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National Cancer Institute®
Ultima Vez Modificado: 1 de marzo del 2002
UI - 11551094
AU - Lindor NM; Dechet CB; Greene MH; Jenkins RB; Zincke MT; Weaver AL;
TI - Wilson M; Zincke H; Liu W Papillary renal cell carcinoma: analysis of germline mutations in the MET proto-oncogene in a clinic-based population.
SO - Genet Test 2001 Summer;5(2):101-6
AD - Department of Medical Genetics, Mayo Clinic, Rochester, MN 55905, USA. email@example.com
Approximately 10% of all renal cell carcinomas (RCCs) present a distinctive papillary histology. Familial papillary RCC (PRCC) has been described, but the majority of cases appear to be sporadic. Recently, germline mutations in the MET proto-oncogene on chromosome 7 have been identified in families with hereditary PRCC. We evaluated 59 patients with PRCC for the frequency of MET germline mutations to determine the value of genetic screening of this patient population. Between 1976 and 1997, 165 patients were identified with PRCC by retrospective chart review. Fifty-nine of 133 surviving patients agreed to provide a family history, a blood specimen, and informed consent for genetic research. DNA was isolated from peripheral blood leukocytes. Denaturing high-performance liquid chromatography (DHPLC) followed by genomic sequencing was performed on eight exons of the MET proto-oncogene, including exons 5-7 of the extracellular domain, exon 14, and exons 16-19 of the tyrosine kinase domain. The 59 patients in this study included 49 men and 10 women with a mean age at diagnosis of 61 years. Bilateral and/or multifocal disease was present in 13 cases (22%). No germline mutations were detected in the studied exons of the MET proto-oncogene (exons previously reported to contain deleterious mutations in familial PRCC). No pathological MET proto-oncogene germline mutations were identified in 59 patients with PRCC. The germline mutation rate in this clinic-based population of individuals with PRCC approaches 0% (CI = 0-6.18). MET proto-oncogene germline mutation screening does not appear to be clinically indicated in patients with PRCC without additional evidence for a genetic predisposition (positive family history, unusual age at onset, bilateral disease).
UI - 11840338
AU - Caldwell MC; Hough C; Furer S; Linehan WM; Morin PJ; Gorospe M
TI - Serial analysis of gene expression in renal carcinoma cells reveals VHL-dependent sensitivity to TNFalpha cytotoxicity.
SO - Oncogene 2002 Jan 31;21(6):929-36
AD - Laboratory of Cellular and Molecular Biology, National Institute on Aging-IRP, National Institutes of Health, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA.
We have used serial analysis of gene expression (SAGE) to investigate the influence of the von Hippel-Lindau (VHL) gene on global gene expression profiles. SAGE libraries were prepared from renal cell carcinoma (RCC) lines that either lack (parental) or express wild-type VHL (wtVHL). Comparison of these libraries revealed some differentially expressed genes (Glut-1, for example) that were known to be influenced by VHL, but the majority of genes had not previously been reported to be affected by the cell's VHL status. The identification of several genes involved in TNFalpha-mediated events prompted us to compare the sensitivity of cells with different VHL status in TNFalpha cytotoxicity assays. Strikingly, VHL-deficient cells were much more resistant to the toxic influence of TNFalpha. We propose that VHL-dependent sensitization of RCC cells to TNFalpha-mediated killing may contribute to VHL's growth suppressive function.
UI - 11830554
AU - Angelo LS; Talpaz M; Kurzrock R
TI - Autocrine interleukin-6 production in renal cell carcinoma: evidence for the involvement of p53.
SO - Cancer Res 2002 Feb 1;62(3):932-40
AD - Department of Bioimmunotherapy, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA.
Interleukin (IL)-6 is an autocrine growth factor for renal cell carcinoma (RCC). We sought to determine whether p53 regulates constitutive IL-6 production. RCC cell lines containing mutant (mut) p53 produced higher levels of IL-6 than those containing wild-type (wt) p53 (P < 0.05). Transfection of wt p53 into RCC cell lines bearing mut p53 (UOK 121LN) or wt p53 (A498 and ACHN) resulted in repression of IL-6 promoter chloramphenicol acetyltransferase activity (P < 0.05). Mutant p53 was either less effective at repressing IL-6 promoter activity (ACHN cells) or enhanced IL-6 promoter activity (A498 cells). A498 cells stably transfected with mut p53 produced higher levels of IL-6 than A498 cells transfected with an empty expression vector (P < 0.05). Electrophoretic mobility shift assays showed decreased binding of CAAT enhancer binding protein, cyclic AMP responsive element binding protein, +/- nuclear factor-kappaB transcription factors to the IL-6 promoter in various RCC cell lines transfected with wt p53 (P < 0.05) but not in those transfected with mut p53. These data suggest that: (a) mutation of p53 contributes to the overexpression of IL-6 in RCC; and (b) wt p53 represses IL-6 expression, at least in part, by interfering with specific transcription factor binding to the IL-6 promoter.
UI - 11642604
AU - Childs RW
TI - Nonmyeloablative blood stem cell transplantation as adoptive allogeneic immunotherapy for metastatic renal cell carcinoma.
SO - Crit Rev Immunol 2001;21(1-3):191-203
AD - National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA. firstname.lastname@example.org
Allogeneic stem cell transplantation has emerged as a potentially curative form of immunotherapy for patients with hematological malignancies that are resistant to conventional chemo/radiotherapy. Donor T cell populations targeting allogeneic minor histocompatibility antigens expressed on the patient's malignant cells are felt to be the driving force of the graft-versus-leukemia reaction, although to date only a handful of these antigens have been fully characterized. Recent data from experimental animal models and limited clinical data in humans suggest that graft-versus-tumor effects, analogous to the graft-versus-leukemia reaction, may be generated against malignancies of epithelial origin. This article reviews the results of a pilot trial demonstrating graft-versus-renal cell carcinoma effects following nonmyeloablative stem cell transplantation, highlighting the potential of allogeneic immunotherapy for treating cancer.
UI - 11750847
AU - Mizutani Y; Nakanishi H; Yoshida O; Fukushima M; Bonavida B; Miki T
TI - Potentiation of the sensitivity of renal cell carcinoma cells to TRAIL-mediated apoptosis by subtoxic concentrations of 5-fluorouracil.
SO - Eur J Cancer 2002 Jan;38(1):167-76
AD - Department of Urology, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan. email@example.com
Cytotoxic chemotherapy has shown little antitumour activity against renal cell carcinoma (RCC). Although immunotherapy is relatively effective against RCC, the response rate is approximately 20%. Therefore, there is an urgent need to increase this response rate. Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL/Apo-2L) is one member of the tumour necrosis factor ligand family that selectively induces apoptosis of cancer cells. Since several cytotoxic anticancer drugs including 5-fluorouracil (5-FU) also mediate apoptosis, we reasoned that combined treatment of cancer cells with TRAIL and drugs might result in synergy and overcome the resistance of the cancer cell. This study has examined whether TRAIL can synergise with 5-FU in both cytotoxic and apoptotic assays against drug-resistant RCC cells. Cytotoxicity was determined by an 1-day microculture tetrazolium dye assay. Synergy was assessed by isobolographic analysis. Treatment of Caki-1 cells with TRAIL in combination with 5-FU resulted in a synergistic cytotoxic effect. Synergy was also achieved in freshly derived RCC cells from 3 patients. The enhanced cytotoxicity was obtained irrespective of the sequence of the treatment, but the highest cytotoxicity was observed when Caki-1 cells were treated with TRAIL and 5-FU simultaneously. The synergy achieved in cytotoxicity with TRAIL and 5-FU was shown to be due to apoptosis. The mechanisms responsible for the synergistic cytotoxicity and apoptosis were examined. Treatment of Caki-1 cells with 5-FU enhanced the expression of p53 and bax, but had no effect on the expression of bcl-2. Incubation of Caki-1 cells with TRAIL enhanced the intracellular accumulation of 5-FU and 5-fluoro-2'-deoxyuridine 5'-monophosphate (FdUMP). Treatment of Caki-1 cells with TRAIL downregulated the expression of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) modestly, and upregulated the expression of orotate phosphoribosyltransferase (OPRT). However, the expression level of thymidine phosphorylase (TP) was not affected by TRAIL. This study demonstrates that combined treatment of RCC cells with TRAIL and 5-FU overcomes their resistance. The sensitisation obtained with freshly isolated RCC cells required low subtoxic concentrations of 5-FU. These findings support the potential application in vivo of a combination of TRAIL and 5-FU in the treatment of TRAIL/5-FU-resistant RCC.
UI - 11857297
AU - Delahunt B; Kittelson JM; McCredie MR; Reeve AE; Stewart JH; Bilous AM
TI - Prognostic importance of tumor size for localized conventional (clear cell) renal cell carcinoma: assessment of TNM T1 and T2 tumor categories and comparison with other prognostic parameters.
SO - Cancer 2002 Feb 1;94(3):658-64
AD - Department of Pathology, Wellington School of Medicine, University of Otago, Wellington, New Zealand. firstname.lastname@example.org
BACKGROUND: The T1 and T2 classifications of the International Union Against Cancer TNM classification system for renal cell carcinoma are based on primary tumor size, and in various editions of the classification, the cut points between T1 and T2 have been amended to provide clinical utility. In the current edition, the T1/T2 cut point is less than or equal to and greater than 7 cm. and more recently a subdivision of the T1 classification (less than or equal to and < 4 cm) has been proposed to identify patients suitable for partial nephrectomy. This study investigates the prognostic significance of tumor size in a series of organ-confined clear cell renal cell carcinomas. METHODS: One hundred thirty cases of organ-confined clear cell renal cell carcinomas, with a minimum of 5 years' follow-up, were identified from the New South Wales Cancer Registry. Tumor size was compared with survival using the method of Kaplan and Meier for TNM size categories, and proportional hazards regression was used for assessing size as a continuous variable. Proportional hazards regression also was used for multivariable comparisons of size and other prognostic parameters (Fuhrman grade, AgNOR score, and Ki-67 index) against survival. RESULTS: Of 116 cases for which tumor dimension was recorded, 25 patients had died of cancer-related causes. Primary tumor size ranged from 12 to 140 mm (mean, 57.3 mm). The association between survival and size was significant irrespective of the TNM classification and was also significant when size was modeled continuously (P = 0.000125, hazard of death increased by 3.51 times for each doubling of tumor size). On univariate analysis, Fuhrman grade (P = 0.04) and AgNOR score (P = 0.015) were associated with survival; however, on multivariate analysis only tumor size retained significance. CONCLUSIONS: Although the cut point of T1 and T2 TNM categories and the proposed T1 subdivision cut point correlate with survival, our finding that size is a continuous variable indicates that as a prognostic parameter for clear cell renal cell carcinoma, primary tumor size is relative rather than indicative. Copyright 2002 American Cancer Society. DOI 10.1002/cncr.10255
UI - 11147860
AU - Jackson RJ; Loh SC; Gokaslan ZL
TI - Metastatic renal cell carcinoma of the spine: surgical treatment and results.
SO - J Neurosurg 2001 Jan;94(1 Suppl):18-24
AD - Department of Neurosurgery, Baylor College of Medicine, The University of Texas MD Anderson Cancer Center, Houston 77030, USA.
OBJECT: Renal cell carcinoma (RCC) is an aggressive malignancy that frequently metastasizes. When RCC metastasizes to the spine, significant pain and neurological dysfunction often follow. Because systemic therapy and radiotherapy have a limited effect in controlling spinal disease, surgery is frequently required; however, there are very few published series specifically addressing the role and benefits of the surgical treatment for this disease. The authors conducted a retrospective study to review their experience with the surgical treatment of metastatic RCC of the spine, paying particular attention to methodology and patient neurological status, pain relief, and survival. METHODS: Between January age 55 years, range 16-82 years) underwent 107 spinal operations for metastatic RCC. Indications for surgery included disabling pain (94 [88%] of 107 procedures) and/or neurological dysfunction (55 [51%] of 107 procedures). The anatomical location and extent of tumor determined the choice of an anterior, posterior, or combined surgical approach. Internal fixation was performed in all but three patients. Preoperative embolization was required in approximately one half of the patients. Radiotherapy was performed in 40 patients prior to surgery, and immuno- and chemotherapy were administered in 70 patients either pre- or postoperatively. After an average follow-up duration of 15 months, 57 patients had died. Kaplan-Meier analysis revealed a median postoperative survival of 12.3 months. Significant pain reduction, as indicated by a visual analog pain scale, was achieved in 84 (89%) of the 94 cases presenting with disabling pain. Neurological improvement was seen in 36 (65%) of the 55 patients. The major morbidity and 30-day mortality rates were 15% (16 of 107 procedures) and 2% (two of 107 procedures), respectively. CONCLUSIONS: In selected patients with metastatic RCC of the spine, resection followed by stabilization can provide pain relief and neurological preservation or improvement.
UI - 11850836
AU - Vortmeyer AO; Huang SC; Pack SD; Koch CA; Lubensky IA; Oldfield EH;
TI - Zhuang Z Somatic point mutation of the wild-type allele detected in tumors of patients with VHL germline deletion.
SO - Oncogene 2002 Feb 14;21(8):1167-70
AD - Molecular Pathogenesis Unit, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, Building 10, Room 5D37, Bethesda, MD 20892, USA.
The majority of patients with Von Hippel-Lindau (VHL) disease are affected by a VHL germline mutation involving one copy of the VHL gene. Loss of heterozygosity of the second VHL allele can be consistently demonstrated in tumor tissue from these patients, suggesting that allelic deletion is a very early or even initiating event for tumorigenesis. Approximately 20% of VHL disease patients, however, exhibit germline deletion of one entire copy or at least a substantial part of the VHL gene. To investigate the nature of the "second genetic hit" in this patient population, we analysed two renal cell carcinomas and one CNS hemangioblastoma from three unrelated patients for genetic changes of the second copy of the VHL gene. All three tumors showed retention of one VHL allele by FISH. Single-strand conformation polymorphism and mutation analysis of microdissected tumor DNA revealed somatic point mutations of the wild-type VHL copies in each of the three tumors. The results indicate that the "two hit model" is equally applicable to patients with VHL germline mutation and VHL germline deletion. In contrast to tumors from patients with VHL germline mutation, however, point mutations of the wild-type allele can be detected in tumors from patients with VHL germline deletion.
UI - 11793370
AU - Schraml P; Struckmann K; Hatz F; Sonnet S; Kully C; Gasser T; Sauter G;
TI - Mihatsch MJ; Moch H VHL mutations and their correlation with tumour cell proliferation, microvessel density, and patient prognosis in clear cell renal cell carcinoma.
SO - J Pathol 2002 Feb;196(2):186-93
AD - Institute of Pathology, University of Basel, Schonbeinstrasse 40, CH-4031 Basel, Switzerland. Peter.Schraml@unibas.ch
Mutations of the von Hippel-Lindau (VHL) gene are considered critical for the initiation of clear cell renal cell carcinoma. The VHL protein is involved in regulation of the cell cycle and neo-vascularization. In this study, the association of VHL mutations with tumour cell proliferation, angiogenesis, and clinical outcome was analysed in 113 clear cell renal cell carcinomas. The degree of angiogenesis and tumour cell proliferation was immunohistochemically determined by counting microvessels (microvessel density, anti-CD34 antibody) and cells with proliferating activity (Ki-67 labelling index, MIB-1 antibody). Forty-eight different VHL sequence alterations were found in 38 of 113 patients (34%) by direct sequencing. Nineteen VHL mutations were frameshifts and nonsense mutations, predicted to change the open reading frame of VHL. These 'loss-of-function' mutations correlated with worse prognosis in univariate analysis (p=0.02). Tumour grade, stage, microvessel density, and tumour cell proliferation were not associated with VHL alterations. These findings may indicate that 'loss-of-function' VHL mutations are involved in the progression of a clear cell renal cell carcinoma subset, whereas regulation of angiogenesis and proliferation of renal carcinoma in vivo is apparently not directly influenced by VHL alterations. Copyright 2001 John Wiley & Sons, Ltd.
UI - 11561691
AU - Berg WJ; Schwartz L; Yu R; Mazumdar M; Motzer RJ
TI - Phase II trial of irofulven (6-hydroxymethylacylfulvene) for patients with advanced renal cell carcinoma.
SO - Invest New Drugs 2001;19(4):317-20
AD - Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA.
The aim of this study was to determine the antitumor activity of irofulven (6-hydroxymethylacylfulvene) in patients with advanced renal cell carcinoma (RCC). Eligible patients had advanced renal cell carcinoma with bidimensionally measurable disease, a Karnofsky performance status of at least 70, life expectancy of greater than three months, no prior treatment with chemotherapy, and no evidence of brain metastases. Irofulven was administered at a dose of 11 mg/m2 by 5-min intravenous infusion, on 5 consecutive days. Cycles were repeated every 28 days. Thirteen patients were enrolled in this study and 12 were evaluable for response. Of the twelve evaluable patients, no major responses were achieved. Eight patients had stable disease as best response. Toxicity included myelosuppression and gastrointestinal side effects. At the dose and schedule used in this trial, irofulven did not produce clinical response in RCC.
UI - 11561693
AU - Kuebler JP; King GW; Triozzi P; Moore T; Kraut EH
TI - Phase II study of pyrazoloacridine in metastatic renal cell carcinoma.
SO - Invest New Drugs 2001;19(4):327-8
AD - Grant/Riverside Hospital, Columbus, OH, USA.
UI - 11769879
AU - Moyad MA
TI - Obesity, interrelated mechanisms, and exposures and kidney cancer.
SO - Semin Urol Oncol 2001 Nov;19(4):270-9
AD - Department of Surgery, University of Michigan Medical Center, Ann Arbor 48109-0330, USA.
Obesity has been shown to increase the risk or be associated with numerous conditions from cardiovascular disease and type II diabetes to erectile dysfunction and osteoarthritis. Obesity may also be associated with numerous cancers, and kidney cancer or renal-cell cancer (RCC) may have one of the strongest correlations to obesity compared with cancer at any other site. Almost every epidemiologic investigation has demonstrated an association that tends to affect women more than men, but both genders are impacted. In general, past studies suggest that with increasing weight, a threshold point exists whereby a certain range of body mass index dramatically changes risk. Men and women at the most extreme ends of obesity tend to have the highest risk or only risk in past studies. Individuals at the more extreme ends of obesity may be affected by an almost indefinite number of mechanisms and exposures that could determine incidence and possibly prognosis. For example, higher estrogen levels, elevated insulin levels, a greater concentration of growth factors in adipose tissue, hypertension, cholesterol metabolism abnormalities, and immune malfunction are just some of the potential mechanisms that may increase kidney cancer risk. Obese individuals may also have lower serum levels of vitamin D and engage in less physical activity. Smoking or genetic predisposition to RCC may synergistically contribute to the effect of obesity on risk. The potential mechanisms and associations are numerous and complex. Regardless of the actual cancer risk now and in the future, the overall effect of obesity on general health is clear, and this should be kept in mind in the discussion between health professional and patient.
UI - 11769880
AU - Moyad MA
TI - Review of potential risk factors for kidney (renal cell) cancer.
SO - Semin Urol Oncol 2001 Nov;19(4):280-93
AD - Department of Surgery, University of Michigan Medical Center, Ann Arbor 48109-0330, USA.
Renal cell cancer (RCC) is responsible for a small percentage of total cancer cases and deaths throughout the world, but the incidence rates of RCC have been steadily increasing over the past decade, whereas numerous other cancers have stabilized or even decreased in number. Even in countries that were observed to have a lower incidence of this disease many are now experiencing large increases in the rates of this cancer. Most kidney cancers are RCC, and blacks are currently experiencing RCC rates that are higher than any other race. Older individuals are also at a higher risk compared with young individuals, but this observation may also be changing. The reasons for these potential increases are not understood beyond the partial impact and greater use of newer diagnostic procedures. Other reasons for higher rates of RCC and a better understanding of which individuals may be at the highest risk need to be examined to provide the clinician with possible clues as to who should be tested and what prevention measures should be offered. Most of the past investigations into risk factors have been case-control or retrospective studies, but some generalizations can still be made. Family history and genetics seem to increase risk, but overall are responsible for a small number of the total cases. Smoking, obesity, and even hypertension seem to be risk factors for RCC. Reducing these behaviors and conditions may also reduce the risk of RCC. Healthier eating habits (fruits and vegetables, and a lower caloric intake) and more physical activity may also reduce the risk of RCC. Therefore, it is possible that the increases in RCC may also be due, in part, to unhealthy lifestyle factors that have been on the increase over the past several decades. Recommendations for cardiovascular disease prevention should also be applied to patients or clinicians concerned about RCC risk. Finally, numerous occupations, occupational exposures, reproductive and hormonal changes or manipulations, and a variety of other factors may impact risk, but overall their contribution seems small compared with other more consistent risk factors.
UI - 11826016
AU - Takahashi M; Kahnoski R; Gross D; Nicol D; Teh BT
TI - Familial adult renal neoplasia.
SO - J Med Genet 2002 Jan;39(1):1-5
AD - Laboratory of Cancer Genetics, Van Andel Research Institute, Grand Rapids, MI 49503, USA.
Our understanding of the molecular mechanisms underlying the tumorigenesis of renal cell carcinoma (RCC) has partially come from studies of RCC related familial cancer syndromes such as von Hippel-Lindau (VHL) disease and hereditary papillary RCC (HPRC). These studies have led to the identification of RCC related genes, which, besides allowing accurate diagnosis of these diseases, have been found mutated or abnormally expressed in the sporadic counterparts of these familial renal tumours. To date, a number of renal tumour related syndromes have been described. We review recent advances in this field and discuss a genetic approach to managing familial cases of renal tumours occasionally encountered by cancer geneticists and urologists.
UI - 11848468
AU - Scheltema JM; Romijn JC; van Steenbrugge GJ; Schroder FH; Mickisch GH
TI - Inhibition of apoptotic proteins causes multidrug resistance in renal carcinoma cells.
SO - Anticancer Res 2001 Sep-Oct;21(5):3161-6
AD - Department of Urology, Erasmus University and Academic Hospital, Rotterdam, The Netherlands.
Renal Cell Carcinomas (RCCs) exhibit strong resistance to the most chemotherapeutic treatments probably due to the expression of various multidrug resistance (MDR) genes. Overexpression of P-glycoprotein (Pgp) is established as one such factor, but other mechanisms such as at-MDR, characterized by attenuated DNA-topoisomerase II (topoII) activity, may be functional as well. In addition, regulating proteins involved in apoptosis can exhibit multidrug resistant features. However, prevention of apoptosis as a mechanism of MDR has not yet been assessed in RCC, nor has the cytotoxicity of a variety of chemotherapeutic agents known to trigger apoptotic or necrotic cell death been tested in RCC in a systematic fashion. Using immunohistochemistry and Western blotting, Bcl-2 and Bax expression was determined in a panel of multidrug resistant RCC lines featuring Pgp and/or at-MDR. The results were related to apoptotic activity and kind of cell death in these cell lines, demonstrated by incubation with Hoechst 33342 and propidium iodide after treatment with various cytotoxic agents and quantitated by MTT. In the drug resistant sublines, some decreased Bax and strongly increased Bcl-2 expression was seen by immunohistochemistry indicating prevention of apoptosis as a distinct feature of MDR in RCC. This was confirmed by Western blotting. Sublines revealed significant resistance for all drugs, except for CC-313 and DiMIQ. However, these drugs induced necrotic cell death, in contrast to all other drugs tested, which induced apoptotic cell death. We conclude that, in chemoselected RCC sublines, multidrug resistance appears to be functional due to inhibition of apoptosis, apart from the MDR1 and at-MDR resistance mechanisms. CC-313 and DiMIQ are very potent cytotoxic agents in RCC, probably because they do not kill by induction of apoptosis.
UI - 11848472
AU - Koga F; Arai K; Kamai T; Abe H; Yoshida K
TI - Fas labeling status does not correlate with apoptosis of renal cell carcinoma in vivo.
SO - Anticancer Res 2001 Sep-Oct;21(5):3193-7
AD - Department of Urology, Dokkyo University School of Medicine, Shimotsuga-gun, Tochigi, Japan. email@example.com
BACKGROUND: Contribution of the Fas system to apoptosis of renal cell carcinoma (RCC) was investigated in vivo. MATERIALS AND METHODS: Tissues from 30 RCC cases were immunostained for Fas and Fas ligand (FasL) to assess associations between Fas labeling status of RCC, indices of FasL-positive tumor-infiltrating mononuclear cells (FasL-TIM) and apoptotic indices (AI) of RCC. RESULTS: In all cases, tumor cells co-expressed Fas and FasL; strongly and diffusely in 13 cases (43%) and weakly in 17 (57%). Despite the constitutive co-expression of Fas and FasL, AI was low in most cases (median, 7 per 1,000 tumor cells; range, 1 to 257). The Fas labeling status did not significantly associate with AI while FasL-TIM index positively correlated with AI. CONCLUSION: These results suggest that the Fas system is not the principal mechanism of apoptosis of RCC while activated tumor-infiltrating mononuclear cells induce apoptosis via mechanisms other than the Fas system.
UI - 11848517
AU - Ramp U; Mahotka C; Kalinski T; Ebel E; Gabbert HE; Gerharz CD
TI - Topotecan (Hycamtin) responsiveness in human renal carcinoma cell lines of the clear cell and papillary types.
SO - Anticancer Res 2001 Sep-Oct;21(5):3509-17
AD - Institute of Pathology, Heinrich Heine University, Duesseldorf, Germany.
BACKGROUND: Since no effective therapeutic approach is yet known for metastatic renal cell carcinoma (RCC), we analyzed the effects of topotecan (Hycamtin), a novel topoisomerase I-inhibitor, in RCC cell lines of the clear cell and papillary/chromophilic types. MATERIALS AND METHODS: The anti-proliferative and apoptosis-inducing effects of topotecan were analyzed in 20 RCC cell lines by MTT-assay and light microscopic apoptosis counting. Moreover, Bcl-2 and Bax expression was investigated by Northern blot and immunocytochemistry while the p53 mutation status was analyzed by DNA sequencing. RESULTS: Exposure to clinically relevant concentrations of topotecan (i.e. < or = 1 microg/ml) resulted in a significant (p<0.05) dose-dependent reduction of cell number in 17 out of 20 RCC cell lines. The reduction of cell number was paralleled by an increase in apoptotic cell death. Papillary/chromophilic RCCs exhibited a significantly (p<0.05) more pronounced responsiveness to topotecan than clear cell RCCs. Moreover, the effects of topotecan proved to be superior to those of 5-fluorouracil (5-FU), an anticancer drug currently used in the therapy of RCCs. No correlation became evident between responsiveness to topotecan and the expression levels of Bcl-2 and Bax. Moreover, the response to topotecan could not be correlated with the p53 mutation status of our RCC cell lines. CONCLUSION: Clinically relevant concentrations of topotecan induced apoptosis in RCC cell lines more effectively than 5-FU. Further testing will show whether topotecan-induced apoptosis can be exploited for the treatment of RCCs in vivo as well.
UI - 11867357
AU - Parker AS; Cerhan JR; Lynch CF; Ershow AG; Cantor KP
TI - Gender, alcohol consumption, and renal cell carcinoma.
SO - Am J Epidemiol 2002 Mar 1;155(5):455-62
AD - Department of Health Sciences Research, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA. firstname.lastname@example.org
The nature of the association between alcohol consumption and renal cell carcinoma (RCC) is not well understood, but there are indications of effect modification by gender. The authors report data from a population-based case-control study conducted in Iowa from 1986 to 1989. RCC cases (261 men and 145 women) were identified through the Iowa Cancer Registry, while controls (1,598 men and 831 women) were randomly selected from the general population, frequency matched on age and gender. Subjects provided detailed information on a mailed questionnaire regarding demographic, anthropometric, lifestyle, dietary, and medical history risk factors. In age-adjusted analysis, there was a decrease in risk for women who reported consuming more than three servings (median among drinkers) of alcohol per week (odds ratio = 0.5, 95% confidence interval: 0.2, 0.9) compared with never drinkers. No evidence of an association among men was noted (odds ratio = 1.1, 95% confidence interval: 0.8, 1.5). Multivariate adjustment for anthropometric, lifestyle, smoking, and dietary factors did not alter the findings. Analysis by type of alcohol suggested that the inverse association was strongest for beer consumption, but estimates were imprecise. These findings suggest an inverse association of alcohol consumption and RCC development among women but not among men.
UI - 11870503
AU - Hotakainen K; Ljungberg B; Paju A; Rasmuson T; Alfthan H; Stenman UH
TI - The free beta-subunit of human chorionic gonadotropin as a prognostic factor in renal cell carcinoma.
SO - Br J Cancer 2002 Jan 21;86(2):185-9
AD - Department of Clinical Chemistry, Helsinki University Central Hospital, Biomedicum Helsinki, Rm A418a Haartmaninkatu 8, FIN-00029, Helsinki, Finland. email@example.com
The free beta-subunit of human chorionic gonadotropin beta is expressed in several nontrophoblastic tumours and this is usually associated with aggressive disease. Little is known about human chorionic gonadotropin beta expression in renal cancer. We determined the pretreatment levels of human chorionic gonadotropin beta in serum of patients with renal cell carcinoma, and studied whether elevated levels predicted the clinical outcome. Serum samples were collected before surgery from 177 patients with renal cell carcinoma and from 84 apparently healthy controls. Human chorionic gonadotropin beta in serum was measured by a highly sensitive time-resolved immunofluorometric assay. The prognostic value of human chorionic gonadotropin beta, and of usual clinical and pathological variables was analyzed by the Kaplan-Meier method, the log rank test and Cox multiple hazard regression. The serum concentrations of human chorionic gonadotropin beta were increased in 23% of the renal cell carcinoma patients and they were significantly higher in patients with renal cell carcinoma than in controls (P<0.0001). The concentrations did not correlate with clinical stage and histopathological grade, but patients with increased human chorionic gonadotropin beta levels had significantly shorter survival time than those with levels below the median (cut-off 1.2 pmol l(-1), P=0.0029). In multivariate analysis human chorionic gonadotropin beta, tumour stage and grade were independent prognostic variables. The serum concentration of human chorionic gonadotropin beta is an independent prognostic variable in renal cell carcinoma. The preoperative value of human chorionic gonadotropin beta in serum may be used to identify patents with increased risk of progressive disease. Copyright 2002 The Cancer Research Campaign
UI - 11849150
AU - Bromwich E; Aitchison M
TI - How should patients be followed up after radical nephrectomy for renal cell cancer?
SO - BJU Int 2002 Jan;89(1):1-4
AD - Department of Urology, Gartnavel General Hospital, Glasgow, UK. firstname.lastname@example.org
UI - 11849151
AU - Latif Z; Watters AD; Bartlett JM; Underwood MA; Aitchison M
TI - Gene amplification and overexpression of HER2 in renal cell carcinoma.
SO - BJU Int 2002 Jan;89(1):5-9
AD - Department of Surgery, Glasgow Royal Infirmary, Glasgow, UK. email@example.com
OBJECTIVE: To determine the frequency of HER2 genetic abnormalities in renal cell carcinoma (RCC) and hence assess the potential suitability of Herceptin immunotherapy. PATIENTS AND METHODS: Tumours from 27 patients with RCC were assessed; all patients had undergone nephrectomy. Benign renal tissue from the nephrectomy specimens was studied in seven patients. Gene amplification was assessed using fluorescent in-situ hybridization, and protein over-expression using immunohistochemistry. RESULTS: Twenty-four patients had clear cell renal carcinoma, two had papillary renal carcinoma and one a sarcomatoid variant carcinoma. There was no HER2 amplification in the tumours or the benign renal tissue. Polysomy 17 was detected in 11 of 27 tumours (41%) and increased HER2 copy number in seven (26%). Both polysomy 17 and increased HER2 copy number were absent in the benign renal tissue. Three tumours (11%) and six of the seven benign renal tissue samples over-expressed the HER2 protein. CONCLUSIONS: HER2 amplification is absent and protein over-expression uncommon in RCC. This casts doubt on the suitability of Herceptin in the treatment of RCC.
UI - 11111187
AU - Nonomura N; Ono Y; Nozawa M; Fukui T; Harada Y; Nishimura K; Takaha N;
TI - Takahara S; Okuyama A Bacillus Calmette-Guerin perfusion therapy for the treatment of transitional cell carcinoma in situ of the upper urinary tract.
SO - Eur Urol 2000 Dec;38(6):701-4;discussion 705
AD - Department of Urology, Osaka University Medical School, Suita City, Osaka, Japan. firstname.lastname@example.org
OBJECTIVES: The aim of this study is to evaluate the efficacy and safety of intrarenal bacillus Calmette-Guerin (BCG) instillation as a treatment for transitional cell carcinoma in situ (CIS) of the upper urinary tract. METHODS: Diagnostic criteria of upper urinary tract CIS were (1) positive urinary cytology, (2) negative multiple random biopsy of the bladder and prostatic urethra, (3) negative radiographic findings in the upper urinary tract and (4) two serial positive cytologies in selective ipsilateral urine sampling from the pyeloureteral system. Eleven patients diagnosed as having upper urinary tract CIS were enrolled in this study. Thus, 11 renal units were treated with BCG instillation. After placing a 6-french Double-J stent, BCG (80 mg) in 40 ml saline was instilled into the bladder weekly, 6 times in total as one course. RESULTS: At the end of one course, 9 cases showed negative urinary cytology. Among these 9 cases, 2 showed recurrence in the upper urinary tract after 4 months and 8 months of disease-free interval, respectively. These 2 cases have received an additional course of BCG instillation, but the urinary cytology did not normalize. Mean recurrence-free time was 19.6 months. Of the other 7 cases who responded to the first course of instillation, 6 cases were alive with no evidence of the disease. The remaining patient died of rectal cancer with no evidence of transitional cell carcinoma (TCC). Of the 2 cases who showed positive urinary cytology even after the first course, 1 underwent nephroureterectomy. The other case was diagnosed as having malignant lymphoma 3 months after the end of this instillation therapy, and he died of malignant lymphoma. As side effects, 8 cases (72.7%) showed bladder irritability, and 4 presented fever higher than 38 degrees C. However, no patient needed antitubercular treatment. CONCLUSION: As for the short-term response, BCG instillation for the treatment of upper urinary tract CIS is considered to be effective and safe. Longer follow-up and further experience with this treatment are required.
UI - 11700888
AU - Mai KT; Landry DC; Robertson SJ; Commons AS; Burns BF; Thijssen A;
TI - Collins J A comparative study of metastatic renal cell carcinoma with correlation to subtype and primary tumor.
SO - Pathol Res Pract 2001;197(10):671-5
AD - Department of Laboratory Medicine, The Ottawa Hospital, Ontario, Canada. email@example.com
Clear cell (CRCC), papillary (PRCC) and chromophobe (CHRC) renal cell carcinoma (RCC) are the three most frequent subtypes of RCC. The rate and distribution of their metastatic lesions have not been well documented. We compared metastatic RCC according to subtype and primary tumor characteristics to better understand their behavior and to aid in the diagnosis of metastatic RCC. Pathology reports and clinical charts related to 283 CRCC, 48 PRCC and 13 CHRCC, including their respective sarcomatoid variants, were reviewed. A hundred and thirty-seven CRCC, 5 PRCC and 1 CHRCC with metastases were identified. CRCC and non-CRCC (PRCC and CHRCC) had different patterns of metastasis and primary tumor growth. CRCC metastases were predominantly distributed in lungs, bone, brain, lymph nodes, and adrenal glands. The associated primary CRCC measured 1.5 to 15 cm, were of all grades and stages, and were often associated with invasion of small or large veins. Three PRCC had regional lymph node metastases, 1 PRCC had both regional and mediastinal lymph node metastases. Bone metastasis was present in 1 case each of PRCC and CHRCC. One PRCC with metastasis solely to regional nodes measured 4 cm. The other 4 cases of PRCC with regional lymph node and/or distant metastases as well as the CHRCC with distant metastases were greater than 8 cm in diameter. In metastasizing and non-metastasizing non-CRCC, invasion of small veins was rare and invasion of renal veins was not seen. We cannot comment with any certainty on the metastatic behavior of CHRCC. In our experience, PRCC tend to loco-regional invasion with lymph node spread. They have a low potential for vascular invasion and distant metastases that likely occur only at late stages of the disease. CRCC has a propensity for vascular invasion and may be associated with distant metastasis at an early stage. Therefore, metastatic RCC at a distant location are most likely to be of CRCC origin than PRCC origin.
UI - 11773466
AU - Mothes H; Heidet L; Arrondel C; Richter KK; Thiele M; Patzer L; Sado Y;
TI - Gubler MC; Antignac C; Scheele J Alport syndrome associated with diffuse leiomyomatosis: COL4A5-COL4A6 deletion associated with a mild form of Alport nephropathy.
SO - Nephrol Dial Transplant 2002 Jan;17(1):70-4
AD - Department of General and Visceral Surgery, Friedrich-Schiller-University Jena, Bachstrasse 18, D-07740 Jena, Germany. Henning.firstname.lastname@example.org
BACKGROUND: The X-linked Alport syndrome (AS) is an inherited nephropathy due to mutations in the COL4A5 gene, encoding the alpha5 chain of type IV collagen, a major component of the glomerular basement membrane (GBM). Here, we report a new kindred with the rare association of X-linked AS and diffuse leiomyomatosis (DL), which is a tumourous process involving smooth muscle cells of the oesophagus, the tracheobronchial tree and, in females, the genital tract. For this syndrome, an almost constant association of large COL4A5 rearrangements with a severe juvenile form of nephropathy has been described for male patients. METHODS: DNA rearrangement at the COL4A5-COL4A6 locus was studied in several members of this family using polymerase chain reaction and pulsed field gel electrophoresis. Furthermore, immunohistochemical staining of tumour and skin samples was performed. RESULTS: The affected patients in this family carry a 120 kb deletion by which the COL4A5 exon 1 and COL4A6 exons 1, 1', and 2 are removed. Immunohistochemical investigation of a skin biopsy of an affected male patient confirmed the absence of both the alpha5 and the alpha6 chains of type IV collagen in the basement membrane of the skin. Surprisingly, both affected male patients had a rather mild renal phenotype. CONCLUSIONS: This report shows that, contrary to what has been reported to date, patients suffering from AS associated with DL can be associated with a late onset renal failure (adult) form of nephropathy.
UI - 11847024
AU - Ravaud A; Bay JO
TI - [Update on renal cell carcinoma]
SO - Bull Cancer 2002 Jan;89(1):31-6
AD - Institut Bergonie, Centre regional de lutte contre le cancer, 229, cours de l'Argonne, 33076 Bordeaux Cedex. email@example.com
Authors have selected and presented radiofrequency tissue ablation for primary renal tumors and cellular therapy with dendritic cells or nonmyeloablative allogeneic transplantation as the main results in 2000-2001 on renal cell carcinoma. Furthermore other points are developed as hypertension increasing the risk of renal cell carcinoma, chromosomal events until renal cell carcinoma and prognosis of incidentally detected tumors.
UI - 11693562
AU - Weinstein MH; Dal Cin P
TI - Genetics of epithelial tumors of the renal parenchyma in adults and renal cell carcinoma in children.
SO - Anal Quant Cytol Histol 2001 Oct;23(5):362-72
AD - Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA. firstname.lastname@example.org
The classification of renal cell carcinomas has been affected by both the delineation of new histologic subtypes and the understanding that recognized histomorphologic patterns are reflective of specific sets of cytogenetic abnormalities. In fact, standard methods of clinicopathologic study and cytogenetic analysis have been cooperatively contributory in the evolution of current concepts regarding the biologic nature and classification of renal parenchymal epithelial tumors. In this review, the current classification scheme for these tumors is discussed from the perspective of both the defining histologic and cytogenetic features. Limited molecular data are described as well.
UI - 11880070
AU - Mejean A; Chretien Y; Vogt B; Cazin S; Balian C; Thiounn N; Dufour B
TI - Coloepiploic mobilization during left radical nephrectomy for renal cell carcinoma is indicated to reduce the risk of iatrogenic splenectomy.
SO - Urology 2002 Mar;59(3):358-61
AD - Department of Urology, Hopital Necker, Paris, France.
OBJECTIVES: To determine whether coloepiploic mobilization (CEM) is indicated to reduce the incidence of iatrogenic splenectomy during left radical nephrectomy for renal cell carcinoma. The incidence of iatrogenic splenectomy during a left nephrectomy is estimated to be between 1.4% and 24%. In a recent study, we reported that the incidence of iatrogenic splenectomy was 8% during a left nephrectomy performed for renal cell carcinoma through a transperitoneal anterior subcostal incision. METHODS: A left radical nephrectomy was performed in 233 consecutive patients for renal cell carcinoma through a transperitoneal anterior subcostal incision with a CEM procedure in which the left colonic flexure was completely detached from the epiploa. Perioperative and postoperative complications, including splenic injury, were noted in a database. The mean patient age was 51.3 years (range 21.3 to 90.2). The mean tumor size was 58 mm (range 15 to 230). RESULTS: An iatrogenic splenectomy was required in 3 patients, and in 1 patient, a splenic injury was treated conservatively. The incidence of iatrogenic splenectomy accompanying left radical nephrectomy was 1.3%. The mean operative time was 120 minutes (range 80 to 240). The mean time to normal gut motility was 3.4 days (range 2 to 11) and to discharge from the hospital it was 9.3 days (range 6 to 19). Regarding CEM, we did not observe any significant abdominal complications. CONCLUSIONS: The incidence of iatrogenic splenectomy during a left radical nephrectomy through a transperitoneal anterior subcostal incision may be reduced by performing the technique of CEM.
UI - 11888084
AU - Witte D; Truong LD; Ramzy I
TI - Transitional cell carcinoma of the renal pelvis the diagnostic role of pelvic washings.
SO - Am J Clin Pathol 2002 Mar;117(3):444-50
AD - Department of Pathology, Baylor College of Medicine and the Methodist Hospital, Houston, TX 77030, USA.
One hundred renal pelvic washings were reviewed blindly for 12 cytologic features. Of 52 washings with tissue confirmation, the cytologic diagnosis
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