Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ABO and Lewis blood group antigens are cell surface carbohydrate determinants formed by the sequential addition of saccharides to precursor backbone structures of membrane lipids and proteins. Suppression of normally active glycosyltransferases results in the absence of antigens that are normally expressed. ABH antigen deletion in malignant and premalignant urothelium has been extensively evaluated; it appears to correlate with significantly higher rates of tumor recurrence and disease progression. However, we have recently shown that the ABH blood group system is differentially expressed in the normal urothelium of secretors in contrast to nonsecretor individuals. The normal urothelium of nonsecretors does not express A, B or H determinants; therefore, deletion of ABH antigens can only be ascertained in secretor individuals. Although nonsecretors only comprise 22-24% of the population, this observation mandates a reevaluation of earlier studies. Deletion of A, B or H antigens is noted in carcinoma in situ (CIS), and in invasive and metastatic transitional cell carcinoma (TCC) of secretor individuals. Increased synthesis or activation of normally quiescent glycosyltransferases in bladder tumors can result in the expression of aberrant tumor-associated blood group antigens. Immunohistochemical analysis has demonstrated that Lewis X (Le(x)) is not detected in normal adult urothelium except for occasional umbrella cells. However, papillomas, CIS and TCC expressed Le(x) in 84% of cases, regardless of grade, stage, blood type or secretor status of the individual. The presence of Le(x)-positive cells in bladder lavage specimens enhanced the detection of urothelial tumor cells, correctly identifying bladder tumors in 253/293 (86%) cases compared to a 63% sensitivity for cytology alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Blood group antigens in normal and neoplastic urothelium. 130 88

At this present time, we feel that there is no role for DNA flow cytometry (FCM), or indeed DNA studies by any other method, to be used as a screening procedure for patients with no prior history of bladder cancer due to the high false-positive rate found when monitoring exfoliated urothelial cells. On the other hand, for patients who have had a superficial transitional cell carcinoma (TCC), which has a documented 50% recurrence rate, and depending on pathological features, a progression rate from 7 to 45%, DNA FCM provides a sensitive method to predict future disease recurrence. It provides an extremely effective way to predict future progression and further acts as a method to monitor changes in the malignant potential of the patient's disease. For those patients with a past history of superficial TCC who develop abnormal ploidy without any overt tumor, 80% will, within the next four years, suffer a disease recurrence. For the patient who has a Ta TCC and receives intravesical Bacillus Calmette-Guerin (BCG), the development of abnormal ploidy in bladder washing specimens is the single best indicator for future disease recurrence. Similarly, a negative DNA FCM of a bladder washing at six months after intravesical therapy is an excellent predictor of no further occurrence. In patients with superficial TCC, ploidy of the initial and recurrent tumor predicts for future progression. Half of those patients with stage Ta bladder cancer with two successive aneuploid bladder tumors develop muscle invasive disease within one year, while three-fourths develop advanced disease within two years after recurrence of their second aneuploid lesion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of DNA flow cytometry as a screening test for bladder cancer. 130 94

The biological effects of expression of mutant ras at different stages of human uroepithelial cell (HUC) tumorigenesis were tested after transfection of EJ/ras into nonestablished HUC and three isogeneic cell lines representing different steps in HUC transformation in vitro. Transfection with EJ/ras failed to immortalize diploid HUC and also failed to cause tumorigenic conversion of a near-diploid SV40-immortalized HUC line (SV-HUC) except at one of six nude mouse inoculation sites. In contrast, EJ/ras-transfected aneuploid low-grade squamous cell carcinoma cells formed undifferentiated, invasive carcinomas at four of six inoculation sites. Furthermore, EJ/ras accelerated tumor growth in MC-ppT11-HA2, an aneuploid high-grade transitional cell carcinoma line, as determined by decreased tumor latent periods and doubling times. These results suggest that EJ/ras contributes to progression, possibly by accelerating tumor growth, but does not in itself cause tumorigenic transformation of uroepithelial cells. To test whether chromosome losses accompanied EJ/ras transformation of SV-HUC, the karyotype of the one SV-HUC tumorigenic transformant obtained (above) was examined. This tumor cell line showed losses of chromosome arms 3p, 10p, 11p, and 18, all of which have been hypothesized to contain genes that suppress cancer development. Therefore, these results also provide new evidence suggesting that genetic losses may be required for mutant ras to contribute to HUC tumorigenic progression.
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PMID:Neoplastic progression by EJ/ras at different steps of transformation in vitro of human uroepithelial cells. 131 69

Human papillomavirus (HPV) detection was done using the polymerase chain reaction technique on tumor tissue from 44 patients with transitional cell carcinoma of the urinary bladder. Only one of the 44 was associated with HPV infection. The HPV-positive patient was not known to have immunodeficiency or genital warts, and the tumor was not morphologically different from the other tumors. Control experiments excluded the possibility that this finding was caused by contamination of the sample. This study confirms that HPV infection is a rare condition in bladder carcinoma.
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PMID:Low incidence of human papillomavirus type 16 DNA in bladder tumor detected by the polymerase chain reaction. 131 Aug 88

A 59-year-old male took total cystourethrectomy on July, 1991, since the bladder tumor recurred 2 years and 4 months after transurethral resection. Six months after total cystourethrectomy, an abnormal mass shadow appeared on the right lower lung field. Metastatic lung tumor was strongly suspected from CT scan. Despite chemotherapy, the pulmonary lesion grew rapidly and the patient died. From the autopsy, metastatic lesions were found in the bilateral lung fields, skin (face, head and abdominal wall), pleura, bilateral kidneys, small intestine and lymph nodes (para-aortic and mesenteric). The primary bladder tumor contained histologically transitional cell carcinoma as the epithelial element and sarcomatous changes with osteoid formation as the non-epithelial elements. Thus, the primary lesion was diagnosed as a malignant mesodermal mixed tumor. However, all of the metastatic lesions showed only sarcomatous changes. Only 10 cases of malignant mesodermal mixed tumor of the bladder have been reported in Japan since Fujita's report. In general, total cystectomy is necessary for the treatment of this disease. It has a poor prognosis; 5 of the 10 patients died within one year after operation.
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PMID:[Malignant mesodermal mixed tumor of the bladder: report of a case]. 132 57

CT scans of the pelvis in 132 patients with bladder tumor were reviewed. Calcifications in the bladder tumor were found in 11 men (8%) including transitional cell carcinoma (n = 6), mucinous adenocarcinoma (n = 4), and malignant mixed mesodermal tumor (n = 1). Calcifications in transitional cell carcinoma were located on the surface of the tumor in all 6 cases: they were nodular in 4 cases, nodular and arched in one, and plaque-like massive calcification in one. In mucinous adenocarcinoma multiple fine punctate calcifications were scattered within the mass in all 4 cases. The CT appearance of calcifications in bladder tumors may be helpful in predicting the histologic type of the tumor.
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PMID:Calcified bladder tumors. CT features. 132 26

The characteristics of one of a group of monoclonal antibodies named BIU-H6 are reported. Using McAb BIU-H6, by ABC-immunohistochemical staining directed against 34 bladder cancers and 5 normal bladders. It was found that BIU-H6 does not react with normal bladder epithelial and adenocarcinoma of the bladder, but with transitional cell carcinoma, squamous cell carcinoma and CIS of the bladder. The staining characters were variant according to the different grade/stage of the cancer. The result shows that BIU-H6 antigen is a tumor associated antigen of poorly differentiated and invasive carcinoma of the bladder.
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PMID:[Characterization of monoclonal antibody (BIU-H) directed against bladder cancer and its pathologic feature]. 132 48

A new human bladder cancer cell line, NTUB1, has been derived from the surgical specimen of a 70-year-old female patient diagnosed with poorly differentiated transitional cell carcinoma. It has been successfully propagated in vitro for over 24 months without evidence of reaching senescence. Population doubling time was about 21 hours at the 32nd passage. It was tumorigenic in nude mice, and the histologic findings of the heterotransplanted tumor resembled the original tumor. Expression of keratin proteins confirmed its epithelial origin. Cytogenetic analysis showed multiple chromosome changes. Anticancer drugs, including thiotepa and adriamycin, were tested in vitro, and the cytotoxicity did not exceed 50% of the control value; likewise, in this patient chemotherapy was not effective. On the other hand, a combination of recombinant tumor necrosis factor and interferon tau in vitro was more effective against this tumor.
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PMID:Characterization of a newly established human bladder carcinoma cell line, NTUB1. 135 47

After the introduction of methotrexate, vinblastine, adriamycin and cisplatin combination (M-VAC) chemotherapy for transitional cell carcinoma (TCC) of the urothelium, the reported response and survival rates improved when compared with the previous regimens. From July 1989 to March 1991, 43 consecutive cases of invasive or metastatic TCC that had received at least one course of M-VAC treatment were collected by a computer-assisted search and analyzed. The overall response rate, including complete response (CR) and partial response (PR), was 44% (CR, 16%; PR, 28%). Tumors originating from the renal pelvis or bladder responded better than those from the ureter (kidney, 57%; bladder, 42%; and ureter 30%). Lymph node, soft tissue, lung metastases and local recurrent tumors had a greater chance of response than bone or liver metastases. Although patients from the blackfoot disease endemic area seemed to respond better than those from the nonendemic area, there was no statistically significant survival benefit. The duration of follow-up ranged from nine to 38 months. The length of survival of nonresponders ranged from one month to 19 months (median, eight months; mean, seven months). Ten of the 19 responders relapsed, and the others were still responding. Three patients (7%) survived two years, disease-free. Although the response rate improved, the chance of long-term survival was still unsatisfactory in our study.
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PMID:Methotrexate, vinblastine, adriamycin and cisplatin (M-VAC) for advanced TCC of urothelium. 136 Feb 98

We analyzed the alteration of int-2, c-erbB-2 and EGFR genes in 32 cases of transitional cell carcinoma of the urinary tract, 15 cases of renal cell carcinoma and 14 cases of prostatic carcinoma by Southern blot hybridization method. Three- to 12 fold amplification of int-2 gene was observed in 4 (12.5%) of 32 transitional cell carcinomas. Of these 4 cases 3 were G3 tumor with muscle invasion and the remaining was G1, pTa tumor with subsequent recurrence of multiple tumors. The other 2 cases (6.3%) with invasive transitional cell carcinoma showed amplification of c-erbB-2 gene. Neither amplification nor gross rearrangement of EGFR gene was detected in transitional cell carcinoma. On the other hand, renal cell carcinomas and prostatic carcinomas had neither amplification nor gross rearrangement of these 3 genes. These results suggest that the int-2 gene located in chromosome locus 11q13 and the c-erbB-2 gene have a specific role in carcinogenesis and in progression of transitional cell carcinoma through their gene amplifications.
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PMID:[int-2 and c-erbB-2 gene amplification in urological cancers]. 136 54


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