of the fimbriated end and nonfimbriated epithelium of fallopian tubes with regard to p53 signature, tubal intraepithelial lesions in transition (TILT), and serous tubal in-situ carcinoma (STIC) in cases of different kinds of serous pelvic cancer. This study immunohistochemically evaluated (by Ki-67 and p53 staining) the presence of p53 signature, TILT lesions, and STIC in 14 consecutive cases of prophylactic salpingo-oophorectomy in women with BRCA-1/2 mutation (bilateral salpingo-oophorectomy), 11 cases of macroscopically inconspicuous adnexae of patients with primary contralateral tubal cancer (TC), 9 cases of primary peritoneal cancer (PPC), and 10 cases of serous ovarian borderline tumors, evaluating the fallopian tubes (using the Sectioning and Extensively Examining the FIMbria protocol), ovarian surface epithelium, and ovarian cortical inclusion cysts. The frequencies of p53 signature, TILT, and STIC were 35.7%, 7.1%, and 0% in cases of prophylactic surgery, 18.2%, 9.1%, and 18.2% in TC, and 11.1%, 0%, and 33.3% in PPC. These precursor lesions were missed during the initial routine screening and were found in the fimbriated end of the fallopian tubes in 94%. In 1 case of PPC, staining for p53 was negative in STIC. The studied adnexal tissue of serous ovarian borderline tumor and ovarian cortical inclusion cysts of all cases showed no alterations according to p53 signature, TILT, or STIC. STIC and p53 signature as precursor lesions of pelvic serous cancer were seen in macroscopically inconspicuous contralateral fallopian tubes in unilateral TC, in patients with elective bilateral salpingo-oophorectomy, and in patients affected by PPC. Therefore, we propose the complete processing of adnexal tissue and the use of step sectioning to establish the correct diagnosis. Immunohistochemistry for p53 and ki-67 may aid in the diagnosis, but is not necessary for routine investigation.
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PMID:p53 signature and serous tubal in-situ carcinoma in cases of primary tubal and peritoneal carcinomas and serous borderline tumors of the ovary. 2180 88

Recent new data in the pathogenesis of serous pelvic cancer and the introduction of serous tubal in situ carcinoma (STIC) and its precursors have raised the question that whether all primary peritoneal cancers (PPC) are in fact of tubal origin. Therefore, the present study evaluates the frequency of STIC and its precursor lesions in cases that were diagnosed as PPC using the morphologic criteria of the most recent WHO classification. The present study evaluates immunohistochemically (Ki-67 and p53 staining) the presence of STIC and its precursor lesions (p53 signature, serous tubal intraepithelial lesion [STIL]) in the completely processed Fallopian tubes of 46 consecutive PPCs. STIC was detected in 10 patients (21.7%) and p53 signature in 9 cases (19.6%). No STIL was observed. All except 1 STIC occurred at the fimbriated end of the Fallopian tube, and a bilateral involvement was detected in 2 cases. These precursor lesions were missed during the initial routine screening. Repeated staining for p53 was negative in STIC in 2 cases. STIC and p53 signature as precursor lesions of pelvic serous cancer are detected in some but not all the cases of primary serous peritoneal cancer. There might be the 2 different carcinogenetic pathways within PPC, and further studies are required to identify the source of serous cancer in cases without an STIC lesion.
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PMID:Serous tubal in situ carcinoma (STIC) in primary peritoneal serous carcinomas. 2372 5

Early detection of sporadic pelvic serous carcinoma remains an elusive goal. In women at high risk for hereditary breast and ovarian cancer syndrome who undergo prophylactic salpingectomy, systematic pathologic examination of the fallopian tubes will detect occult tubal cancer, mostly in the fimbriae, of a minority of women. Such tubal cancers are the putative precursor to advanced-stage pelvic cancer. We hypothesized that early tubal cancer detection can also be accomplished in women at low risk using a similar approach. In this study, we performed complete and systematic examination of the fallopian tubes removed during surgery performed for benign indications. Among 522 women, 4 cases of serous tubal intraepithelial carcinoma (STIC) were identified. Three of these cases would have gone undetected using the current standard of care of sampling only a single random section of the tube. The fourth case was accompanied by occult ovarian carcinoma. The fimbriae contained STIC in 3 of the 4 cases and atypical mucosa in 1 case in which the STIC was in the nonfimbriated portion of the tube. The morphologic and immunohistochemical features (aberrant p53 and MIB-1) of these STICs were similar to those expected in high-risk women. All 4 patients with STIC underwent BRCA1 and BRCA2 gene testing; no germline mutations were identified in any patient. An additional 11 specimens contained atypical mucosal proliferations that fell short of morphologic and immunohistochemical criteria for STIC. Two of these 11 fulfilled criteria for a serous tubal intraepithelial lesion, and the remaining atypical proliferations exhibited normal p53 and MIB-1. For most specimens, the fimbriae could be completely submitted in 1 or 2 cassettes per tube. These results demonstrate that systematic examination of the tubal fimbriae can serve as a form of early detection of sporadic tubal cancer without incurring significant labor or cost. We propose that the tubal fimbriae should be completely examined in all patients undergoing benign surgery even if there are no clinical features to suggest risk for hereditary breast and ovarian cancer syndrome.
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PMID:Early detection of high-grade tubal serous carcinoma in women at low risk for hereditary breast and ovarian cancer syndrome by systematic examination of fallopian tubes incidentally removed during benign surgery. 2482 Mar 99