Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P52742 (pT3)
 1,034 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A retrospective analysis of 59 patients with renal pelvic and ureter cancer (56 transitional cell carcinomas, 2 squamous cell carcinomas, and 1 adenocarcinoma), which were treated surgically, was performed in relation to postoperative recurrence, particularly distant metastasis. Of the 59 cases, postoperative recurrences developed as distant metastasis in 9 cases (15.3%), as bladder cancer in 19 cases (32.2%) and as contralateral renal pelvic and ureter cancer (bilateral metachronous cancer) in 3 cases (5.1%). Three of the 9 cases with the development of distant metastasis were squamous cell carcinoma or adenocarcinoma, and the others transitional cell carcinoma. All the metastases occurred within 2 years. In cases with transitional cell carcinoma, nonpapillary tumor, grade 3, high stage (pT3 and pT4), positive vascular invasion and IFN beta or gamma had a significant influence on the rate of distant metastasis. On the other hand, location, diversity and previous or coexistent bladder cancer did not seem to be related to the frequency of the development of distant metastasis. Thus, tumor aggressiveness was the only predictive valuable of the development of distant metastasis after surgery for renal pelvic and ureter cancer.
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PMID:[Recurrence following surgery for primary renal pelvic and ureter cancer--clinicopathologic analysis of distant metastasis]. 149 3

In 106 consecutive patients with localized prostate cancer digital rectal examination (DRE), preoperative prostate-specific antigen (PSA) determination and results of systematic sextant biopsies (TRUS 6Bx) of the prostate were analyzed for their value in the estimation of the aggressivity of tumors. In all patients with negative pelvic lymph nodes radical retropubic prostatectomy was performed. Tumor aggressiveness was defined as capsular penetration (pT2 versus pT3) or positive surgical margins in patients with pT3 tumors. Neither DRE nor preoperative PSA level was helpful in predicting capsular penetration or positive surgical margins. However, the number of positive core biopsies and the identification of Gleason 4 or 5 tumors within positive biopsy specimens correlated with capsular penetration and positive surgical margins. These results can be used to create a score, based on DRE, PSA, TRUS 6Bx, and Gleason 4 or 5, that might be helpful in predicting tumour aggressivity in patients with localized prostate cancer.
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PMID:[Preoperative assessment of tumor aggressiveness in localized prostatic carcinoma]. 748 60

Clear cell renal cell carcinomas (RCCs) are characterized by a deletion of chromosome 3p, which might result in the inactivation of the FHIT (fragile histidine triad) gene, a putative tumour suppressor gene. To explore the relevance of FHIT aberrations for tumour progression and prognosis in clear cell RCCs, FHIT protein expression was analysed in formalin-fixed tissue from 149 clear cell RCCs by immunohistochemistry. FHIT protein expression was found to be markedly reduced in all RCCs, when compared with adjacent non-neoplastic tubule epithelia. Although remaining below the FHIT levels of normal tubule epithelia, a significant increase of FHIT expression became evident from well (G1) to poorly (G3) differentiated clear cell RCCs (p=0.0001) and from low (pT1) to advanced (pT3) tumour stages (p=0.001). The log-rank test demonstrated a significant inverse correlation (p=0.0074) between FHIT expression and tumour aggressiveness as indicated by patient survival. Cox regression analysis revealed that FHIT expression is an independent prognostic parameter (p=0.0139) in clear cell RCCs. In conclusion, clear cell RCCs show a marked reduction of FHIT protein expression when compared with their putative cells of origin. In contrast to other tumour types, however, loss of FHIT protein expression is significantly less pronounced in poorly differentiated RCCs or advanced tumour stages. This versatility of FHIT expression during tumour progression suggests a role for reversible mechanisms of FHIT inactivation during the initiation and progression of clear cell RCCs.
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PMID:FHIT expression in clear cell renal carcinomas: versatility of protein levels and correlation with survival. 1192 Jul 39

Deregulation of apoptosis plays an important role in carcinogenesis, tumor progression, and resistance to chemotherapy. XIAP is considered to be the most potent caspase inhibitor of all known IAP (inhibitor of apoptosis) family members. To explore the relevance of XIAP for progression and prognosis in renal cell carcinomas (RCCs) of the clear-cell type, we analyzed XIAP protein expression in formalin-fixed tissue from 145 clear-cell RCCs by immunohistochemistry. XIAP protein expression was found in 95% of clear-cell RCCs. A significant increase of XIAP expression became evident from well (G1) to poorly (G3) differentiated clear-cell RCCs (P < 0.0001) and from low (pT1) to advanced (pT3) tumor stages (P = 0.0016). Log-rank test showed a significant inverse correlation (P = 0.0174) between XIAP expression and tumor aggressiveness as indicated by patients' survival. Most important, multivariate Cox regression analysis revealed that XIAP expression is an independent prognostic parameter (P = 0.018) in clear-cell RCCs. Our results suggest an important role for XIAP-mediated inhibition of apoptosis during progression of clear-cell RCCs and introduce XIAP expression as a new independent prognostic marker in this tumor type.
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PMID:XIAP expression is an independent prognostic marker in clear-cell renal carcinomas. 1529 70

The laminin-5 gamma 2 chain (LN-5gamma2) is known to be a marker of invasion in several cancer types. Our purpose was to examine the prognostic significance of LN-5gamma2 expression in different areas of individual colorectal cancers (CRCs) by using tissue microarrays (TMAs), and to clarify the optimal areas for prognostic assessment. Using formalin-fixed paraffin-embedded tissue blocks of pT3 primary CRCs resected from 120 patients, we constructed TMA blocks of tissue core specimens taken from the submucosal invasive front, subserosal invasive front, central area, and rolled edge of each tumor. Using these four-point TMA sets, cytoplasmic LN-5gamma2 expression was immunohistochemically surveyed, and the area-specific prognostic significance of LN-5gamma2 expression was evaluated. The data revealed that 35, 30, 15 and 10% of the 120 CRCs showed high-grade LN-5gamma2 expression in the submucosal invasive front, subserosal invasive front, central area and rolled edge, respectively. Disease-specific survival curves for the groups with high- and low-grade LN-5gamma2 in the submucosal invasive front and subserosal invasive front were different significantly or of marginal difference (respective 5-year survival rates: 54 and 78% for submucosal invasive front (P=0.030) and 58 and 75% for subserosal invasive front (P=0.055)). Multivariate analysis revealed that the grades of LN-5gamma2 expression in submucosal invasive front (hazard ratio=2.0, P=0.047) and subserosal invasive front (hazard ratio=2.9, P=0.0033) were independent prognostic factors. In contrast, the grades of LN-5gamma2 expression in the central area and rolled edge did not have a significant impact on patient prognosis. Analysis using area-specific four-point TMAs clearly demonstrated that LN-5gamma2 expression in the invasive front largely influences the degree of clinical aggressiveness of CRC and its tendency to metastasize.
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PMID:Prognostic implication of laminin-5 gamma 2 chain expression in the invasive front of colorectal cancers, disclosed by area-specific four-point tissue microarrays. 1551 72

To address the need for new prognostic parameters in advanced colon carcinoma that could add insights into the aggressiveness of tumors, the expression levels of MUC1 recognized by a monoclonal antibody (mAb) MY.1E12 in archival specimens from 123 Japanese patients with colon carcinomas were evaluated by immunohistochemistry to correlate the results with clinicopathological characteristics. The localization of mAb MY.1E12-reactive-MUC1 (MY.1E12-MUC1) was classified into apical, cytoplasmic and stromal types based on the predominant cellular distribution. The MUC1 mRNA levels revealed by in situ hybridization were not a determinant for the localization types of MY.1E12-MUC1. Immunostaining of MY.1E12-MUC1 was recognized in the cancerous epithelia of pT1 carcinoma in 61%, pT2 in 78%, pT3 in 98% and pT4 in 90% of the cases at the deepest invading sites. At the deepest invading sites, apical-type localization was found to predominate in pT1 carcinoma, but stromal-type localization was found to increase in pT2-4 carcinomas in parallel with the depth of invasion. The frequency of synchronous distant organ metastasis at the time of diagnosis tended to be higher in cases of pT3 and pT4 carcinomas in the stromal-type localization-dominant group than in cases in the apical-type localization-dominant group. The post-surgical survival outcome of cases of pT3 and pT4 carcinomas was significantly poorer in the former than in the latter (P = 0.002). The stromal-type localization of MY.1E12-MUC1 may be a phenotype serving as a unique biological feature associated with the tumor aggressiveness of advanced colon carcinoma.
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PMID:Expression of MUC1 recognized by monoclonal antibody MY.1E12 is a useful biomarker for tumor aggressiveness of advanced colon carcinoma. 1555 88

The overall outcome of gallbladder carcinoma has not been favorable because of frequent recurrence at distant sites after surgery. A high-level expression of MUC1 recognized by a monoclonal antibody (mAb), MY.1E12, is correlated with poor survival in several types of carcinomas. There is a need to find new prognostic parameters that can give further insights into tumor aggressiveness of the disease. Immunohistochemistry was performed to determine the expression level of mAb MY.1E12-reactive-MUC1 (MY.1E12-MUC1) in 79 cases of gallbladder carcinoma of different depths of invasion and to determine the correlation of the expression level with clinicopathological findings. The cellular distribution of MY.1E12-MUC1 was heterogeneous among carcinomas of different depths of invasion. Immunohistochemical localization was classified into apical, cytoplasmic and stromal types based on the predominant cellular distribution. In 35 cases of pT2 carcinoma in which curative resections had been performed, the localization was apical type in 54%, cytoplasmic type in 66%, and stromal type in 56% of the cases at the deepest invading sites in the subserosal layer. Postsurgical recurrences at distant sites were seen in 11 of 18 cases of pT2 carcinoma (61%) that had more than or equal to 10% of the cancerous epithelia showing stromal localization of MY.1E12-MUC1 at the deepest invading sites (stromal group) and in 3 of 17 cases (18%) that had less than 10% of the cancerous epithelia showing stromal localization (nonstromal group). The postsurgical 5-year survival rate was significantly poorer in the former (54%) than in the latter (79%; P = 0.049). In 38 cases of pT3 and pT4 carcinomas, the frequency of synchronous distant organ metastasis at the time of diagnosis was significantly higher in cases in the stromal group (61%) than in cases in the nonstromal group (20%). Moreover, in 73 cases of pT2, pT3 and pT4 carcinomas, the expression rate of abnormal localization of E-cadherin was significantly higher in the stromal group (63%) than in the nonstromal group (30%). The MUC1 mRNA levels revealed by in situ hybridization would not be a determinant important for the stromal localization. The stromal localization of MY.1E12-MUC1 may be a phenotype serving as a unique biological feature associated with the tumor aggressiveness of gallbladder carcinoma, such as the tendency to form distant organ metastasis.
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PMID:Expression of MUC1 recognized by a monoclonal antibody MY.1E12 is a useful biomarker for tumor aggressiveness of carcinoma of the gallbladder. 1555 92

Screen-detected (SD) breast cancers are smaller and biologically more indolent than clinically presenting cancers. An often debated question is: if left undiagnosed during their preclinical phase, would they become more aggressive or would they only increase in size? This study considered a registry-based series (1988-1999) of 3329 unifocal, pT1a-pT3 breast cancer cases aged 50-70 years, of which 994 were SD cases and 2335 clinical cases. The rationale was that (1) the average risk of lymph node involvement (N+) is lower for SD cases, (2) nodal status is the product of biological aggressiveness and chronological age of the disease, (3) for any breast cancer, tumour size is an indicator of chronological age, and (4) for SD cases, tumour size is specifically an indicator of the duration of the preclinical phase, that is, an inverse indicator of lead time. The hypothesis was that the relative protection of SD cases from the risk of N+ and, thus, their relative biological indolence decrease with increasing tumour size. The odds ratio (OR) estimate of the risk of N+ was obtained from a multiple logistic regression model that included terms for detection modality, tumour size category, patient age, histological type, and number of lymph nodes recovered. A term for the detection modality-by-tumour size category interaction was entered, and the OR for the main effect of detection by screening vs clinical diagnosis was calculated. This increased linearly from 0.05 (95% confidence interval: 0.01-0.39) in the 2-7 mm size category to 0.95 (0.64-1.40) in the 18-22 mm category. This trend is compatible with the view that biological aggressiveness of breast cancer increases during the preclinical phase.
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PMID:Screen-detected vs clinical breast cancer: the advantage in the relative risk of lymph node metastases decreases with increasing tumour size. 1585 34

The aim of this study was to determine whether the excess risk of axillary lymph node metastases (N+) differs between interval breast cancers arising shortly after a negative mammography and those presenting later. In a registry-based series of pT1a-pT3 breast carcinoma patients aged 50-74 years from the Italian screening programmes, the odds ratio (OR) for interval cancers (n=791) versus the screen-detected (SD) cancers (n=1211) having N+ was modelled using forward stepwise logistic regression analysis. The interscreening interval was divided into 1-12, 13-18, and 19-24 months. The prevalence of N+ was 28% among SD cancers. With a prevalence of 38%, 42%, and 44%, the adjusted (demographics and N staging technique) OR of N+ for cancers diagnosed between 1-12, 13-18, and 19-24 months of interval was 1.41 (95% confidence interval 1.06-1.87), 1.74 (1.31-2.31), and 1.91 (1.43-2.54), respectively. Histologic type, tumour grade, and tumour size were entered in turn into the model. Histologic type had modest effects. With adjustment for tumour grade, the ORs decreased to 1.23 (0.92-1.65), 1.58 (1.18-2.12), and 1.73 (1.29-2.32). Adjusting for tumour size decreased the ORs to 0.95 (0.70-1.29), 1.34 (0.99-1.81), and 1.37 (1.01-1.85). The strength of confounding by tumour size suggested that the excess risk of N+ for first-year interval cancers reflected only their higher chronological age, whereas the increased aggressiveness of second-year interval cancers was partly accounted for by intrinsic biological attributes.
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PMID:Breast screening: axillary lymph node status of interval cancers by interval year. 1845 1

OBJECTIVE To evaluate a contemporary series of patients with incidental prostate cancer detected by transurethral resection of the prostate (TURP) and undergoing radical prostatectomy (RP). PATIENTS AND METHODS Between 1998 and 2004, 1931 patients had TURP for obstructive voiding symptoms and suspected BPH. Incidental prostate cancer was found in 104 (5.4%); 26 of these patients had a RP. The pathological staging and treatment of these patients were reviewed retrospectively and the follow-up results obtained. RESULTS Of the 26 patients who had RP, 17 had T1a and nine had T1b carcinoma of the prostate. After RP, six (35%) in the T1a group had no residual tumour (pT0) and 11 (65%) had pT2 cancer; the respective incidence in those with T1b was two and seven, with no pT3 disease in either group. The preoperative Gleason grading did not correspond well with that after RP; 30% of the patients had upgraded Gleason scores and 42% showed either downgrading or no residual tumour, with 81% having Gleason scores of <7. After a median follow-up of 47 months, one patient is receiving hormonal therapy because of biochemical relapse. Conclusion Subsequent to stringent PSA testing and prostate biopsy when indicated, the rate of incidental prostate cancer is low. Furthermore, substantially many patients will harbour either no residual cancer or tumours with favourable characteristics in their RP specimens. However, there is currently no possibility to reliably predict the absence of aggressive prostate cancer after TURP, and thus safely recommend observation instead of further therapy. Therefore, patients with incidental prostate cancer need to be counselled individually. The decision 'treatment or no treatment' should be determined by the patients' age and life-expectancy, tumour aggressiveness in the TURP specimen and the prostate-specific antigen level after TURP.
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PMID:Outcome of radical prostatectomy for incidental carcinoma of the prostate. 2126 82


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