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W R Fair

Publications and source records attributed to W R Fair.

At least 109 records · Page 6Linked to original sources
PubMed1994

Association of P53 nuclear overexpression and tumor progression in carcinoma in situ of the bladder.

We investigated the prevalence and clinical relevance of p53 nuclear overexpression, as detected by antibody PAb1801 and immunohistochemistry, in 33 patients with carcinoma in situ of the bladder. Median followup was 124 months. Disease progressed in 16 patients (48%) during followup. The association between p53 nuclear overexpression and tumor progression was assessed by multivariate analysis, controlling for possible confounding variables, such as patient age and sex, presence of associated stage Ta bladder tumor and adjuvant bacillus Calmette-Guerin therapy. Patients were stratified into 2 groups according to the per cent of tumor cells displaying p53 nuclear overexpression: group 1-18 with less than 20% tumor cells positive and group 2-15 with 20% or more tumor cells positive. Disease progressed in 3 patients (16.7%) in group 1 and in 13 (86.7%) in group 2 (p < 0.0001). Detection of p53 nuclear overexpression in 20% or more tumor cells was the only independent marker of tumor progression in univariate and multivariate analyses (p = 0.004, adjusted relative risk 8.6, 95% confidence interval 2 to 40). Death specifically from bladder cancer was also associated with this altered pattern of p53 expression (p = 0.01, Fisher's exact test). We conclude that p53 nuclear overexpression is an early event in bladder cancer, occurring in 48% of cases of carcinoma in situ of the bladder. Our results also suggest that p53 nuclear overexpression offers significant clinical information and may be a useful tool in the selection of therapy for patients with carcinoma in situ of the bladder.

Aged↗
PubMed1994

The management of patients with nonseminomatous germ cell tumors of the testis with serologic disease only after orchiectomy.

Management of patients with nonseminomatous germ cell tumors of the testis who have persistently elevated serum tumor marker levels (alpha-fetoprotein and/or human chorionic gonadotropin) following orchiectomy and no clinical evidence of disease is controversial. We reviewed our experience with 15 such patients at our cancer center between March 1977 and November 1991. Group 1 (11 patients) underwent initial retroperitoneal lymph node dissection and group 2 (4 patients) received primary chemotherapy. All group 1 patients required subsequent chemotherapy for retroperitoneal disease or persistent marker elevation, whereas only 1 of the 4 who received primary chemotherapy required later surgery. We conclude that tumor marker elevation in this setting is usually indicative of systemic tumor, which is best treated primarily by initial chemotherapy.

Adult↗
PubMed1994

Neuroendocrine differentiation in metastatic prostatic adenocarcinoma.

Neuroendocrine differentiation of prostatic adenocarcinoma has received considerable attention in recent years. The objectives of this study were to characterize the incidence, pattern of distribution and peptide hormone immunoreactivities of neuroendocrine differentiated tumor cells in prostatic carcinoma metastases; determine the correlation of neuroendocrine differentiation and deoxyribonucleic acid content in lymph node metastases, and determine the prognostic role of neuroendocrine differentiation of metastases in stage D1 cancer. We examined immunohistochemically 62 metastatic lesions (41 pelvic lymph nodes and 21 bone metastases) for the presence of chromogranin-A expressing tumor cells. Of 41 lymph nodes and 21 bone metastases 19 (46%) and 11 (52%), respectively, contained chromogranin-A immunoreactive cells. These cells were commonly found to comprise the minority of tumor cells in the metastases and typically were distributed in a dispersed pattern. Serotonin and peptide hormone immunocytochemistry in 19 cases (12 lymph nodes and 7 bone metastases) demonstrated neuroendocrine cells containing thyroid-stimulating hormone and serotonin in 17 (89%) and 10 (53%), respectively. All 7 bone metastases contained thyroid-stimulating hormone immunoreactive cells. The presence of chromogranin-A positive cells did not correlate statistically with deoxyribonucleic acid content of lymph node metastases nor with disease specific survival in patients with stage D1 prostate cancer. Our results indicate that a substantial proportion of prostate cancer metastases contain a subpopulation of cells expressing a neuroendocrine phenotype similar to primary tumors. These cells are capable of elaborating certain biogenic amines and peptide hormones. However, in stage D1 prostate cancer nodal lesions expressing neuroendocrine differentiation do not appear to have significant prognostic value.

Adenocarcinoma↗
PubMed1994

Immunohistochemical determination of p53 protein nuclear accumulation in prostatic adenocarcinoma.

Abnormalities of the TP53 gene are currently the most common genetic alterations associated with human malignancy. The study of altered patterns of p53 protein expression in primary prostate cancer has to date yielded a much lower incidence of alteration compared to bladder, colon, lung and breast cancer. However, the analysis of prostate cancer metastases has been limited. The objective of our study was to determine the prevalence of p53 nuclear accumulation in primary, metastatic and hormone refractory prostatic adenocarcinoma, and to characterize its relationship with conventional clinicopathological variables. We used 2 antibodies (mouse monoclonal PAb 1801 and rabbit polyclonal CM-1) and an immunohistochemical method in 93 paraffin embedded tumors (48 primary tumors, 29 lymph node metastases and 16 bone metastases) to assess p53 nuclear accumulation. Overall, p53 nuclear accumulation was observed in 19 tumors (20%), including 17 with PAb 1801 and CM-1 immunoreactivities, and 2 with CM-1 immunoreactivity only. The pattern of p53 immunoreactivity was heterogeneous in most tumors, with only 3 cases exhibiting homogeneous staining. Primary, lymph node and bone metastases exhibited p53 nuclear staining in 9 of 48 (19%), 2 of 29 (7%) and 8 of 16 (50%) cases, respectively (p = 0.003). In 6 of 10 primary hormone refractory tumors (60%) and in 3 of 38 primary hormone naive tumors (8%) p53 nuclear immunoreactivity was expressed (p = 0.002). P53 nuclear accumulation was significantly more common in higher grade primary tumors (p = 0.007). Our results suggest that p53 nuclear accumulation is relatively uncommon in prostate cancer. However, p53 nuclear accumulation appears to be associated with advanced stages of disease, as illustrated by its relatively higher occurrence in hormone refractory tumors and bone metastases. Furthermore, the significantly greater prevalence of p53 accumulation in bone metastases is currently the highest reported for prostate cancer.

Adenocarcinoma↗
PubMed1994

Clinical and pathobiological effects of neoadjuvant total androgen ablation therapy on clinically localized prostatic adenocarcinoma.

Neoadjuvant total androgen ablation therapy leads to involutional changes in prostatic carcinoma and may have the potential to downstage operable prostate cancers. We studied 27 clinically localized prostatic carcinomas after 3 months of combined treatment with a luteinizing hormone-releasing hormone agonist, goserelin acetate, and the antiandrogen flutamide, followed by radical retropubic prostatectomy, for changes in the serum prostate-specific antigen (PSA) level, changes in prostatic volume, therapy-induced histopathologic changes, DNA ploidy, and proliferative activity. Ten hormonally untreated, grade-matched prostatic adenocarcinomas served as controls. The mean pretherapy serum PSA level was 17.5 ng/ml, and posttherapy PSA levels were all < 4.0 ng/ml, with 18 men having undetectable levels. The mean reduction in prostatic volume following hormonal therapy was 37% (range 16-52%). Pathologic staging confirmed 20 pT2N0, six pT3N0, and one pT3N1. All prostates showed residual adenocarcinoma (extremely focal in seven cases [26%] with loss of glandular architecture, cytoplasmic vacuolization, and nuclear pyknosis. High-grade adenocarcinoma was nondiploid in 25% of hormonally treated prostates and 80% of 10 untreated controls. Immunostaining for proliferating cell nuclear antigen showed > 10% nuclear reactivity in 33% of treated carcinomas and 90% of untreated carcinomas. In conclusion, 3 months of neoadjuvant androgen ablation for localized prostatic carcinoma significantly lowers serum PSA and prostatic volume and produces involutional changes in residual carcinomas that mimic high-grade disease. However, pretreated carcinomas have predominantly a diploid DNA content and low proliferative activity as opposed to untreated carcinomas. Thus, grading of pretreated adenocarcinomas by conventional methods may be misleading. Preoperative total androgen ablation has a profound effect on a subset of prostatic carcinoma cells, possibly by facilitating programmed cell death.

Adenocarcinoma↗
PubMed1994

Experience with neoadjuvant diethylstilboestrol and radical prostatectomy in patients with locally advanced prostate cancer.

OBJECTIVE: To report our experience with neoadjuvant endocrine therapy and radical retropubic prostatectomy (RRP) in patients with locally advanced prostate cancer. PATIENTS AND METHODS: Fifty-five patients with prostatic adenocarcinoma (18 clinical stage B2/3, 27 clinical stage C, and 10 clinical stage D0) were treated with diethylstilboestrol (DES) 3 mg/d (median time 12 weeks, range 5-36) followed by pelvic lymph node dissection and planned RRP. Clinical response was monitored bi-weekly with serum prostate-specific antigen (PSA), serum acid phosphatase and digital rectal examination. RESULTS: The median pre-treatment serum PSA was 20.4 ng/ml (range 1.2-620). The median post-treatment, pre-operative serum PSA was 0.4 ng/ml. Twenty-seven (49%), 41 (75%) and 54 (98%) patients had serum PSA levels that were undetectable, < 1.0 ng/ml and < 4.0 ng/ml respectively. In 15 patients, transrectal ultrasound measurement of prostatic volume changes was performed, and all demonstrated prostate volume reduction (median reduction 35%, range 18-45). All 55 patients underwent pelvic lymphadenectomy, with 47 (85%) undergoing RRP. Of the eight patients not undergoing RRP, three had negative lymph nodes but prostate resection was not deemed feasible and five had nodal metastases as determined by frozen section analysis. Final pathological stage revealed the following distribution: organ confined tumours, 18 (33%); capsular perforation with negative surgical margins, seminal vesicles and lymph nodes, seven (13%); seminal vesicle and/or margin involvement with negative lymph nodes, 18 (33%); lymph node metastases, 12 (22%). Neither pre-therapy serum PSA nor serum PSA response was predictive of final pathological stage. With a median follow-up interval of 26 months (range 12-49), 21 patients (38%) have undetectable serum PSA without adjuvant therapy. CONCLUSIONS: Our results indicate that despite clinical evidence suggestive of downstaging, the majority of patients with locally advanced prostatic carcinoma managed with neoadjuvant DES and RRP continue to have pathological evidence of extraprostatic carcinoma.

Adenocarcinoma↗
PubMed1994

Neoadjuvant chemotherapy for invasive bladder cancer: prognostic factors for survival of patients treated with M-VAC with 5-year follow-up.

PURPOSE: To determine survival in patients with muscle-invasive bladder cancer treated with neoadjuvant chemotherapy and to analyze prechemotherapy and postchemotherapy factors for prognostic significance. PATIENTS AND METHODS: The survival of 111 patients with T2-4N0M0 bladder cancer treated with neoadjuvant methotrexate, vinblastine, doxorubicin, and cisplatin (M-VAC) was assessed. Prechemotherapy and postchemotherapy factors were analyzed for correlation with survival. Factors found to be significant on univariate analysis were subjected to multivariate analysis using Cox's proportional hazards model. RESULTS: The median follow-up duration was 5.3 years. Initial tumor (T) stage (P = .0001), presence of ureteral obstruction (P = .0074), and presence of a palpable mass (P = .0039) were the only pretreatment factors found to be significant on univariate analysis. Postchemotherapy surgery was performed in 81 patients. In these cases, postchemotherapy clinical stage and pathologic stage were significant factors on univariate analysis. In the multivariate analysis, the initial prechemotherapy T stage and the postchemotherapy pathologic stage (pT stage) were the only two factors to demonstrate independent significance. An association between downstaging postchemotherapy and survival was observed for patients with extravesical disease (T < or = 3B) at the start of treatment. In this subset, the 5-year survival rate was 54% for patients with downstaging versus 12% for those without downstaging. This association was not observed for patients with bladder-confined disease (T < or = 3A) at presentation. CONCLUSION: The stage of bladder cancer at presentation and at postchemotherapy pathologic staging are independent prognostic factors for long-term survival in patients treated with neoadjuvant chemotherapy. Downstaging after neoadjuvant chemotherapy was associated with improved survival in patients with muscle-invasive bladder cancers, but only for those with extravesical disease (T > or = 3B) pretreatment. Randomized comparisons will be required to assess the impact of chemotherapy on overall survival.

Adult↗
PubMed1994

Differential expression of protein kinase C isozyme messenger RNAs in dunning R-3327 rat prostatic tumors.

Adenocarcinoma of the prostate is the second leading cause of cancer deaths in men. The protein kinase C (PKC) family of signal transducing kinases has been implicated in neoplastic transformation and progression in other tissues, and some evidence suggests roles for PKC in prostate growth and neoplasia. We have detected expression of eight specific PKC isozyme mRNAs (alpha, beta, gamma, delta, epsilon, eta, theta, and zeta) in normal rat whole prostate and found some of these to be differentially expressed in certain Dunning R-3327 rat prostatic adenocarcinoma sublines. PKC zeta mRNA was detected in normal prostate and Dunning H tumor, whereas an alternatively spliced form of PKC zeta RNA was found in Dunning G tumor and normal brain. Both forms of PKC zeta RNA were markedly reduced in the androgen insensitive, highly metastatic Dunning AT-3, MAT-Lu, and MAT-LyLu tumors. We have cloned and report the sequence of the novel portion of the alternatively spliced form of PKC zeta RNA, which is polyadenylated and present in cytoplasm.

Adenocarcinoma↗
PubMed1993

Allelic deletions in renal tumors: histopathological correlations.

Allelic loss on the short arm of chromosome 3 (3p) is considered to be one of the early detectable events in the pathogenesis of renal cell carcinoma (RCC). Conflicting reports, however, suggest that this event may be absent in some renal tumors. The present study attempts to further define subgroups of renal tumors associated with 3p deletions. In addition, we have also attempted to identify late genetic events associated with tumorigenesis and tumor progression. Eighty-two primary renal tumors (69 RCC and 13 oncocytic tumors) were analyzed by restriction fragment length polymorphism analysis directed at chromosomes 3, 11p, 17p, and 18q. Results were correlated with histopathological information. Deletions of 3p were seen in nonpapillary RCC of all cell types, but were absent in oncocytic and most papillary tumors. Among the 60 nonpapillary RCC, significant correlations were seen between deletion of 17p and tumor grade (P = 0.037), P stage (P = 0.027), and nodal metastases (P = 0.042). We therefore conclude that 3p deletions, although not specific to any cell type or histological pattern of RCC, are seen in a majority of clear cell nonpapillary RCC but are absent in oncocytic and most papillary tumors. Additional allelic losses on chromosome 17p are associated with advanced disease and, therefore, may be related to tumor progression. Further studies on larger series of patients with extended follow-up will be necessary to investigate the prognostic value of molecular genetic markers in RCC.

Alleles↗
PubMed1993

Genetic alterations in bladder cancer.

To see whether genetic alterations follow a sequence of events leading to bladder cancer progression, 60 paired bladder tumours and normal tissues were analysed with polymorphic DNA markers, correlating loss of heterozygosity (LOH) at candidate tumour suppressor gene sites with pathological indices of poor clinical outcome. Distinct genotypic patterns were associated with early and late stages of bladder cancer. 9q deletions were observed in all superficial papillary tumours (Ta) and almost all tumours invading the lamina propria (T1), suggesting that this event associates with the development of superficial bladder tumours. However, 3p, 5q, and 17p deletions were absent in the Ta tumours but were identified in invasive bladder cancers. Two genetic pathways characterise the evolution of superficial bladder tumours. 9qLOH was detected in most Ta tumours, but in only 43% of muscle invasive neoplasms. Our hypothesis is that certain chromosomal abnormalities have a defined role in bladder tumour development, whereas others correlate with pathological indices of poor clinical outcome.

Alleles↗
PubMed1993

Characterization of neuroendocrine differentiation in human benign prostate and prostatic adenocarcinoma.

BACKGROUND: This report describes an immunohistopathologic analysis characterizing the incidence, pattern of distribution, and hormonal content of neuroendocrine (NE) cells in human benign prostate and prostatic adenocarcinoma. METHODS: Formaldehyde-fixed, paraffin-embedded material from 15 benign prostates, 31 primary prostatic adenocarcinomas, 16 metastatic lesions, 21 primary tumors treated with short-course diethylstilbestrol (DES), and 10 specimens from hormone-refractory patients were examined. NE cells were identified using silver histochemistry and a panel of immunohistochemical NE markers (chromogranin-A, serotonin, neuron-specific enolase), and specific peptide hormone antibodies. RESULTS: NE cells were identified in all benign prostates. NE cells were identified in 77% of primary untreated adenocarcinomas with no significant differences with respect to pathologic stage. NE cells were found isolated and dispersed in the tumor, composing the minority of malignant cells. Double-labeling and serial section immunohistochemistry demonstrated the coexpression of prostate-specific antigen (PSA) in NE cells. In addition to serotonin, some tumors expressed multiple hormone immunoreactivities. NE cells were identified in 56% of metastatic deposits, with a similar pattern of distribution. In DES-treated cases, NE cells were found consistently in the adjacent benign epithelium, whereas 52% of tumors contained NE cells. Hormone-refractory tumors contained NE cells in 60% of cases. CONCLUSIONS: This analysis demonstrates that a significant proportion of primary and metastatic prostatic adenocarcinomas contain a subpopulation of NE cells, the expression of which does not appear to be suppressed with androgen ablation and does not correlate with pathologic stage. Furthermore, NE cells coexpress PSA, suggesting a common precursor cell of origin. The elaboration of biogenic amines and neuropeptides suggests that NE cells dispersed in prostatic carcinoma may play a paracrine growth-regulatory role.

Adenocarcinoma↗
PubMed1993

Identification of a new receptor subtype for tumor necrosis factor-alpha.

Two distinct receptors, which bind both tumor necrosis factor-alpha and tumor necrosis factor-beta (TNF-alpha and TNF-beta), have been previously identified and cloned from transformed cells. The present study identifies a novel receptor subtype in normal human liver which binds TNF-alpha but not TNF-beta. TNF-alpha but not TNF-beta competes for 125I-TNF-alpha binding and incorporation into affinity-labeled complexes in human liver plasma membranes (HLPM). Antisera to the cloned receptors competed for 125I-TNF-alpha binding to plasma membranes isolated from various transformed cell lines but not to HLPM. However, mRNAs corresponding in size to both known TNF receptors were detected in liver RNA, making it likely that post-transcriptional modifications account for the TNF-alpha specificity of HLPM. These observations suggest that the effects of TNF-alpha and TNF-beta on some normal tissues may be more distinct than previously realized.

Antibodies, Monoclonal↗
PubMed1993

The role of neoadjuvant hormonal manipulation in localized prostatic cancer.

BACKGROUND: Although hormonal manipulation is standard therapy for patients with metastatic prostatic cancer, its use in localized disease in combination with surgical extirpation of the gland has not been investigated thoroughly and systematically. METHODS: The authors report their initial pilot studies using preoperative neoadjuvant endocrine therapy. RESULTS: Although marked reduction in serum prostate-specific antigen (PSA) levels occurred in all patients, the PSA level after endocrine manipulation did not predict the pathologic stage. In addition, immunohistochemical staining of the radical prostatectomy specimen for PSA, in several patients with a zero serum PSA level, after endocrine therapy revealed intense PSA staining in the cancer cells but not in benign epithelium. The effects on tumor downstaging were inconclusive. Overall, only 33% of patients had organ-confined disease, but in some patients, complete tumor regression (PO) occurred. CONCLUSIONS: Neoadjuvant hormonal therapy in prostatic cancer, although definitely not standard therapy, bears investigation. In addition to the effect on the "index" cancer, it also provides an opportunity to evaluate the effect of hormonal agents on microfocal ("early") cancer and known precursors of malignant change. Therefore, it may provide a means of assessing agents of potential use in the development of chemopreventive strategies.

Administration, Oral↗
PubMed1993

Molecular cloning of a complementary DNA encoding a prostate-specific membrane antigen.

Recently, a novel M(r) 100,000 prostate-specific membrane glycoprotein (PSM) has been detected by the prostate-specific monoclonal antibody 7E11-C5, raised against the human prostatic carcinoma cell line LNCaP. The PSM antigen is expressed exclusively by normal and neoplastic prostate cells and metastases. We now report the molecular cloning of a full-length 2.65-kilobase complementary DNA encoding the PSM antigen from a human LNCaP complementary DNA library by polymerase chain reaction using degenerate oligonucleotide primers. Analysis of the complementary DNA sequence has revealed that a portion of the coding region, from nucleotide 1250 to 1700, has 54% homology to the human transferrin receptor mRNA. The deduced polypeptide has a putative transmembrane domain enabling the delineation of intra- and extracellular portions of this antigen. In contrast to prostate-specific antigen and prostatic acid phosphatase which are secreted proteins, PSM as an integral membrane protein may prove to be effective as a target for imaging and cytotoxic targeting modalities.

Amino Acid Sequence↗
PubMed1993

Nuclear overexpression of p53 protein in transitional cell bladder carcinoma: a marker for disease progression.

BACKGROUND: Approximately one third of the patients with superficially infiltrative transitional cell (T1-TNM pathological staging system) bladder carcinoma who are treated with transurethral resection alone have disease progression. Despite precise pathologic staging and grading, clinical outcome in these patients is not predictable. Recent reports reveal that mutations of the p53 tumor suppressor gene (also known as TP53) occur commonly in bladder cancers. PURPOSE: The aim of this study was to investigate the hypothesis that altered patterns of expression of the protein product(s) of the mutated p53 tumor suppressor gene are associated with tumor progression in patients with T1 bladder cancer. METHODS: We examined deparaffinized tumor tissue specimens from transurethral resection in 43 patients with T1 bladder cancer who had not received adjuvant therapy. Nuclear overexpression of p53 protein was detected by immunohistochemical analysis using the mouse monoclonal antibody PAb1801, which stains both wild-type and mutant p53 proteins. The data were then correlated with the following conventional prognostic variables: age, sex, histologic presence of associated carcinoma in situ, and vascular invasion of tumor. Disease progression rates per 100 person-years were calculated. RESULTS: Median follow-up was 119 months. None of the urothelial and stromal cells from normal bladder specimens showed nuclear overexpression of p53 protein, but patients with T1 bladder tumors could be stratified into two groups with different patterns of staining for p53 protein. Eighteen patients (42%) had no more than 20% tumor cells with positive nuclear staining (group A), while the remaining 25 patients (58%) had 20% or more tumor cells with nuclear immunoreactivity (group B). Patients in group B had a significantly lower progression-free interval (P < .001). Disease progression rates were 20.5% per year for group B and 2.5% for group A. CONCLUSION: These results suggest that T1 bladder cancers exhibiting nuclear overexpression of p53 protein have a higher probability of disease progression. This study also suggests that p53 overexpression is an important prognostic factor in these patients and may be useful in selecting appropriate therapy. IMPLICATIONS: Large prospective studies are needed to confirm these results and to evaluate nuclear overexpression of p53 protein as a prognostic marker in bladder cancer.

Adult↗
PubMed1993

Hypocellular bladder wash specimens and their clinical significance.

Bladder wash flow cytometry specimens containing less than 1,000 cells were defined as hypocellular. Between June 1981 and December 1990, 5,676 bladder wash flow cytometry specimens were collected, of which 142 (2.5%) were deemed hypocellular. Of the 132 evaluable patients with hypocellular specimens 34 (30%) had documented evidence of carcinoma compared to 52% for the entire population. Among the 34 patients 30 had transitional cell carcinoma, of which 12 were carcinoma in situ, 9 stage Ta or T1 and 9 stage T2 or greater. Thus, there was no obvious relationship between stage or grade of carcinoma versus probability of a hypocellular specimen. Differences in irrigation techniques of different urologists in the operating room using general anesthesia versus catheter and cystoscopic irrigation in the outpatient clinic are discussed as possible explanations for the hypocellular specimens.

Biopsy↗
PubMed1993

The management of clinically unconfirmed positive urinary cytology.

An aggressive evaluation of extravesical sites of disease in patients with clinically unconfirmed positive urinary cytology findings is indicated only in previously untreated asymptomatic or symptomatic patients (group 1) and in those with a complete response to intravesical therapy who are without evidence of disease for 1 year (group 4). Patients who have positive urinary cytology findings immediately after complete transurethral resection of bladder tumors or intravesical therapy will almost always have recurrent bladder transitional cell carcinoma and do not require aggressive extravesical evaluation initially. Transurethral resection prostate biopsy between the 5 and 7 o'clock positions along the entire length of the prostatic urethra is the technique of choice for detecting transitional cell carcinoma of the prostate, since other less invasive techniques frequently underestimate the extent of disease. In the absence of radiographic disease, bilateral ureteral lavage cytology is the technique of choice to identify the upper tract as the source of a positive urinary cytology result. Rigid and flexible ureteropyeloscopy should be performed only in the presence of radiographic or cytological evidence of upper tract transitional cell carcinoma, or in patients with a history of upper tract disease who have suspected relapse on the basis of a positive urinary cytology result.

Carcinoma, Transitional Cell↗