Relevant bibliographies by topics / Metastatic papillary renal-Cell cancer

Academic literature on the topic 'Metastatic papillary renal-Cell cancer'

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Published: 25 May 2024

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Journal articles on the topic "Metastatic papillary renal-Cell cancer"

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Sidana, Abhinav, Amit L. Jain, Meet Kadakia, Spencer Krane, Julia C. Friend, Akhil Muthigi, Martha Ninos, Joanna H. Shih, and Ramaprasad Srinivasan. "Predictors of mortality in metastatic papillary renal cell cancer." Journal of Clinical Oncology 35, no. 6_suppl (February 20, 2017): 509. http://dx.doi.org/10.1200/jco.2017.35.6_suppl.509.

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509 Background: While studies have established several prognostic factors determining mortality in metastatic clear cell renal cell cancer patient, similar analysis has been lacking in metastatic papillary renal cell cancer (pRCC) patients. We aim to determine the predictors of mortality in metastatic pRCC patients. Methods: Retrospective evaluation of the medical records of patients with metastatic pRCC seen at National Cancer Institute (2000-2014) was undertaken. Patient demographics, tumor characteristics, and outcomes were studied. Kaplan-Meier Survival analysis was done to estimate overall survival (OS). Cox proportional-hazards regression analysis was done to identify predictors of All cause mortality (ACM) in this population. Results: 106 consecutive patients with metastatic pRCC were identified. The median age and follow up time after the diagnosis of metastases was 50 years (11-80) and 33.8 mon (2.3-246.7) respectively. Twenty one (19.8%) and 42 (39.6%) patients had papillary type 1 and papillary type 2 renal cancers respectively; in 43 (40.5%) patients, tumors were classified as papillary, not otherwise specified. Half (53) of patients had hereditary origin of pRCC. Median estimated OS of entire cohort was 37.5 mon. There was no difference in survival between patients with hereditary or sporadic pRCC (p = 0.80) or among patients with different subtypes of pRCC (p = 0.79). On univariate analysis, elevated serum corrected calcium elevated lactate dehydrogenase, Neutrophil-lymphocyte ratio (NLR), platelet-lymphocyte ratio, and presence of malignant ascites significantly affected the patients’ prognosis. Corrected Calcium (p = 0.03) and NLR (p = 0.004) were found to be independent predictors of ACM on multivariate analysis. Conclusions: To our knowledge, this is the largest single center series evaluating survival and predictors of survival in metastatic pRCC. Metastatic pRCC patients with elevated NLR and serum corrected calcium are significantly associated with relatively poor OS when compared to patients without these findings. If validated in larger multi-institutional cohorts, it might be reasonable to incorporate corrected calcium and NLR in nomograms predicting ACM in metastatic pRCC.
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Carlo, Maria Isabel, Nabeela Khan, Yingbei Chen, James Hsieh, A. Ari Hakimi, Chung-Han Lee, Darren R. Feldman, Robert J. Motzer, and Martin Henner Voss. "The genomic landscape of metastatic non-clear cell renal cell carcinoma." Journal of Clinical Oncology 35, no. 6_suppl (February 20, 2017): 474. http://dx.doi.org/10.1200/jco.2017.35.6_suppl.474.

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474 Background: Non-clear cell renal cell carcinoma (nccRCC) encompasses about 20% of RCC cases and includes a number of subtypes that vary clinically and molecularly. Compared to ccRCC, these tumors have more limited sensitivity to conventional anti-VEGF agents and mTOR inhibitors, and there is clear need for better therapies. Analysis of genomic alterations in potentially targetable pathways may lead to novel therapeutic development strategies. Methods: We retrospectively analyzed tumors from 112 patients with metastatic nccRCC with targeted next-generation sequencing (NGS) across a panel of >340 cancer-relevant genes. Matched tumor and normal was used to facilitate somatic calling. We report on recurrent alterations observed for nccRCC variants. Results: Median age was 53 years (range 12-77), 67% were male; 47% presented with metastatic disease and 53% with localized disease that later metastasized. NGS was performed on tissue from primary tumors (57%) or metastatic sites (43%). Subtype classifications included unclassified (44%), papillary (21%), chromophobe (13%), translocation (12%), and other (9%). The most frequently altered genes by subtype are included in table. 36% of unclassified or papillary tumors had a mutation in a putative driver gene amenable to targeted therapies, including MET, NOTCH1, SMARCB1, TSC1, TSC2, PIK3CA, and FGFR3. 3 chromophobe tumors and 1 translocation tumor had a mutation in a potentially targetable pathway. Conclusions: The mutation profiles of metastatic nccRCC vary by papillary, chromophobe, and translocation subtype, with unclassified tumors most approximating papillary subtype. Unclassified and papillary subtypes harbor frequent mutations in potentially targetable pathways that merit further investigation. [Table: see text]
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Graham, Jeffrey, Connor Wells, Frede Donskov, Jae-Lyun Lee, Anna Paola Fraccon, Felice Pasini, Camillo Porta, et al. "Cytoreductive nephrectomy in metastatic papillary renal cell carcinoma: Results from the International Metastatic Renal Cell Carcinoma Database Consortium (IMDC)." Journal of Clinical Oncology 36, no. 6_suppl (February 20, 2018): 581. http://dx.doi.org/10.1200/jco.2018.36.6_suppl.581.

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581 Background: There is evidence that cytoreductive nephrectomy (CN) may be beneficial in metastatic renal cell carcinoma (mRCC), but the role of CN in patients with papillary histology is unclear. Methods: Using the IMDC database, a retrospective analysis was performed on patients with papillary mRCC treated with or without CN. Baseline characteristics and IMDC risk factors were collected. Median overall survival (OS) was determined for both patient groups. Multivariable Cox regression analysis was performed to control for imbalances in individual IMDC risk factors. Results: In total, 353 patients with papillary mRCC with (n = 75) or without (n = 278) a component of clear cell histology were identified. Median follow-up time was 57.1 months (95% CI 32.9-77.8) and the OS from the start of first-line targeted therapy for the entire cohort was 13.2 months (95% CI 12.0-16.1). Baseline characteristics are in Table 1 and patients who had CN were more likely to be younger, with better KPS, and have sarcomatoid histology. Median OS in patients with CN was 16.3 months (95% CI 13.1-19.2), compared to 8.6 months (95% CI 6.1-12.2; p < 0.0001) in the no CN group. When adjusted for individual IMDC risk factors, the hazard ratio (HR) of death for CN was 0.62 (95% CI 0.45-0.85; p = 0.0031). Conclusions: The use of CN in patients with mRCC and papillary histology appears to be associated with improved survival when compared to no CN after adjustment for risk criteria. A clinical trial in this rare population may not be possible but this data does corroborate with clear cell literature. [Table: see text]
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Dudani, Shaan, Guillermo de Velasco, Connor Wells, Chun Loo Gan, Frede Donskov, Camillo Porta, Anna Fraccon, et al. "Characterizing sites of metastatic involvement in metastatic clear-cell, papillary, and chromophobe renal cell carcinoma." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): 5071. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.5071.

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5071 Background: There exists considerable biological and clinical variability between histologic variants of metastatic renal-cell carcinoma (mRCC). Data reporting on sites of metastatic involvement in less common histologies of mRCC are sparse. We sought to characterize the frequency of metastatic site involvement across the three most common histologies of mRCC: clear-cell (ccRCC), papillary (pRCC), and chromophobe (chrRCC). Methods: Using the International mRCC Database Consortium (IMDC) database, patients with mRCC starting systemic therapy between 2002-2019 were identified and sites of metastases at the time of systemic therapy initiation were documented. Patients with multiple sites of metastatic involvement were included in analyses of all groups to which they had metastases. The primary outcomes were prevalence of metastatic site involvement and overall survival (OS). Patients with mixed histology were excluded. Results: 10,105 patients were eligible for analysis. Median age at diagnosis was 60, 72% were male and 79% underwent nephrectomy. 92%, 7% and 2% of patients had ccRCC, pRCC, and chrRCC, respectively. Frequency of metastatic site involvement across the histologic subtypes is shown in Table. Lung, adrenal, brain and pancreatic metastases were more frequent in ccRCC, lymph node involvement was most frequent in pRCC, and liver metastases were most frequent in chrRCC. Median OS for ccRCC varied by site of metastatic involvement, ranging between 16 months (brain/pleura) and 50 months (pancreas). OS by site of metastatic involvement was compared between histologies for the four most common sites of metastases (lung, lymph nodes, bone, liver). As compared to patients with ccRCC, patients with pRCC had lower OS regardless of site of metastasis (p < 0.05). Power was limited and thus differences in OS between ccRCC and chrRCC were not detectable. Conclusions: Sites of metastatic involvement differ based on histology in mRCC. These data highlight the clinical and biologic variability between histologic subtypes of mRCC and constitute the largest cohorts of patients with metastatic pRCC and chrRCC to report on sites of metastases. Sites of Metastatic Involvement by Histology. [Table: see text]
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Motzer, Robert J., Jennifer Bacik, Tania Mariani, Paul Russo, Madhu Mazumdar, and Victor Reuter. "Treatment Outcome and Survival Associated With Metastatic Renal Cell Carcinoma of Non–Clear-Cell Histology." Journal of Clinical Oncology 20, no. 9 (May 1, 2002): 2376–81. http://dx.doi.org/10.1200/jco.2002.11.123.

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PURPOSE: To define outcome data for patients with metastatic renal cell carcinoma (RCC) with histology other than clear-cell type, including collecting duct (or medullary carcinoma), papillary, chromophobe, and unclassified histologies. PATIENTS AND METHODS: Sixty-four patients with metastatic non–clear-cell RCC histology were the subjects of this retrospective review. Included in the analysis were 22 (8%) of 286 patients from a clinical trials database, 19 of 1,166 patients from a surgery database, and 23 of 357 patients from a pathology database. RESULTS: The prevalent histology was collecting duct, present in 26 (41%) patients. The number of patients with chromophobe and papillary histologies was 12 (19%) and 18 (28%), respectively. Eight (12%) of the patients had tumors that could not be classified for specific tumor histology. Among the 43 patients treated with 86 systemic therapies, including 37 cytokine therapies, two patients (5%) were observed to have a partial response. The median overall survival time was 9.4 months (95% confidence interval, 8 to 14 months). The survival was longer for patients with chromophobe tumors compared with collecting duct or papillary histology, and this group included four patients with survival of greater than 3 years. CONCLUSION: RCC consists of a heterogeneous group of tumors including clear-cell, papillary, chromophobe, collecting duct, and unclassified cell types. Non–clear-cell histologies constitute less than 10% of patients in general populations of patients with advanced RCC treated on clinical trials. Metastatic non–clear-cell RCC is characterized by a resistance to systemic therapy and poor survival, with the survival for patients with chromophobe tumors longer than that for patients with metastatic collecting duct or papillary RCC. Treatment with novel agents on clinical trials is warranted.
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Ronnen, Ellen A., G. Varuni Kondagunta, Nicole Ishill, Lesley Spodek, Paul Russo, Victor Reuter, Jennifer Bacik, and Robert J. Motzer. "Treatment outcome for metastatic papillary renal cell carcinoma patients." Cancer 107, no. 11 (2006): 2617–21. http://dx.doi.org/10.1002/cncr.22340.

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Elabbady, Ahmed, Ryan Boudreau, and Vahid Mehrnoush. "Rapid metachronous bladder metastasis of type 2 papillary renal cell carcinoma." Archive of Clinical Cases 10, no. 2 (May 18, 2023): 93–96. http://dx.doi.org/10.22551/2023.39.1002.10249.

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Renal cell carcinoma (RCC) frequently spreads to distant organs like the lung, lymph nodes, bone, and liver. However, there have been some reports of RCC bladder metastasis. We present a case of a 61-year-old man presented with total painless gross hematuria. The patient had a history of right radical nephrectomy for papillary (type 2) RCC, high-grade, pT3a with negative surgical margins. There was no evidence of metastases on 6-month surveillance CT. After one-year post-operation, at this current admission, the cystoscopy discovered a solid bladder mass away from the trigone in the right lateral bladder wall. The resected bladder mass was metastatic papillary RCC with PAX-8 positive but GATA-3 negative on immunostaining. A positron emission tomography scan confirmed multiple lung, liver, and osseous metastases. This case report can highlight the importance of having bladder metastasis in RCC mind, although rare, and may necessitate the surveillance measures like urine analysis at more frequent interval and CT Urography instead of regular CT to detect the RCC metastatic bladder cancer at early stage.
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Steiner, T., J. Roigas, H. Kirchner, C. Doehn, H. Heynemann, M. Siebels, S. Loening, et al. "Clinical course of patients with metastatic papillary renal cell carcinoma." Journal of Clinical Oncology 24, no. 18_suppl (June 20, 2006): 14591. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.14591.

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14591 Background: For a long time it has been discussed, whether patients (pts.) with metastatic papillary renal cell carcinoma (mRCC pap) demonstrate different behaviour compared to those with clear cell mRCC. Methods: Clinical data of 61 pts. with mRCC pap were retrospectively assessed at 8 treatment centres. Results: Median follow-up was 20 (1–114) months, median age at time of diagnosis was 62 (24–85) years. Men were affected predominantly (50/61 pts.; 82%). 21 pts. (34%) showed metastases at time of diagnosis. The remaining 40 pts. had metachroneous metastatic disease. Mean time to metastases development was 30.4 (3–143; median 16.5) months. Metastatic sites were: lung (37; 61%), bone (24; 38%), liver (20; 33%), lymph nodes (24; 38%). Local recurrences occurred in 17 pts. (28%). Others sites of metastatic disease were brain in 6 pts. (10%), peritoneal carcinosis in 5 pts. (8%) and others. A surgical approach was performed primarily in 11 pts. (18%): lung 2; local recurrence and lymphomas 7; liver 1; brain 1. 26/61 pts. with metastatic disease received an immuno- (interferon-a ± interleukin-2) or immunochemotherapy (in combination with vinblastine or 5-fluorouracile) as first line treatment. In total, 42/61 pts. (69%) received an interferon- or interleukin-based immunotherapy. No treatment at all was performed in 12 pts. (20%) because of poor performance status. 5/42 pts. (11.4%) achieved an objective response to immuno(chemo)therapy. In the Kaplan-Meier-analysis, median overall survival after diagnosis of metastatic disease was estimated to be 13 ± 1.5 (95% CI 9.9–16) months for the entire study group and 12 ± 2.5 (95% CI 7.1–16.3) from the beginning of systemic treatment. Conclusions: Clinical data of a large population of pts. with mRCC pap have been assessed in this retrospective analysis for the first time. Compared to pts. with clear cell mRCC, these patients are characterized by: I) more frequent local recurrences; II) lower remission rates to immuno(chemo)therapeutic approaches; III) poorer prognosis with regard to overall survival. These findings should be taken into account when planning future studies. No significant financial relationships to disclose.
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Yonese, Ichiro, Masaya Ito, Kosuke Takemura, Takao Kamai, and Fumitaka Koga. "A Case of Metastatic Hereditary Leiomyomatosis and Renal Cell Cancer Syndrome-Associated Renal Cell Carcinoma Treated with a Sequence of Axitinib and Nivolumab Following Cytoreductive Nephrectomy." Journal of Kidney Cancer and VHL 7, no. 2 (July 20, 2020): 6–10. http://dx.doi.org/10.15586/jkcvhl.2020.148.

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Hereditary leiomyomatosis and renal cell cancer syndrome (HLRCC) associated renal cell carcinoma (RCC) is an aggressive form of type 2 papillary RCC caused by deficiency of the fumarate hydratase gene. For patients with metastatic disease, no standard treatment has been established with dismal prognosis. We report a case of metastatic HLRCC-associated RCC in a 65-year-old Japanese male whose clinical features mimicked advanced renal pelvic cancer. A durable response was achieved with a sequence of axitinib and nivolumab after cytoreductive and diagnostic nephrectomy. Their potential therapeutic roles in the management of metastatic HLRCC-associated RCC have been discussed based on its molecular and biological backgrounds.
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Schrader, A. J., S. Rauer-Bruening, P. J. Olbert, A. Hegele, J. Rustemeier, and R. Hofmann. "Incidence and long term prognosis of papillary renal cell carcinoma." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): e16020-e16020. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e16020.

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e16020 Background: Papillary renal cell carcinoma (pRCC) represents the largest subgroup of non clear-cell kidney cancer. In this study we assessed tumour characteristics and long-term prognosis of patients with pRCC in comparison with conventional clear-cell cancer (ccRCC). Methods: We evaluated 744 patients who had undergone renal surgery for RCC between 1990 and 2005. The mean follow-up was 5.6 years. Results: Both groups pRCC and ccRCC were alike concerning age, body mass index, and the incidence of regional lymph node or distant metastasis at diagnosis. The percentage of male patients was higher in pRCC than in ccRCC (73.8 vs. 60.3%, p = 0.006). Even though patients with pRCC presented more often with smaller (p = 0.039) and low grade tumours (p = 0.006), there was no statistically significant difference in tumour recurrence or tumour related death. Moreover, looking at the whole cohort Kaplan-Meier curves revealed no differences regarding tumour specific survival between pRCC and ccRCC (p = 0.94; 5-year survival 78% vs. 77%). However, we observed a trend towards an improved outcome for organ confined (pT1–2) cancer, but a significantly inferior prognosis for locally advanced stage (pT3–4) and/or metastatic papillary tumours at the time of renal surgery. However, applying multivariate analysis including age, sex, and tumour grade, histology could neither be retained as a significant independent prognostic marker in the metastatic setting (p = 0.068, cox regression analysis) nor in a subgroup analysis focussing on patients with advanced cancer (pT3–4 and/or N+/M+; p = 0.064, cox regression analysis). Conclusions: Even though pRCC and ccRCC differ significantly in many aspects including histology and genetic alterations, in all, their long term prognosis is comparable. As we could not confirm a favourable clinical course for pRCC in general, standardized aftercare programmes and - if necessary - systemic treatment, especially in the era of novel targeted drugs, are also needed for this common RCC subtype. In addition, routine histologic subtyping of pRCC is strongly recommended. No significant financial relationships to disclose.
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Dissertations / Theses on the topic "Metastatic papillary renal-Cell cancer"

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De, Vries-Brilland Manon. "Caractérisation du microenvironnement immunitaire des carcinomes papillaires du rein." Electronic Thesis or Diss., Angers, 2023. http://www.theses.fr/2023ANGE0017.

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Article 1 : Inhibiteurs de points de contrôle dans le carcinome rénal papillaire métastatique : le carcinome papillaire à cellules rénales (pRCC) est le CCR à cellules non claires (nccRCC) le plus courant et une entité distincte, bien qu'hétérogène, associée à de mauvais pronostics. Le paysage thérapeutique du pRCC métastatique (mpRCC) reposait jusqu'à présent sur des thérapies ciblées, imitant les développements antérieurs dans le carcinome rénal métastatique à cellules claires. Cependant, les antiangiogéniques ainsi que les inhibiteurs de mTOR ne conservent qu'une activité limitée dans le mpRCC. Alors que le développement d'inhibiteurs de points de contrôle immunitaires (ICI) est actuellement en cours chez les patients atteints de mpRCC, notre objectif était de discuter des données d'activité précoces et du potentiel de futures stratégies thérapeutiques en monothérapie ou en association. L'expression de points de contrôle immunitaires tels que PD-L1 et de cellules immunitaires infiltrantes dans le pRCC pourrait fournir des informations sur leur immunogénicité potentielle, bien que celle-ci soit actuellement mal décrite. Sur la base de données rétrospectives et prospectives, l'efficacité de l'ICI en monothérapie reste limitée. Les associations avec des inhibiteurs de la tyrosine-kinase, notamment avec des inhibiteurs anti-MET, présentent des taux de réponse prometteurs et pourraient entrer dans la norme de soins chez les patients non traités. Un travail collaboratif est nécessaire pour affiner le paysage moléculaire et immunitaire du pRCC et poursuivre les efforts visant à mettre en place des essais cliniques prédictifs basés sur des biomarqueurs dans ces tumeurs rares.Article 2 : Analyses complètes du microenvironnement tumoral immunitaire dans le carcinome papillaire à cellules rénales. Contexte : le carcinome papillaire à cellules rénales (pRCC) est le CCR à cellules non claires (nccRCC) le plus courant et associé à de mauvais résultats dans le contexte métastatique. Dans cette étude, nous avions pour objectif d'évaluer de manière exhaustive le microenvironnement tumoral immunitaire (TME), largement inconnu, des patients atteints de pRCC métastatique et d'identifier des cibles thérapeutiques potentielles. Méthodes : nous avons effectué une analyse quantitative de l'expression génique du TME en utilisant la méthodologie du compteur MCP, sur 2 cohortes indépendantes de pRCC localisés (n=271 et n=98). Nous avons ensuite caractérisé le TME, en utilisant l'immunohistochimie (n = 38) et le séquençage d'ARN (RNA-seq) (n = 30) sur des pRCC métastatiques de la cohorte prospective de l'essai AXIPAP. Résultats : le clustering non supervisé a identifié 2 « sous-types de TME » dans chacune des cohortes : le « immuno-enrichi » et le « immuno-faible ». Au sein de la cohorte de l'essai AXIPAP, le cluster « immuno-enrichi » était significativement associé à un plus mauvais pronostic. selon la médiane de survie globale à 8 mois (IC95%, 6-29) versus 37 mois (IC95%, 20-NA, p=0,001). Les 2 signatures immunitaires, Teff et JAVELIN Renal 101 Immuno signature, prédictives de La réponse aux inhibiteurs de point de contrôle immunitaire (IPC) dans le ccRCC était significativement plus élevée dans le groupe « enrichi sur le plan immunitaire » (p < 0,05 ajusté). Enfin, 5 gènes différentiellement surexprimés ont été identifiés, correspondant principalement aux populations de lymphocytes B. Conclusion : pour la première fois, en utilisant RNA-seq et IHC, nous avons mis en évidence un sous-type immunitaire TME spécifique du pRCC métastatique, significativement plus infiltré par la population T et Bimmune. Ce groupe « immunoenrichi » semble avoir un pronostic plus défavorable et pourrait avoir une valeur prédictive potentielle de réponse à l’immunothérapie, justifiant la confirmation de ces résultats dans une cohorte de pRCC métastatiques traités par CPI et en association avec des thérapies ciblées
Article 1: Checkpoint inhibitors in metastatic papillary renal cell carcinoma : papillary Renal Cell Carcinoma (pRCC) is the most common non-clear cell RCC (nccRCC) and a distinct entity, although heterogenous, associated with poor outcomes. The treatment landscape of metastatic pRCC (mpRCC) relied so far on targeted therapies, mimicking previous developments in metastatic clear-cell renal cell carcinoma. However, antiangiogenics as well as mTOR inhibitors retain only limited activity in mpRCC. As development of immune checkpoint inhibitors (ICI) is now underway in patients with mpRCC, we aimed at discussing early activity data and potential for future therapeutic strategies in monotherapy or combination. Expression of immune checkpoints such as PD-L1 and infiltrative immune cells in pRCC could provide insights into their potential immunogenicity, although this is currently poorly described. Based on retrospective and prospective data, efficacy of ICI as single agent remains limited. Combinations with tyrosine-kinase inhibitors, notably with anti-MET inhibitors, harbor promising response rates and may enter the standard of care in untreated patients. Collaborative work is needed to refine the molecular and immune landscape of pRCC, and pursue efforts to set up predictive biomarker-driven clinical trials in these rare tumors. Article 2 : Comprehensive analyses of immune tumor microenvironment in papillary renal cell carcinoma. Background : papillary Renal CellCarcinoma (pRCC) is the most common non-clear cell RCC (nccRCC), and associated with poor outcomes in the metastatic setting. In this study, we aimed to comprehensively evaluate the immune tumor microenvironment (TME) ,largely unknown, of patients with metastatic pRCC and identify potential therapeutic targets. Methods : we performed quantitative gene expression analysis of TME using MCP-counter methodology, on 2 independent cohorts of localized pRCC (n=271 and n=98). We then characterized the TME, using immunohistochemistry (n=38) and RNA-sequencing (RNA-seq) (n=30) on metastatic pRCC from the prospective AXIPAP trial cohort. Results: unsupervised clustering identified 2 "TME subtypes", in each of the cohorts : the “immune-enriched” and the “immune-low”.Within AXIPAP trial cohort, the “immune-enriched” cluster was significantly associated with a worse prognosis according to the median overall survival to 8 months (95%CI, 6-29) versus 37 months (95%CI, 20-NA,p=0.001).The 2 immune signatures, Teff and JAVELIN Renal 101 Immuno signature, predictive of response to immune checkpoint inhibitors (CPI) in ccRCC, were significantly higher in the “immune-enriched” group (adjusted p<0.05). Finally, 5 differentially overexpressed genes were identified, corresponding mainly to B lymphocyte populations. Conclusion : for the first time, using RNA-seqand IHC, we have highlighted a specific immune TME subtype of metastatic pRCC, significantly more infiltrated with T and Bimmune population. This “immune-enriched” group appears to have a worse prognosis and could have a potential predictive value for response to immunotherapy, justifying the confirmation of these results in a cohort of metastatic pRCC treated with CPI and incombination with targeted therapies
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Bartrolí, Comellas Mariona. "Prognostic markers and therapeutic targets for metastatic renal cell carcinoma." Doctoral thesis, Universitat de Barcelona, 2018. http://hdl.handle.net/10803/664198.

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Targeting cancer metastasis has gained considerable importance in the recent years when aiming to increase patients’ overall survival. In Renal Cell Carcinoma (RCC), the discovery of metastatic biomarkers and targets is still required, as most patients present metastatic disease at the time of diagnosis. Therefore, the aim of this thesis is the discovery of new biomarkers and targets of metastatic RCC using two variants of a patient-derived orthoxenograft (PDOX) animal model of clear cell RCC (ccRCC). Indeed, PDOX models have recently gained significant relevance for studying the progression of cancer and metastasis, due to their better mimicking of the histology, the metastatic capacity and treatment responses of human cancers. To this purpose, previous results had sequenced the two variants of this PDOX model, both at DNA and at RNA level, and had performed a FISH analysis. Firstly, Carboxypeptidase E (CPE), which was one of the highest expressed genes in the metastatic variant, has demonstrated to play a role in invasion when it is secreted to the medium, even though its overexpression alone is not sufficient to generate metastasis in vivo. In addition, it has showed a clear association to ccRCC and an inverse correlation with the overall survival of these patients. Secondly, we have studied two molecules of the coagulation pathway due to its relevance as one of the most upregulated pathways at RNA level. On the one hand, Factor XIII (FXIII or F13) has shown to be related to CPE in vivo, despite the overexpression of both molecules is not sufficient to develop all the metastatic cascade. However, it also affects the overall survival of ccRCC patients, highlighting these two molecules as possible biomarkers for this type of cancer. On the other hand, Coagulation Factor II Thrombin Receptor (F2R or PAR1) has demonstrated to play a role in metastasis, since its inhibition reduces both the early and late phases of this process. With the use of F2R inhibitors and the clinical association of the coagulation pathway to worse prognosis, this thesis opens new opportunities for the treatment of metastasis and cancer malignization. In summary, we have discovered new metastatic biomarkers and targets which, together with further validations, especially in the clinical setting, are proposed to be useful for RCC patients in the future.
Recentment, l’estudi de la metàstasi ha guanyat importància amb l’objectiu d’augmentar la supervivència dels pacients amb càncer. En el càncer renal (RCC), el descobriment de biomarcadors metastàtics i dianes terapèutiques és necessari degut a que la majoria de pacients presenten metàstasi en el moment del diagnòstic. L’objectiu d’aquesta tesi ha estat el descobriment de nous biomarcadors i dianes terapèutiques pel càncer renal metastàtic a través de dues variants d’un model animal orthoxenograft (PDOX) de RCC de cèl·lula clara (ccRCC). Els models PDOX han guanyat molta importància en l’estudi de la progressió del càncer i la metàstasi, ja que mimetitzen la histologia, la capacitat metastàtica i la resposta als tractaments. Prèviament, s’havien seqüenciat les dues variants d’aquest model PDOX tant a nivell de DNA com de RNA, juntament amb un anàlisi FISH. En primer lloc, la Carbxoxipeptidasa E (CPE), un dels gens més expressats en la variant metastàtica, ha demostrat ser important en la invasió quan és secretada al medi, tot i no ser suficient per generar metàstasi in vivo. A més, s’ha associat amb el ccRCC i anti-correlacionat amb la supervivència d’aquests pacients. En segon lloc, hem estudiat dues molècules de la cascada de coagulació, una de les més alterades en nivells de RNA. Hem demostrat que el Factor XIII (FXIII o F13) està relacionat amb CPE in vivo, malgrat que l’expressió de les dues molècules no és suficient per a que es desenvolupi la metàstasi. Tot i així, el F13 afecta la supervivència de pacients amb ccRCC, suggerint aquestes dues molècules com a possibles biomarcadors d’aquest tipus de càncer. A més, la inhibició del Receptor del Factor de Coagulació II (F2R) ha demostrat reduir les fases inicials i finals del procés metastàtic. Així doncs, l’ús d’inhibidors de F2R, juntament amb el fet que la cascada de coagulació es relaciona amb el pronòstic dels pacients, fa que aquesta tesi obri noves oportunitats per al tractament de la metàstasi i la malignització del càncer. En resum, hem descobert nous biomarcadors i dianes terapèutiques que, juntament amb futures validacions, sobretot en clínica, poden ser útils per als pacients metastàtics de ccRCC.
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Perrier-Trudova, Victoria. "Molecular characterization of hereditary and sporadic papillary renal cell carcinoma type 2 (PRCC2)." Thesis, Paris, EPHE, 2015. http://www.theses.fr/2015EPHE3085.

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Le cancer du rein papillaire de type 2 (PRCC2) est un cancer très agressif avec un potentiel métastatique élevé et pour lequel il n’y a pas de traitement efficace. La forme héréditaire de PRCC2 est associée au syndrome rare de la léiomyomatose cutanéo-utérine héréditaire (HLRCC). HLRCC est due à une mutation germinale hétérozygote du gène Fumarate Hydratase (FH) qui code l'enzyme du cycle de Krebs, la Fumarase. Le déficit en fumarase induit l’accumulation de fumarate et active les voies de signalisation du facteur de transcription inductible par l’hypoxie (HIF) et des espèces réactives de l’oxygène (ROS). Néanmoins, aucune mutation du gène FH n’a été rapportée dans les cas de PRCC2 sporadiques. Le projet de recherche porte sur la caractérisation moléculaire des PRCC2 héréditaires et sporadiques. Notre analyse du transcriptome a identifié des différences entre les signatures moléculaires des PRCC2 héréditaires et sporadiques. Cependant, l’étude d’immunohistochimie n'a pas révélé de biomarqueurs potentiels. Les analyses bio-informatiques de profils d’expression génique ont révélé que les tumeurs PRCC2 héréditaires et sporadiques partagent une dérégulation de la voie principale NRF2/KEAP1. Il a été montré que la surexpression de AKR1B10 (Aldo-Keto Reductase Family 1 Membre B10) est la conséquence directe de l’activation de l'élément de réponse antioxydant (ARE). Finalement, nous avons établi un nouveau modèle in vitro de lignée cellulaire, NCCFH1 (FH-/-), issue d’un patient HLRCC. NCCFH1 représente une plateforme idéale pour les études fonctionnelles, métaboliques et thérapeutiques. Bortézomib pourrait être la meilleure alternative thérapeutique pour les patients avec PRCC2
Papillary Renal Cell Carcinoma type 2 (PRCC2) is known to be a very aggressive type of kidney cancer with a high metastatic potential, poor outcome and absence of effective therapy. Hereditary form of PRCC2 is associated with rare hereditary leiomyomatosis and renal cell carcinoma (HLRCC). HLRCC is characterized by germline heterozygous mutations in the Fumarate Hydratase (FH) gene that encodes an enzyme of the Krebs cycle, Fumarase. It has been shown that the accumulation of fumarate induces activation of Hypoxia Inducible Factor (HIF) and ROS (Reactive Oxygen Species) pathways. Nevertheless, no FH gene mutation has been reported in sporadic PRCC2 tumors. The goal of this study is to better characterize hereditary and sporadic PRCC2. Our transcriptome analysis identified the set of genes that are differentially expressed between the two types of PRCC2. Subsequent immunohistochemistry screening did not reveal any potential diagnostics biomarkers. Further, the comprehensive computational analysis of gene profiling data revealed that hereditary and sporadic PRCC2 share the similar molecular signature with NRF2-KEAP1 axis deregulation as one of the major pathway in both forms. We demonstrated that over expression of Aldo-keto reductase family 1 member B10 (AKR1B10) is the direct consequence of the antioxidant response element (ARE) activation shared in hereditary and sporadic tumors. Finally, we have established FH-deficient cell line (NCCFH1) a new preclinical model of hereditary PRCC2. It presents the perfect platform for studying the metabolic features and testing new therapies for hereditary PRCC2, while bortezomib appears to be a potential efficient therapeutic option
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Zastrow, Stefan, Anh Phuong, Immanuel von Bar, Vladimir Novotny, Oliver W. Hakenberg, and Manfred P. Wirth. "Primary Tumor Size in Renal Cell Cancer in Relation to the Occurrence of Synchronous Metastatic Disease." Karger, 2014. https://tud.qucosa.de/id/qucosa%3A70551.

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Objectives: To investigate the controversially discussed relationship between tumor size and the occurrence of primary synchronous metastatic disease in renal cell cancer (RCC). Patients and Methods: A consecutive RCC cohort of 2,058 patients (150 primary metastatic) who underwent surgery between 1995 and 2010 was investigated. Rates of synchronous metastases were calculated for stratified groups of tumor size. Uni- and multivariate logistic regression models were calculated for the correlation of tumor size with primary metastatic disease. Results: The rate of metastatic disease increased with increasing tumor size. Tumor size was significantly correlated with synchronous metastatic disease (p < 0.001, c-index 0.772), but for RCCs ≤ 4 cm in size no significant correlation was found. Regarding tumors ≤ 5 cm in size, the correlation became significant (p = 0.028, c-index 0.621). A multivariate logistic regression model for the prediction of synchronous metastatic disease including tumor size, age and comorbidity yielded a significant c-index of 0.82 and was used to construct a nomogram. Conclusion: Our data confirm the correlation between tumor size and the rate of synchronous metastatic disease. Small renal tumors <4 cm in size have a low risk of synchronous metastatic disease. The risk becomes significantly associated with tumor size for tumors ≤ 5 cm.
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Ambrosetti, Damien. "Carcinomes rénaux : caractérisation moléculaire et des voies métaboliques dépendant des mécanismes hypoxiques." Thesis, Nice, 2015. http://www.theses.fr/2015NICE4143/document.

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Les carcinomes rénaux (RCC) sont subdivisés en plusieurs sous-types, définis selon des critères histologiques, phénotypiques et génétiques. Le diagnostic différentiel de ces tumeurs est primordial avec des conséquences pronostiques et thérapeutiques. Génétique et diagnostic : Nous avons étudié les données cliniques, histologiques, immunohistochimiques et génétiques d'une série de RCC papillaires (PRCC) de type 1 et 2. Une caractérisation génomique exhaustive complétée par NGS nous a permis de classer les PRCC de type 2 dans plusieurs groupes d'évolution variable. Nos résultats fournissent des informations inédites sur la pathogenèse des PRCC qui donnent des pistes pour un traitement personnalisé. Métabolisme, grade tumoral et phénotype : Dans une série de RCC à cellules claires (ccRCC), nous avons analysé les caractéristiques de ces tumeurs et l'expression des protéines impliquées dans le métabolisme et les isoformes de HIF. Cette étude nous a permis de mettre en évidence quantitativement une corrélation entre l'expression de MCT1, GLUT1 et CAXII et le grade de Fuhrman, et qualitativement une localisation périphérique de HIF2alpha et la co-localisation des protéines HIF2alpha et HAF. Stratégies théranostiques : Dans l’optique de définir les traitements les plus appropriés pour les patients atteints de RCC, nous avons fait un parallèle entre la sensibilité aux thérapies ciblées des patients (in vivo) et de cellules dérivées de la tumeur initiale (in vitro). Nous avons démontré que la réponse chez les patients et dans les cellules était équivalente et donc que des tests in vitro sont une piste pour définir des traitements personnalisés des patients atteints de ccRCC
Renal carcinomas (RCC) are divided into several subtypes, defined by histological, genetic and phenotypic criteria. The differential diagnosis of these tumors is important with prognostic and therapeutic implications. Genetics and diagnosis: We studied the clinical, histological, immunohistochemical and genetic of papillary RCC (PRCC) type 1 and 2 cohort. An extensive genomic characterization completed by NGS has allowed us to classify type 2 PRCC in several groups of variable clinical evolution. Our results provide new information on the pathogenesis of PRCC that provide perspectives for personalized treatment. Metabolism, tumor grade and phenotype: In a series of clear cell RCC (ccRCC), we analyzed the characteristics of these tumors and the expression of proteins involved in the metabolism and isoforms of HIF. This study allowed us to demonstrate quantitative correlation between the expression of MCT1, GLUT1 and CA XII and Fuhrman grade, and qualitatively peripheral HIF2alpha localization and co-localization of proteins HIF2alpha and HAF. Theranostic strategies: In order to define the most appropriate treatment for patients with RCC, we made a parallel between sensitivity to targeted therapies of patients (in vivo), and cells derived from the original tumor (in vitro). We have demonstrated that the response in patients and in cells and was similar, thus in vitro assays are a way to define personalized treatment for ccRCC
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Roigas, Jan. "Chemoimmuntherapie und immunologische Bedeutung von 70 kiloDalton Hitzeschockproteinen beim metastasierten Nierenzellkarzinom." Doctoral thesis, [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=97263438X.

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Albiges-Sauvin, Laurence. "Caractérisation des Carcinomes Papillaires du Rein." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T070.

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Les Carcinomes Papillaires du Rein (pRCC) représentent la seconde forme histologique de cancers du rein . Ils correspondent à une entité hétérogène de tumeurs subdivisées en type I et type II sur leurs caractéristiques anatomopathologiques. Leur pronostic au stade métastatique est inferieur à celui des carcinomes à cellules claires. Les caractéristiques biologiques des pRCC sont mal connues et n’ont pas permis de développer jusqu'à ce jour de thérapeutiques spécifiques.Ce travail propose, en première partie, une synthèse des données disponibles biologiques, anatomo-pathologiques, thérapeutiques et pronostiques des pRCC. Cette synthèse a fait l’objet d’une publication. ( Albiges et al. The Oncologist 2012)Le second volet est dédié à l’analyse de la place du proto-oncogène MET au sein des pRCC de type I et II et plus particulièrement les différentes modalités d’activation de ce gène. Cette analyse (i) caractérise les anomalies quantitatives de l’ADN du gène MET (CGH array pour les pRCC de type II et CGMA pour les pRCC de type I) et leur corrélation au niveau d’expression génique; (ii) recherche l’existence de mutations activatrices du domaine tyrosine kinase par séquençage du gène MET chez les pRCC de type I; et (iii) analyse également les niveaux d’expression du ligand et des co-activateurs de ce récepteur MET. Ces résultats sont en cours de publication (Albiges et al. Clinical Cancer Research)Le troisième et dernier volet de ce travail vise à identifier des pistes biologiques propres aux pRCC par l’analyses de sous groupes distinguable en termes de profils d’expression génique et surtout par l’analyses des anomalies de l’ADN identifiées par CGH array des pRCC de type II, couplées aux données de transcriptome
Papillary renal cell carcinomas (pRCC) are the second most common form of Renal Carcinomas and belongs to the non clear cell carcinomas family. This tumour type is an heterogeneous group of tumours usually subdivided in type I and type II according to pathological features. The prognosis of pRCC in the metastatic setting is worse to clear cell carcinoma’s prognosis. Biological characteristics of pRCC are poorly known and did not allow the development of specific targeted therapies.This work first presents a synthesis of published data regarding biology, pathology, therapeutics and prognosis of pRCC. This review has been published. (Albiges et al. The Oncologist 2012)Second part is dedicated to the analysis of MET proto-oncogene across pRCC. The main focus is to assess MET activation drivers. This analysis (i) characterises MET gene DNA copy number alterations (CGH array for type II pRCC and CGMA approach for Type I pRCC) and their correlation with gene expression profiling; (ii) assess activating mutations within the tyrosine kinase of MET gene in the type I pRCC; and (iii) investigate expression level of ligand and co-activators of MET receptor. This analysis is under publication. (Albiges et al. Clinical Cancer Research)Third and last part of this work aims at identifing new biological pathway specific to pRCC using clustering of gene expression profiling and DNA abnormalities assessed by CGHarray inthe type II pRCC subtypes with matching gene expression data
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GOBBO, Stefano. "CLEAR CELL-PAPILLARY RENAL CELL CARCINOMA." Doctoral thesis, 2014. http://hdl.handle.net/11562/706768.

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Il carcinoma renale papillare a cellule chiare e il carcinoma renale con stroma leiomuscolare sono due entità recentemente descritte in letteratura, a comportamento biologico non aggressivo e composte da elementi a citoplasma chiaro e basso grado nucleare, la cui distinzione dai principali istotipi renali e in particolare dal carcinoma renale a cellule chiare di tipo convenzionale risulta spesso complessa. In questa tesi sono stati studiati 14 carcinomi renali papillari a cellule chiare e 7 carcinomi renali con stroma leiomuscolare, utilizzando un ampio pannello immunoistochimico e diverse metodiche di biologia molecolare, allo scopo di definirne maggiormente i caratteri comuni e permettere una loro distinzione più efficace dai più comuni istotipi tumorali renali. Entrambe le entità descritte hanno presentato diffusa espressione di CK7, CAIX e costante negatività per AMACR. E’ stata inoltre evidenziata la frequente positività per i marcatori 34βE12 e GATA3. I tumori hanno evidenziato inoltre un profilo genetico stabile, l’assenza di alterazioni del gene VHL e di perdita del cromosoma 3p. Un solo caso, con caratteristiche morfologiche e in parte immunofenotipiche e genetiche del gruppo dei carcinomi renali papillari a cellule chiare, ha presentato negatività per 34βE12, GATA3 e presenza di alterazioni a carico del gene VHL ed è pertanto stato riclassificato come carcinoma renale a cellule chiare. L’insieme dei caratteri descritti, comuni ai carcinomi renali papillari a cellule chiare e a quelli con stroma leiomuscolare, permettono di distinguerli dagli istotipi renali “convenzionali” e di ipotizzare una loro origine comune. Tuttavia, la presenza di casi con caratteri in parte sovrapponibili al carcinoma renale a cellule chiare sottolinea la necessità dell’utilizzo di più metodiche diagnostiche per loro il riconoscimento nella pratica clinica.
Clear cell papillary renal cell carcinoma (CCPRCC) is renal neoplasm that has been recently proposed to be added to the current WHO classification of renal tumors. We collected and described a series of these neoplasms, in order to get insights to their clinico-pathological and molecular profiles. We identified 14 CCPRCC. A first level of Immunohistochemical analysis was performed using CK7, CD10, AE1/AE3, alpha-methylacyl-CoA racemase, PV, S100A1, α-SMA, caldesmon and desmin. We also performed FISH analysis using probes for chromosome 3 and 3p25, array CGH, VHL sequencing and methylation analysis on a part of the cases. Than with a second level of immunoistochemical analysis, we investigated the immunoexpression of 34βE12, CK1, CK5, CK10, CK14 and GATA3, looking for specific markers. The mean age of the patients was 61, including 9 males and 5 females. The average tumor diameter was 2,62 cm. CCPRCC presented a thick encapsulation and a tubule-papillary or tubule-cystic morphology composed of clear cells with low-grade nuclei. With the first level of immunoistochemical analyses all cases were positive for CK7 and AE1-AE3 and negative for P504S, Parvalbumin, HMB45 and cathepsin K; 75% and 62% of cases were positive respectively for CD10 and S100A1. No deletion of chromosome 3p, significant VHL methylation or changes in copy number was detected in any case, whereas only one CCPRCC showed VHL mutation and presented deletions in chromosome 3 and 6 at CGH analysis. The second level immunoistochemical analysis showed that 13 of 14 cases of CCPRCC express 34βE12. The immunoexpression of CK14 had the same result of 34βE12. All cases were negative for Ck1 and CK10; only 4 cases of CCPRCC were positive for CK5. GATA3 was expressed in 7 of 13 (54%) cases of CCPRCC. Comparing as control the immunoexpression of 292 cases of conventional clear cell RCC 34βE12 (or CK14) was expressed in 0,3% and GATA3 was expressed in 1% of the cases giving to them a strong specific meaning. We concluded that CCPRCC show strong and diffuse positivity for CK7 and do not show 3p deletion, VHL mutation or methylation abnormalities. These tumors show a genomic stability after wide whole genomic analysis. We propose the immunoistochemical markers 34βE12 (or CK14) and GATA3 as specific markers useful for the identification of these distinct renal neoplasms.
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TSAI, YI-TA, and 蔡易達. "The molecular mechanisms of Sorafenib and GW5074 anti-cancer combination therapy in metastatic renal cell carcinoma." Thesis, 2017. http://ndltd.ncl.edu.tw/handle/51617077893198827872.

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博士
國防醫學院
醫學科學研究所
105
Mitochondria are the powerhouses of cells and targets of cancer therapeutics. The unique role of Raf proteins in the mitochondria provides a strong rationale to target mitochondrial Raf proteins. However, Raf inhibitor monotherapy induces serine 338 phosphorylation of C-Raf (pC-RafS338) subsequent to mitochondrial translocation and impedes therapy. Currently, no selective mitochondrial targeted cancer therapeutics is available. This study identified a unique combination therapy of Raf inhibitors, sorafenib and GW5074, and targeted mitochondrial function instead of the canonical Raf signalling pathway, irrespective of upstream Ras and Raf mutation status. The GW5074 was bound to C-Raf and induced C-Raf conformation change, which enhanced sorafenib binding. This drug-target interaction facilitated the S308 phosphorylation of DAPK (pDAPKS308) translocation from the mitochondria to the cytoplasm, causing mitochondrial dysfunction and ROS generation. ROS facilitated PP2A dephosphorylation of DAPK at serine 308, disassembled the C-Raf and DAPK complex in the cytoplasm, and induced profound cancer cells necroptosis.
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Books on the topic "Metastatic papillary renal-Cell cancer"

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Wong, Han Hsi, Basma Greef, and Tim Eisen. Treatment of metastatic renal cancer. Edited by James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0089.

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Metastatic renal cancer is resistant to standard chemotherapy. Although some patients with indolent disease can be initially managed with observation, the majority of patients will require aggressive treatment soon after diagnosis. Options include cytoreductive nephrectomy, resection of a solitary metastasis in highly selected cases, or systemic therapy options. The TKIs sunitinib and pazopanib are currently the first-line treatments of choice. Whilst axitinib and cabozantinib have important roles in the second line the PD-1 checkpoint inhibitor, nivolumab, is now established as standard second line therapy. Inhibitors of the mammalian target of rapamycin (mTOR) pathway, everolimus and temsirolimus, interleukin-2 as well as the anti-angiogenic antibody bevacizumab have also been shown to be effective. The treatment paradigm of metastatic renal cancer is constantly changing as evidence from clinical trials continues to emerge. With the development of agents addressing novel targets such as T-cell regulation, the future certainly looks brighter for patients diagnosed with this disease.
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Eisen, Tim. The patient with renal cell cancer. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0172.

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Renal cancer is the commonest malignancy of the kidney and worldwide, accounts for between 2% and 3% of the total cancer burden. The mainstay of curative treatment remains surgery. There have been significant advances in surgical technique, the most important ones being nephron-sparing surgery and laparoscopic nephrectomy. The medical treatment of advanced renal cell cancer has only improved markedly in the last decade with the development of antiangiogenic tyrosine-kinase inhibitors, inhibitors of mammalian target of rapamycin, and a diminished role for immunotherapy.Tyrosine-kinase inhibitor therapy results in reduction of tumour volume in around three-quarters of patients and doubles progression-free survival, but treatment is not curative. The management of side effects in patients on maintenance tyrosine-kinase inhibitors has improved in the last 3 years, although still presents difficulties which have to be actively considered.The molecular biology of renal cell carcinoma is better understood than for the majority of solid tumours. The commonest form of renal cancer, clear-cell carcinoma of the kidney, is strongly associated with mutations in the von Hippel–Lindau gene and more recently with chromatin-remodelling genes such as PBRM1. These genetic abnormalities lead to a loss of control of angiogenesis and uncontrolled proliferation of tumour cells. There is a very wide spectrum of tumour behaviour from the extremely indolent to the terribly aggressive. It is not currently known what accounts for this disparity in tumour behaviour.A number of outstanding questions are being addressed in scientific and clinical studies such as a clearer understanding of prognostic and predictive molecular biomarkers, the role of adjuvant therapy, the role of surgery in the presence of metastatic disease, how best to use our existing agents, and investigation of novel targets and therapeutic agents, especially novel immunotherapies.
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Chapman, Hannah, and Christine Elwell. Renal and bladder cancer. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0167.

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This chapter addresses the diagnosis and management of bladder and renal cancers. In the UK, bladder cancer is the fourth most common cancer in men, and the eighth most common cancer in women. Bladder cancer arises from the bladder urothelium, and is typically a papillary transitional cell carcinoma. Chronic infection with the parasite Schistosoma haematobium is associated with squamous cell carcinoma of the bladder, and is most prevalent in Egypt and sub-Saharan Africa. Renal cancer accounts for 3% of cancers in adults in the UK and, in most cases, is a renal cell carcinoma arising from proximal renal tubule epithelium. A further 5%–10% of renal cancers are transitional cell (urothelial) carcinomas of the renal pelvis. Benign kidney tumours, such as cysts, are also common.
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Jafri, Mariam, and Eamonn R. Maher. Genetics and molecular biology of renal cancer. Edited by James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0084.

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Renal cell carcinoma (RCC) is the exemplar of how the understanding of the molecular pathogenesis of rare inherited disorders can inform an understanding of the key pathways involved in the pathogenesis of sporadic cancer. In this chapter we describe the clinical and pathological features of the inherited kidney cancer syndromes: von Hippel Lindau disease (VHL); Birt-Hogg-Dube syndrome; hereditary leiomyomatosis and renal cancer syndrome; succinate dehydrogenase disorders; hereditary papillary renal cancer; and translocation-associated kidney cancer. Though individually rare, recognition of individuals with familial kidney cancer is important as they present specific clinical challenges to the urological surgeon because of their propensity to develop multicentric/bilateral tumours. Furthermore, different familial RCC predisposition syndromes are associated with different extra renal clinical features and have specific surveillance needs. Despite differences in clinical features, there is some overlap in the molecular pathophysiology between the disorders and these highlight the key signalling pathways for RCC oncogenesis.
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Cassidy, Jim, Donald Bissett, Roy A. J. Spence OBE, Miranda Payne, Gareth Morris-Stiff, and Madhumita Bhattacharyya. Gynaecological cancers. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199689842.003.0020_update_001.

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Genitourinary cancers examines the malignancies arising in the kidney, ureter, bladder, prostate, testis, and penis. Renal cancer has high propensity for systemic spread, largely mediated by overexpression of vascular endothelial growth factor (VEGF). Treatments include surgery, immunotherapy, and targeted therapy. Wilms tumour, a childhood malignancy of the kidney, warrants specialist paediatric oncology management to provide expertise in its unique pathology, staging, and treatment, often with surgery and chemotherapy. Cancer of the bladder and ureters, another tobacco related cancer, may present as either superficial or invasive disease. The former is managed by transurethral resection and intravesical therapy. The latter may require radical surgery, preoperative chemotherapy, or radiotherapy. Prostate cancer, the commonest male cancer, is an androgen dependent malignancy. It has attracted controversy with regards to PSA screening, and potential over treatment with radical prostatectomy. Division into low, intermediate, and high risk disease according to tumour grade, stage, and PSA helps in deciding best treatment, antiandrogen therapy for metastatic disease, radiotherapy and adjuvant hormone therapy for locally advanced disease, either surgery or radiotherapy for early intermediate risk disease, and active monitoring for low risk cases. Testicular cancer divides according to pathology into seminoma, nonseminomatous germ cell tumours (NSGCT), and mixed tumours, the latter two frequently producing tumour markers, alpha-fetoprotein (AFP) and/or human chorionic gonadotrophin (HCG). Stage I disease is managed by inguinal orchidectomy and surveillance or adjuvant chemotherapy. More advanced disease is managed by chemotherapy, with high probability of cure in the majority. Penile cancer, often HPV related, can be excised when it presents early, but delay in presentation may lead to regional and systemic spread with poor prognosis.
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Book chapters on the topic "Metastatic papillary renal-Cell cancer"

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Mulders, Peter F. "Treatment Strategies in Metastatic Renal Cell Carcinoma." In Renal Cancer, 343–59. Totowa, NJ: Humana Press, 2001. http://dx.doi.org/10.1385/1-59259-144-2:343.

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Powles, Tom, and Axel Bex. "Integration of Surgery in Metastatic Renal Cancer." In Renal Cell Carcinoma, 257–77. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-062-5_15.

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Vives Dilme, Roser, Juan Gómez Rivas, Riccardo Campi, Javier Puente, and Jesús Moreno Sierra. "Cytoreductive Nephrectomy in Metastatic Renal Cell Carcinoma." In Robotic Surgery for Renal Cancer, 237–45. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-11000-9_24.

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Branscheid, D., S. Pomer, S. Krysa, and I. Vogt-Moykopf. "Survival After Lung Surgery for Metastatic Renal Cancer." In Contemporary Research on Renal Cell Carcinoma, 30–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78609-9_4.

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Matrana, Marc, Bradley Atkinson, and Nizar M. Tannir. "Combinatorial and Sequential Targeted Therapy in Metastatic Renal Cell Carcinoma." In Kidney Cancer, 225–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-21858-3_15.

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Matrana, Marc R., Bradley J. Atkinson, and Nizar M. Tannir. "Combinatorial and Sequential Targeted Therapy in Metastatic Renal Cell Carcinoma." In Kidney Cancer, 315–34. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17903-2_19.

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Bergerot, Paulo, Kathy Burns, Dhruv Prajapati, Rachel Fox, Meghan Salgia, and Sumanta K. Pal. "Advances in the Treatment of Metastatic Renal Cell Carcinoma." In Cancer Treatment and Research, 127–37. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-93339-9_6.

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Bollack, C., D. Jacqmin, J. P. Bergerat, J. Ford, R. Herbrecht, P. Dufour, F. Oberling, G. Prevost, P. Salze, and J. Jurascheck. "Recombinant Interferon Alpha Plus Vinblastine in Metastatic Renal Cell Cancer: Updated Results." In Immunotherapy of Renal Cell Carcinoma, 75–81. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75853-9_12.

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Childs, Richard W., and Cristian A. Carvallo. "Allogeneic Hematopoietic Blood-Cell Transplantation As Immunotherapy for Metastatic Renal Cell Carcinoma." In Cancer Immunotherapy at the Crossroads, 279–93. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-743-7_15.

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Ryan, Charles J. "Developments in the Management of Genitourinary Malignancies: Prostate Cancer and Renal Cell Carcinoma." In From Local Invasion to Metastatic Cancer, 533–44. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-087-8_44.

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Conference papers on the topic "Metastatic papillary renal-Cell cancer"

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Li, Fang, Qiuyu Jiang, Jinyuan Zhang, Xintao Jing, Xiaofei Wang, and Chen Huang. "Pan-cancer analysis of CDCA2 and its function in papillary renal cell carcinoma." In ICBBT 2022: 2022 14th International Conference on Bioinformatics and Biomedical Technology. New York, NY, USA: ACM, 2022. http://dx.doi.org/10.1145/3543377.3543391.

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Kim, Ji-Yeon, Se-Hoon Lee, Jong-Il Kim, Jong-Yeon Shin, and Dae seog Heo. "Abstract 1888: Target sequencing of papillary renal cell carcinoma, type 2, using custom-made kidney cancer panel." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1888.

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Yao, Qian, Jianfeng Li, and Dexi Liu. "Abstract 4412: Combining cytokine gene therapy with conventional cancer chemotherapyfor treatment of metastatic renal cell carcinoma." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4412.

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Roseweir, Antonia K., Tahir Qayyum, Robert Jones, Grenville Oades, Michael Aitchison, and Joanne Edwards. "Abstract 14: The effect of Src family kinase inhibitors in non-metastatic clear cell renal cancer." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-14.

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Khandelwal, Jaanki, Devaki S. Surasi, Sergio P. Klimkowsky, Nathaniel Wilson, Mohammad J. Moussa, Matthew Campbell, Amishi Shah, et al. "523 Nivolumab and ipilimumab in patients with metastatic non-clear cell renal cell carcinoma at MD Anderson Cancer Center." In SITC 38th Annual Meeting (SITC 2023) Abstracts. BMJ Publishing Group Ltd, 2023. http://dx.doi.org/10.1136/jitc-2023-sitc2023.0523.

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Beom, Seung-Hoon, Sejung Park, Woo Sun Kwon, Sang Joon Shin, Soo-Youl Kim, Nam Hoon Cho, and Sun Young Rha. "Abstract A053: Significance of Transglutaminase 2 expression on clinical outcome in metastatic renal cell carcinoma." In Abstracts: AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics; October 26-30, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1535-7163.targ-19-a053.

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Farace, Françoise, Marine Gross - Goupil, Elodie Tournay, Melissa Taylor, Catherine Hill, and Bernard Escudier. "Abstract 372: Circulating endothelial progenitor cell levels predict survival benefit in metastatic renal cell cancer patients treated with antiangiogenic agents." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-372.

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Seok, Han Kyung, Raven Peter, Awrey Shannon, Li Estelle, Fazli Ladan, Gleave Martin, and So Alan. "Abstract A36: Knockdown of integrin-linked kinase reduces invasive and metastatic potential of renal cell carcinoma." In Abstracts: AACR Special Conference: The Translational Impact of Model Organisms in Cancer; November 5-8, 2013; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1557-3125.modorg-a36.

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Harris, Wayne B., Dana C. Nickleach, Yuan Liu, Omer Kucuk, and Viraj A. Master. "Abstract C15: Inflammation-free survival as a surrogate endpoint for overall survival in patients with metastatic renal cell carcinoma." In Abstracts: Sixth AACR Conference: The Science of Cancer Health Disparities; December 6–9, 2013; Atlanta, GA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7755.disp13-c15.

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Bensalem, Assia, and Kamel Bouzid. "Abstract B202: Hand-foot syndrome, the main side effect of patients with metastatic renal cell carcinoma treated with sunitinib." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-b202.

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You might also be interested in the extended bibliographies on the topic 'Metastatic papillary renal-Cell cancer' for particular source types:
Journal articles
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