Готові списки джерел за темами / Translocation renal cell carcinoma

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Добірка наукової літератури з теми "Translocation renal cell carcinoma"

Автор: Grafiati

Опубліковано: 11 березня 2023

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Статті в журналах з теми "Translocation renal cell carcinoma"

Armah, Henry B., and Anil V. Parwani. "Xp11.2 Translocation Renal Cell Carcinoma." Archives of Pathology & Laboratory Medicine 134, no. 1 (January 1, 2010): 124–29. http://dx.doi.org/10.5858/2008-0391-rsr.1.

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Abstract Xp11.2 translocation renal cell carcinomas (RCCs), a recently recognized distinct subtype, are rare tumors predominantly reported in young patients. They comprise at least one-third of pediatric RCCs, and only few adult cases have been reported. They are characterized by various translocations involving chromosome Xp11.2, all resulting in gene fusions involving the transcription factor E3 (TFE3) gene. In recent years, at least 6 different Xp11.2 translocation RCCs have been identified and characterized at the molecular level. These include a distinctive RCC that bears a translocation with the identical chromosomal breakpoints (Xp11.2, 17q25) and identical resulting ASPL-TFE3 gene fusion as alveolar soft part sarcoma. They typically have papillary or nested architecture and are composed of cells with voluminous, clear, or eosinophilic cytoplasm. Their most distinctive immunohistochemical feature is nuclear labeling for TFE3 protein. Although only limited data are available so far, they are believed to be rather indolent, but there have been increasing, recent reports of an aggressive clinical course in adult cases. The consistent immunohistochemical staining for TFE3 in all RCC with unusual histology, regardless of patient age, is likely to expand the spectrum of Xp11.2 translocation RCC with respect to age, clinical behavior, and molecular abnormalities.

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Geller, James I., Pedram Argani, Adebowale Adeniran, Edith Hampton, Angelo De Marzo, Jessica Hicks, and Margaret H. Collins. "Translocation renal cell carcinoma." Cancer 112, no. 7 (2008): 1607–16. http://dx.doi.org/10.1002/cncr.23331.

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Kothari, KanchanS, PragatiA Sathe, LeenaP Naik, and BhuvaneshwariM Kandalkar. "Xp11 translocation renal cell carcinoma." Indian Journal of Pathology and Microbiology 56, no. 4 (2013): 471. http://dx.doi.org/10.4103/0377-4929.125383.

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Neagu, O., A. Petrescu, G. Berdan, L. Mitrache, S. Varban, P. Argani, and V. Jinga. "Xp11.2 translocation renal cell carcinoma." European Urology Supplements 17, no. 12 (October 2018): e2694. http://dx.doi.org/10.1016/s1569-9056(18)33533-4.

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Ross, Hillary, and Pedram Argani. "Xp11 translocation renal cell carcinoma." Pathology 42, no. 4 (June 2010): 369–73. http://dx.doi.org/10.3109/00313021003767348.

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Ross, Hillary, Morris Edelman, and Pedram Argani. "Xp11 Translocation Renal Cell Carcinoma." Pathology Case Reviews 15, no. 1 (January 2010): 3–6. http://dx.doi.org/10.1097/pcr.0b013e3181d2cfc2.

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Caliò, Anna, Diego Segala, Enrico Munari, Matteo Brunelli, and Guido Martignoni. "MiT Family Translocation Renal Cell Carcinoma: from the Early Descriptions to the Current Knowledge." Cancers 11, no. 8 (August 3, 2019): 1110. http://dx.doi.org/10.3390/cancers11081110.

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The new category of MiT family translocation renal cell carcinoma has been included into the World Health Organization (WHO) classification in 2016. The MiT family translocation renal cell carcinoma comprises Xp11 translocation renal cell carcinoma harboring TFE3 gene fusions and t(6;11) renal cell carcinoma harboring TFEB gene fusion. At the beginning, they were recognized in childhood; nevertheless, it has been demonstrated that these neoplasms can occur in adults as well. In the nineties, among Xp11 renal cell carcinoma, ASPL, PRCC, and SFPQ (PSF) were the first genes recognized as partners in TFE3 rearrangement. Recently, many other genes have been identified, and a wide spectrum of morphologies has been described. For this reason, the diagnosis may be challenging based on the histology, and the differential diagnosis includes the most common renal cell neoplasms and pure epithelioid PEComa/epithelioid angiomyolipoma of the kidney. During the last decades, many efforts have been made to identify immunohistochemical markers to reach the right diagnosis. To date, staining for PAX8, cathepsin K, and melanogenesis markers are the most useful identifiers. However, the diagnosis requires the demonstration of the chromosomal rearrangement, and fluorescent in situ hybridization (FISH) is considered the gold standard. The outcome of Xp11 translocation renal cell carcinoma is highly variable, with some patients surviving decades with indolent disease and others dying rapidly of progressive disease. Despite most instances of t(6;11) renal cell carcinoma having an indolent clinical course, a few published cases demonstrate aggressive behavior. Recently, renal cell carcinomas with TFEB amplification have been described in connection with t(6;11) renal cell carcinoma. Those tumors appear to be associated with a more aggressive clinical course. For the aggressive cases of MiT family translocation carcinoma, the optimal therapy remains to be determined; however, new target therapies seem to be promising, and the search for predictive markers is mandatory.

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de Oliveira, C. V. L., G. R. Bechara, S. R. Zacchi, M. C. L. de Miranda, G. Z. Pinho, and M. M. L. de Miranda. "MiT family translocation renal cell carcinoma." Journal of Pediatric Surgery Case Reports 45 (June 2019): 101190. http://dx.doi.org/10.1016/j.epsc.2019.101190.

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Argani, Pedram. "MiT family translocation renal cell carcinoma." Seminars in Diagnostic Pathology 32, no. 2 (March 2015): 103–13. http://dx.doi.org/10.1053/j.semdp.2015.02.003.

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Bambury, Richard Martin, Claire Brady, Aoife McCarthy, Stewart Fleming, Nicholas J. Mayer, and Derek Gerard Power. "Translocation renal cell carcinomas: An evolving entity." Journal of Clinical Oncology 30, no. 5_suppl (February 10, 2012): 472. http://dx.doi.org/10.1200/jco.2012.30.5_suppl.472.

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472 Background: Translocation renal cell carcinomas (RCCs) are a novel, rare and distinct clinicopathological entity. The term refers to RCCs with overexpression of transcription factor E3 (TFE3) due to translocation involving the Xp11 locus or less commonly with overexpression of transcription factor EB (TFEB) due to a t(6:11) translocation. In children it is estimated that these tumours account for 40% of RCCs but in adults this proportion is estimated to be 1-4%. As these neoplasms are only recently recognised, outcome data are premature. We report 2 cases of translocation RCC in an Irish regional cancer centre and describe clinicopathological characteristics and early outcome. Methods: In our recent practice, 2 renal cell carcinomas were suspected to be translocation tumours based on morphology and immunohistochemical features (RCC+/CK7-/EMA-). Using immunohistochemistry we tested for expression of TFE3 and TFEB. Results: Both tumours were translocation RCCs. The first case was a 74 year old lady who presented with right upper quadrant pain and had a 9cm right renal mass with no metastatic disease on CT imaging. Radical nephrectomy was performed and histology revealed a pT3aN2, Fuhrman grade 4 renal cell carcinoma with papillary architecture and eosinophillic hyaline nodules within many of the papillae. Staining for TFE3 showed focal nuclear positivity consistent with an Xp11 translocation RCC. She remains disease free 6 months post surgery. The second case was a 46 year old man with an incidental finding of a right renal mass on ultrasound abdomen performed after a new diagnosis of haemochromatosis. Staging CT imaging revealed no metastatic disease and he underwent laparoscopic nephrectomy. Histology revealed a pT1aNx, Fuhrman grade 3 renal cell carcinoma with predominantly alveolar architecture and focal papillary and microcystic areas. Staining for TFEB was positive consistent with a t6:11 translocation RCC. He remains disease free 5 months post surgery. Conclusions: We report 2 new cases of this rare subset of RCC. The therapeutic implications for patients with these mutations are as yet unclear. We plan to update with ongoing follow-up and identification of new cases to determine the clinical behaviour of these rare cancers in the Irish setting.

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Дисертації з теми "Translocation renal cell carcinoma"

Wake, Naomi Catherine. "Identification and functional analysis of a novel renal cell carcinoma (RCC) susceptibility gene from an RCC associated constitutional chromosomal translocation." Thesis, University of Birmingham, 2013. http://etheses.bham.ac.uk//id/eprint/3964/.

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Familial renal cell carcinoma (RCC) only accounts for 3% of all RCC, yet the study of these inherited forms has provided important insights into the more common sporadic RCC. Somatic VHL inactivation is found in 70% of sporadic clear cell RCC (ccRCC) though is rarely found in other forms of RCC including papillary and chromophobe types. VHL-independent RCC tumourigenesis is poorly understood and current research involves identifying novel RCC candidate genes to further understand the mechanisms involved. In this study a constitutional balanced translocation, t(5;19)(p15.3;q12), associated with familial RCC was characterised using an oligonuleotide CGH array followed by genomic sequencing and the previously uncharacterised gene, UBE2QL1, was found to be disrupted by the 5p15.3 breakpoint. UBE2QL1 expression was down-regulated in 78.6% of sporadic RCC and UBE2QL1 promoter region hypermethylation and gene deletions were detected in 20.3% and 17.3% of sporadic RCC, respectively. Re-expression of UBE2QL1 in deficient RCC cell lines suppressed anchorage independent growth and colony formation. UBE2QL1 shows homology to the E2 class of ubiquitin conjugating enzymes and was shown to possess an active-site cysteine (C88) that is monoubiquitinated in vivo. In addition, UBE2QL1 co-immunoprecipitation and co-localisation studies demonstrated a protein interaction with FBXW7 (an F box protein for the SCF E3 ubiquitin ligase) and was shown to facilitate the degradation of the known FBXW7 substrates, cyclin E1 and mTOR. These findings demonstrate that UBE2QL1 functions as a novel renal tumour suppressor gene and ubiquitin conjugating enzyme.

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Malouf, Gabriel. "Décryptage des changements épigénétiques impliqués dans la transition épithélio-mésenchymateuse et le cancer." Thesis, Paris 11, 2014. http://www.theses.fr/2014PA11T037.

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La transition épithélio-Mésenchymateuse (TEM) est un processus de plasticité cellulaire qui existe dans le développement embryonnaire et qui permet la formation des tissus et organes. Dans la cancérogénèse, ce processus est réactivé par des facteurs de transcription dont l’action implique très probablement un remodelage de la chromatine. La cartographie exacte de ces changements épigénétiques est peu connue à l’échelle du génome entier, même si il y a eu quelques études antérieures explorant les changements de quelques loci de façon bien ciblée. Ce mémoire traite du remodelage épigénétique médié par le facteur de transcription Twist1 dans un modèle de lignée mammaire immortalisée. L’architecture de ce remodelage a été cartographiée grâce à l’utilisation des techniques de haut-Débit pour analyser la méthylation de l’ADN (DREAM) et les modifications des histones (ChIPseq). Nos résultats montrent un changement majeur du méthylome pendant la TEM avec une hyperméthylation focale et une hypométhylation globale des corps des gènes prédominant au niveau des « domaines partiellement méthylés »; ces domaines sont déjà connus dans le développement pour gagner de façon concomitante à leur hypométhylation des marques d’histone répressives. Nous avons aussi observé un remodelage des domaines de l’histone répressive H3K27me3 avec une réduction de leur taille, et surtout le quasi doublement du nombre de gènes bivalents qui accompagne la transition. Le couplage de la méthylation de l’ADN avec le profil des microRNA nous a permis d’identifier le miR-203 comme l’unique microRNA régulé par méthylation de l’ADN durant la TEM; nous avons aussi montré que l’extinction épigénétique du miR-203 est requise pour la TEM et l’acquistion des propriétés de cellules souches. Enfin, nous avons réalisé une caractérisation génétique et/ou épigénétique de deux cancers rares, les carcinomes fibrolamellaires du foie et les carcinomes du rein à translocation. Pour les carcinomes fibrolamellaires du foie, nous avons décrit la nature endocrine de cette tumeur et établi une signature épigénétique basée sur la méthylation de l’ADN pouvant servir à différencier les formes histologiques appelées « pures » des formes « mixtes ». Pour les cancers du rein à translocation, nous avons montré les bases génétiques et épigénétiques de la différence entre les formes pédiatriques et adultes, avec la découverte fréquente du gain du bras chromosomique 17q dans les formes adultes. Nous avons aussi identifié une mutation récurrente dans le gène qui remodèle la chromatine INO80D appartenant à la famille INO80. En conclusion, ce travail explore le rôle de l’étude de l’épigénome pour comprendre la reprogrammation pendant les processus physiologiques comme la TEM d’une part et le cancer d’autre part
The epithelial-Mesenchymal transition (EMT) is a process of cellular plasticity that exists in embryonic development and which allows the formation of tissues and organs. In carcinogenesis, the process is reactivated by transcription factors whose action probably involves chromatin remodeling. The exact mapping of these epigenetic changes is poorly understood genome-Wide, although there have been some previous studies exploring changes in so few well-Targeted loci. This thesis deals with the epigenetic remodeling mediated by the transcription factor Twist1 in a model of human mammary immortalized cell line. The architecture of this remodeling has been mapped through the use of high-Throughput techniques to analyze DNA methylation (DREAM) and histone modifications (ChIPseq). Our results suggest a major change in the EMT methylome with focal hypermethylation and gene body hypomethylation predominantly within "partially methylated domains"; these areas are already known in development to gain repressive histone marks concomitantly with DNA hypomethylation. We also observed landscape remodeling of repressive histone mark H3K27me3 with a reduction in domains size, and especially the almost doubling of the number of bivalent genes. The coupling of DNA methylation with the profile of microRNA has allowed us to identify miR-203 as single microRNA regulated by DNA methylation during EMT; we have also shown that epigenetic suppression of miR-203 is both required for EMT and acquisition of stem cell properties. Finally, we performed a genetic and/or epigenetic characterization of two rare cancers, named fibrolamellar hepatocellular carcinomas and translocation renal cell carcinomas. In fibrolamellar hepatocellular carcinoma, we described the endocrine nature of this tumor and established a signature based on DNA methylation which can be used to distinguish histological forms called "pure" from "mixed" fibrolamellar hepatocellular carcinomas. Regarding translocation renal cell carcinomas, we established the genetic and epigenetic basis of differences between pediatric and adult forms, characterized by frequent gain of 17q gain chromosomal arm in adults. We also identified recurrent mutations in the chromatin remodeling gene INO80D which belongs to INO80 family. In conclusion, this work explores the impact of analyzing the epigenome to understand reprogramming during physiological processes such as EMT and cancer

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Rashidkhani, Bahram. "Diet and renal cell carcinoma /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-163-6/.

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Fallah, Abdul Karim. "Genomic studies in renal cell carcinoma." Thesis, Manchester Metropolitan University, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.528380.

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Al-Sharhan, Mouza Abdulla. "Prognostic factors in renal cell carcinoma." Thesis, University of Newcastle Upon Tyne, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285788.

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Chagnon, Fanny. "A dendritic cell vaccine for murine renal cell carcinoma." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=19400.

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Renal Cell Carcinoma (RCC) has a very high rate of mortality since it does not respond to conventional therapies such as chemotherapy and radiation therapy. Furthermore, in the majority of cases, metastases are already present at the time of diagnosis. The objective of our study is to develop a noval treatment for RCC, using a dendritic cell (DC) vaccine. An animal model of RCC, RENCA, was used to develop the vaccine.

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Giraldo-Castillo, Nicolas. "The Immune Microenvironment in Clear Cell Renal Cell Carcinoma : The heterogeneous immune contextures accompanying CD8+ T cell infiltration in clear cell Renal Cell Carcinoma." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066321/document.

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Dans cette étude, nous avons tenté de décrypter les mécanismes reliant l’augmentation de lymphocytes infiltrant les tumeurs (LIT) T CD8+ et un pronostic clinique défavorable dans le cancer du rein à cellules claires (ccRCC). Pour cela, nous avons déterminé 1) la relation entre le pronostic associé à l'expression d’immune checkpoints et l’infiltrat de cellules dendritiques (DC) et de LT CD8+ et 2) les caractéristiques phénotypiques des LIT T CD8+. L’expression des immune checkpoints a été déterminée par immunohistochimie dans une cohorte de 135 ccRCC. Nous avons constaté que les densités des cellules exprimant CD8, PD-1 et LAG-3 sont corrélées, et associées à une diminution de PFS et OS. Egalement, les patients dont les tumeurs présentent des densités élevées de cellules PD-1+ et PD-L1 et/ou PD-L2 +, ont le taux de survie le plus faible. Des densités élevées de DC immatures isolées dans le stroma tumoral sont associées à une forte expression d’immune checkpoints et à un faible taux de survie chez ces patients. En revanche, les patients présentant un taux de survie prolongé ont une densité élevée de lymphocytes CD8+, des DC matures au sein de structures lymphoïdes tertiaires, ainsi qu’une faible expression d’immune checkpoints. Nous avons analysé les LIT T CD8+ chez 21 patients ccRCC par Cytométrie de Flux. On a trouvé un groupe de patients (8/21) dont les tumeurs sont caractérisées par la surexpression de marqueurs inhibiteurs (PD1 et TIM3) et de d'activation (CD69 et CD38), par l'expansion des cellules T CD8 + mémoires effectrices et un plus grand potentiel d’agressivité. En résumé, nous avons démontré qu’une densité élevée de LIT T CD8+ dans les ccRCC est accompagnée d’une forte expression d’immune checkpoints et d’une réponse immunitaire mal coordonnée dans un sous-groupe de tumeurs agressives
To decipher the potential mechanisms linking increased CD8+ T cell infiltration with an adverse clinical outcome in ccRCC, in this study we determined: 1) the prognosis associated with the expression of immune checkpoints and its coordination with dendritic cell (DC) and CD8+ cell infiltration, and 2) the phenotypic traits of CD8+ tumor infiltrating lymphocytes. The prognosis associated with CD8+ and DC infiltrations, in addition to the expression of immune checkpoints were investigated in a cohort of 135 ccRCC by quantitative immunohistochemistry. We found that the densities of CD8+, PD-1+ and LAG-3+ cells were closely correlated, and independently associated with decreased PFS and OS. In addition, patients whose tumors presented both high densities of PD-1+ cells and PD-L1+ and/or L2+ tumor cells, displayed the worst clinical outcome. High densities of immature DC isolated in the tumour stroma were associated with high expression of immune checkpoints and patients’ poor clinical outcome. In contrast, the presence of mature DC within Tertiary Lymphoid Structures identified, among the tumours with high CD8+-TIL densities, those with low expression of immune checkpoints and prolonged survival. We also investigated the phenotype of freshly isolated CD8+TIL in 21 ccRCC by flow cytometry. We found a group tumors (8/21) characterised by the over-expression of inhibitory (PD-1 and TIM-3) and activation markers (CD69 and CD38), the expansion of the effector memory cell subpopulation (CCR7-CD45RA-), and a trend toward more aggressive features. In summary, we demonstrated that the infiltration with CD8+ TIL in ccRCC is accompanied by the enhanced expression of immune checkpoints and a poorly coordinated immune response in a subgroup of aggressive tumors

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Ronkainen, H. L. (Hanna-Leena). "Novel prognostic biomarkers for renal cell carcinoma." Doctoral thesis, Oulun yliopisto, 2012. http://urn.fi/urn:isbn:9789514297731.

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Abstract Background and aims: Stage and grade are the most widely used prognostic parameters for renal cell carcinoma (RCC). The clinical course of this disease is not, however, always predictable by traditional prognostic factors. In the era of new molecular targeted therapies a more accurate prognostication of RCC patient survival is important for the individualization of treatment and follow-up of patients. Despite exhaustive research there are still no prognostic biomarkers for RCC in clinical practice. In order to find novel prognostic tissue markers for RCC, we examined the expression of 14 biomarkers involved in carcinogenesis and clarified their prognostic significance in RCC. Material and methods: Out of 189 consecutive patients who underwent surgery for kidney cancer at Oulu University Hospital in the 1990s, 152 patients with histologically verified RCC were included in this study. The stage distribution was 70 (46%), 12 (8%), 51 (34%) and 19 (12%) patients with stages I-IV, respectively. The majority of the tumours (83 tumours, 55%) were nuclear grade II and 5 (3%), 40 (27%) and 22 (15%) of the tumours were grades I, III and IV, respectively. Clinical and follow-up data were obtained from patient records, the Finnish Cancer Registry and on demand from the Population Register Centre of Finland. The biomarkers studied included markers of the oxidative and neuroendocrine systems as well as proteins related to cell adhesion and migration, invasion, metastasis, inflammation and immune responses. The expression of various biomarkers was characterized via immunohistochemical tests of archival tumour material. The staining intensity was compared to clinicopathological parameters and patient RCC-specific survival. Results: The 5-year RCC-specific survival was 77%. The expression of Toll-like receptor 9 (TLR9) was an independent marker of favourable RCC-specific survival whereas cytoplasmic myosin VI expression was found to be an independent prognostic factor of poor RCC-specific survival. Cell culture experiments showed how cyclooxygenase-2 (COX-2) expression is regulated by HuR in RCC. HuR and COX-2 immunoexpression were also related to decreased RCC-specific survival. Immunostaining of Keap1 was associated with advanced RCC and a marker of a poorer RCC-specific prognosis. The expression of different neuroendocrine markers was evaluated but we could not establish any prognostic value for them. Conclusions: In particular, TLR9, HuR and myosin VI can be regarded as promising novel prognostic biomarkers in RCC. Stage, however, is the most important single prognostic factor for RCC
Tiivistelmä Munuaissyöpä on vuosikymmenten ajan jatkuvasti yleistynyt. Vaikka se diagnosoidaan nykyisin useimmiten sattumalöydöksenä vatsan alueen kuvantamistutkimuksissa ja hoitomenetelmät ovat viime vuosikymmenten aikana kehittyneet, munuaissyöpäkuolleisuus ei ole laskenut. Munuaissyövän ennusteen määrittäminen voi olla haasteellista. Perinteiset ennustetekijät, levinneisyys ja erilaistumisaste, eivät riitä selittämään kaikkien potilaiden taudinkulkua, eikä munuaissyövälle vielä ole kliinisessä käytössä ennusteellista merkkiainetta. Munuaissyöpähoitojen kehittyessä taudinkulun ennustaminen on yhä tärkeämpää, jotta potilaiden hoito ja seuranta voidaan yksilöidä. Tämän väitöskirjatyön tarkoituksena oli etsiä uusia ennusteellisia kudosmerkkiaineita munuaissyöpäkasvaimille. Väitöskirjatutkimus perustuu 1990-luvulla Oulun yliopistollisessa sairaalassa leikatun 152 munuaissyöpäpotilaan aineistoon. Lähes puolet aineiston kasvaimista edusti levinneisyysluokkaa I, ja yli puolet munuaissyöpäkasvaimista oli hyvin erilaistuneita (tumagradus I ja II). Tutkimuspotilaista kerättiin kattavat seurantatiedot. Leikkauksessa poistettujen munuaissyöpäkasvainten arkistomateriaalista tutkittiin eri merkkiaineiden ilmenemistä. Tutkitut merkkiaineet käsittivät oksidatiivisen ja neuroendokriinisen järjestelmän merkkiaineita sekä valkuaisaineita, jotka liittyvät keskeisiin syövän ominaisuuksiin, kuten solujen välisiin liitoksiin ja solujen liikkumiseen sekä etäpesäkkeiden syntymiseen. Lisäksi tutkittiin merkkiaineita, jotka liittyvät tulehdusreaktioihin ja immuunipuolustukseen. Väitöskirjatutkimus paljasti useita uusia kudosmerkkiaineita, joiden ilmeneminen munuaissyöpäkasvaimessa on yhteydessä potilaan ennusteeseen. Näistä merkittävimpiä ovat myosiini VI, joka liittyy syöpäkasvainten metastasointiin, sekä immuunipuolustuksessa vaikuttava Tollin kaltainen reseptori 9 (Toll-like receptor 9, TLR9). Molemmat merkkiaineet osoittautuivat itsenäisiksi ennustetekijöiksi munuaissyövässä. Muita ennusteeseen vaikuttavia merkkiaineita ovat tutkimuksen mukaan oksidatiivista stressiä aistiva Keap1 sekä immunologisiin reaktioihin liittyvä syklo-oksigenaasi 2 (COX-2) ja sen ilmenemistä säätelevä HuR

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Lawrentschuk, Nathan Leo. "Hypoxia and angiogenesis in renal cell carcinoma." Connect to thesis, 2009. http://repository.unimelb.edu.au/10187/6790.

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Hypoxia is one of the hallmarks of cancer. It was first postulated to occur in solid tumours by Thomlinson and Gray in 1955.1 The presence of hypoxia has been demonstrated in different types of solid tumours.2 Intratumoral hypoxia is caused by the lack of functional blood vessels in proliferating tumour tissue, resulting in low intratumoral oxygen concentrations. If hypoxia is severe or prolonged, cell death occurs.3 Malignant cells can undergo genetic and adaptive changes that allow them to escape from dying of oxygen deprivation. These changes are associated with a more aggressive malignant phenotype 4,5 conferring resistance to radiation 6,7 and chemotherapeutic agents.3,8,9 Hence hypoxia is known to be a key factor responsible for tumour resistance in humans.
Invasive polarographic oxygen sensor measurements have demonstrated hypoxia in solid tumours and it is generally defined to occur at an oxygen tension less than ten mmHg.10 Perhaps of more importance is that hypoxia has been demonstrated to be a prognostic indicator for local control after treatment with radiotherapy in glioma, head and neck and cervical cancers.11-13 It has also been able to predict for survival and the presence of distant metastases in soft tissue sarcomas.14 Finally, the significance of hypoxia in the activation and induction of functional molecules such as hypoxia inducible factors (HIFs) and VEGF, the modulation of gene expression (e.g. carbonic anhydrase IX), increased proto-oncogene levels, activation of nuclear factors and accumulation of other proteins (e.g. TP53) although progressing, is yet to be defined.15,16
Thus, it is of clinical interest to understand the levels of hypoxia and numbers of hypoxic cell populations in tumours, particularly those resistant to radiation and chemotherapy. In doing so clinicians and researchers may formulate more accurate prognostic information and develop treatments targeting hypoxic cells. Renal cell carcinoma (RCC) is a tumour resistant to radiation and chemotherapy that is yet to have its oxygen status investigated.
Although the “gold standard” of oxygen tension measurement is the Polarographic Oxygen Sensor (POS or Eppendorf pO2 histograph), non-invasive means of measuring oxygen status via imaging, immunohistochemistry or serum tumour markers are more practical. As highlighted by Menon and Fraker, it is imperative that reliable, globally usable, and technically simplistic methods be developed to yield a consistent, comprehensive, and reliable profile of tumour oxygenation. Until newer more reliable techniques are developed, existing independent techniques or appropriate combinations of techniques should be optimized and validated using known endpoints in tumour oxygenation status and/or treatment outcomes.17
Hanahan and Weinberg 18 surmised that the field of cancer research has largely been guided by a reductionist focus on cancer cells and the genes within them- a focus that has produced an extraordinary body of knowledge. Looking forward in time, they believe that progress in cancer research would come from regarding tumours as complex tissues in which mutant cancer cells have conscripted and subverted normal cell types (endothelial cells, immune cells, fibroblasts) to serve as active collaborators in their neoplastic agenda. The interactions between the genetically altered malignant cells and these supporting coconspirators will prove critical to understanding cancer pathogenesis and to the development of novel, effective therapies.18
Essentially, the background outlined here not only highlights the core aim of this thesis: to better understand the oxygen status of renal cell carcinoma and the relationship of this to angiogenesis so that better targeted therapies may be pursued in the future; but it also places this research in the context of the future proposed by Hanahan and Weinberg,18 by clearly focusing on collaborators in the neoplastic agenda, rather than just tumour cells themselves, to better understand RCC.

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Morrissey, Catherine. "The molecular pathology of renal cell carcinoma." Thesis, University of Birmingham, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.420407.

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Книги з теми "Translocation renal cell carcinoma"

Bukowski, Ronald M., and Andrew Novick. Renal Cell Carcinoma. New Jersey: Humana Press, 2000. http://dx.doi.org/10.1385/1592592295.

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Campbell, Steven C., and Brian I. Rini, eds. Renal Cell Carcinoma. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-062-5.

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Bukowski, Ronald M., Robert A. Figlin, and Robert J. Motzer, eds. Renal Cell Carcinoma. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-1622-1.

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Bukowski, Ronald M., Robert A. Figlin, and Robert J. Motzer, eds. Renal Cell Carcinoma. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-332-5.

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Oya, Mototsugu, ed. Renal Cell Carcinoma. Tokyo: Springer Japan, 2017. http://dx.doi.org/10.1007/978-4-431-55531-5.

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Figlin, Robert A., W. Kimryn Rathmell, and Brian I. Rini, eds. Renal Cell Carcinoma. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-2400-0.

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Renal cell carcinoma. Shelton, Conn: People's Medical Pub. House, 2009.

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Debruyne, Frans M. J., Ronald M. Bukowski, J. Edson Pontes, and Pieter H. M. de Mulder, eds. Immunotherapy of Renal Cell Carcinoma. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75853-9.

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Bukowski, Ronald M., James H. Finke, and Eric A. Klein. Biology of Renal Cell Carcinoma. New York, NY: Springer New York, 1995. http://dx.doi.org/10.1007/978-1-4612-2536-2.

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M, Bukowski Ronald, Finke James H. 1944-, and Klein Eric A. 1955-, eds. Biology of renal cell carcinoma. New York: Springer-Verlag, 1995.

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Caliò, Anna, Diego Segala, and Guido Martignoni. "MiT Family Translocation Renal Cell Carcinoma." In Encyclopedia of Pathology, 1–4. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-28845-1_4847-1.

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Caliò, Anna, Diego Segala, and Guido Martignoni. "MiT Family Translocation Renal Cell Carcinoma." In Encyclopedia of Pathology, 205–8. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-41894-6_4847.

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Geller, James I., Nicholas G. Cost, and Mariana M. Cajaiba. "TFE/Translocation Morphology Renal Cell Carcinoma." In Rare Kidney Tumors, 93–104. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-96989-3_8.

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Chahoud, Jad, Gabriel G. Malouf, and Nizar M. Tannir. "Translocation Renal Cell Carcinomas." In Rare Genitourinary Tumors, 41–52. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-30046-7_3.

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Russo, Paul. "Renal Cell Carcinoma." In Renal Cancer, 3–33. Totowa, NJ: Humana Press, 2001. http://dx.doi.org/10.1385/1-59259-144-2:003.

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Filippiadis, Dimitrios K., Maria Tsitskari, and Thomas D. Atwell. "Renal Cell Carcinoma." In Image-Guided Interventions in Oncology, 197–213. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-48767-6_11.

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Barker, David W., and Ronald J. Zagoria. "Renal Cell Carcinoma." In Medical Radiology, 103–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/3-540-30003-1_7.

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Nomiya, Takuma, and Hiroshi Tsuji. "Renal Cell Carcinoma." In Carbon-Ion Radiotherapy, 241–49. Tokyo: Springer Japan, 2013. http://dx.doi.org/10.1007/978-4-431-54457-9_28.

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Garcia, Michael A., and Alexander R. Gottschalk. "Renal Cell Carcinoma." In Handbook of Evidence-Based Radiation Oncology, 535–43. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-62642-0_24.

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Monzon, Federico A. "Renal Cell Carcinoma." In Diagnostic Molecular Pathology in Practice, 201–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-19677-5_25.

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Тези доповідей конференцій з теми "Translocation renal cell carcinoma"

Melas, Marilena, Kevin J. McDonnell, Christopher K. Edlund, Sarah J. Tash, Duveen Y. Sturgeon, Chenxu Qu, Charalampos Lazaris, et al. "Abstract 491: Elucidatingde novoPATRR-mediated t(3;8) balanced translocation and clear cell renal cell carcinoma." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-491.

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Ku, Sheng-Yu, Swathi Ramakrishnan, Eric Ciamporcero, Bo Xu, Gissou Azabdaftari, Richard Cheney, and Roberto Pili. "Abstract 2546: HDAC and Hsp90 inhibition as therapeutic strategy for translocation renal cell carcinoma." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2546.

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Damayanti, Nur P., Sreenivasulu Chintala, Ashley Orillion, Remi Adelaiye-Ogala, May F. Elbanna, Pete Hollenhorst, and Roberto Pili. "Abstract 4475: Delineating translocation renal cell carcinoma oncogenesis in cells harboring TFE3 fusion with spliceosome machinery associated genes." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4475.

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Baba, Masaya, Ying Huang, Takanobu Motoshima, Hisashi Hasumi, Yukiko Hasumi, Mitsuko Furuya, Yoji Nagashima, et al. "Abstract 3527: Clarification of the molecular mechanism for cancer development in Xp11.2 translocation renal cell carcinoma." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3527.

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Haddad, Philip A., Dalia Hammoud, and Kevin Gallagher. "Abstract 3525: Epidemiology and clinicopathology prognostic factors of TFEB translocation renal cell carcinoma (TBRCC): Analysis of updated pooled database." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-3525.

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Malouf, Gabriel G., Xiaoping Su, Hui Yao, Christopher G. Wood, Yue Lu, Shoudan Liang, Erika J. Thompson, et al. "Abstract 2980: Integrated transcriptome and methylome sequencing of Xp11 translocation renal cell carcinomas reveal uncoupling of DNA methylation and transcriptional profiles." 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.am2013-2980.

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Ramakrishnan, Swathi, Paula Sotomayor, Kristin Lehet, and Roberto Pili. "Abstract 5016: Epigenetics in 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.am2012-5016.

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Saleem, M. D. "Mediastinal Presentation of Renal Papilalry Cell Carcinoma." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6963.

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Oliveira, Marcos, Jorge Dionísio, Ambrus Szantho, and Duro Da Costa. "Hemorrhagic Endobronchial metastasis of renal cell carcinoma." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.2841.

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Ryu, Hyewon, Solbi Kim, Nayoung Kim, Jin-Man Kim, and Hyo Jin Lee. "Abstract 1549: LAPTM5 in clear cell renal cell carcinoma." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1549.

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Ismail, Mohamed, Monish Aron, Joe Philip, and Faris Abushamma. Renal cell carcinoma – minimally invasive nephron sparing surgery. BJUI Knowledge, January 2022. http://dx.doi.org/10.18591/bjuik.0114.v2.

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Schmidt, Laura S., and W. Marston Linehan. Principles and management of hereditary renal cell carcinoma. BJUI Knowledge, March 2022. http://dx.doi.org/10.18591/bjuik.0095.v2.

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Drake, Richard R., and Alexander Parker. Tissue and Metabolomic Biomarkers of Recurrent Renal Cell Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada592797.

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Stroman, Luke, and Tim O'Brien. Management of renal cell carcinoma with inferior vena cava (IVC) involvement. BJUI Knowledge, January 2022. http://dx.doi.org/10.18591/bjuik.0738.

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Stewart, B. J. Mass Spectrometry Data Set for Renal Cell Carcinoma and Polycystic Kidney Disease Cell Models. Office of Scientific and Technical Information (OSTI), January 2017. http://dx.doi.org/10.2172/1342001.

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Zhou, Xiao, and Guangcheng Luo. A meta-analysis of platelet-lymphocyte ratio: a merit attention prognostic factor in renal cell carcinoma. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2021. http://dx.doi.org/10.37766/inplasy2021.9.0064.

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Shen, Li. A Novel Tumor Antigen and Foxp3 Dual-Targeting Tumor Cell Vaccine Enhances the Immunotherapy in a Murine Model of Renal Cell Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada615157.

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Zhou, Xiao, and Guangcheng Luo. Whether the consistency of tumor thrombus has prognostic significance in patients with renal cell carcinoma—a meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2022. http://dx.doi.org/10.37766/inplasy2022.2.0015.

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Jin, Hongyu, and Man Zhang. Adjuvant targeted therapy combined with surgery for advanced and metastatic renal cell carcinoma: Protocol for a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2020. http://dx.doi.org/10.37766/inplasy2020.11.0093.

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Monti, Martina, Susanna Lunardini, Igino Andrea Magli, Riccardo Campi, Giulia Primiceri, Francesco Berardinelli, Daniele Amparore, et al. Micro-RNA predict response to systemic treatments in meta-static renal cell carcinoma patients: results from a systematic review of the literature. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0086.

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