Renal cell carcinoma : molecular biology, immunology, and clinical management


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Clinical Management

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The study published by Malouf et al. The first cohort was similar to the tumor cohort presented by Bi et al. This cohort underwent targeted sequencing of both matched elements using a custom panel of frequently mutated cancer-related genes and 37 introns frequently rearranged in cancer average exon coverage of x. Also, they did not report using matched normal tissue from any patients in their targeted sequencing analysis, which likely limits the interpretation of copy number aberrations for these tumors.

Kidney Cancer Research

The sequencing results of this cohort stand somewhat in contrast to the results of the study above. In the third sample they saw similar homozygous deletions in VHL but found multiple distinct inactivating mutations in TP53 and phosphatase and tensin homolog PTEN that differed between the two elements. The third case also had a unique amplification of Janus kinase 2 JAK2 in the sarcomatoid element, which, when taken together with the TP53 and PTEN mutations, may suggest a divergent course of evolution for this tumor.

In the second cohort, they analyzed 23 tumors with sRCC arising from a mixture of carcinomatous backgrounds including clear cell, unclassified, collecting duct, papillary, and mucinous tubular and spindle cell carcinoma. Most of these tumors were primary kidney specimens In their third cohort, the investigators employed whole-exome sequencing on four tumors with sccRCC, not microdissected.

They reported a lower overall median mutation rate in these four cases In two of these four cases they went on to test multiple regions from the primary tumors 4 regions in one and two in the other to evaluate intratumoral heterogeneity using Sanger sequencing for VHL and TP53 genes only. For these two cases they report no finding of intratumor heterogeneity in regards to these two genes.

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Integrating the results of these studies helps us answer several questions about the molecular framework of sRCC. First the truncal events and shared genomic aberrations between both the carcinomatous elements and sarcomatoid element seen in both studies confirm that sRCC arises from RCC. Next, the notion that the sarcomatoid element represents a dedifferentiated progression of RCC is supported by the increased overall mutational burden and copy number aberrations seen in the sarcomatoid elements compared to the carcinomatous elements from Bi et al.

The increase in aberrations of known cancer genes TP53 , NF2 , CDKN2A also supports the sentiment that the sarcomatoid elements are driving pathogenesis in these tumors.


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Oda et al. The carcinomatous elements, or background histology, for this cohort included both mixed and granular subtypes, somewhat limiting the application of these results. While Bi et al.

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The latter study included diverse primary RCC histologies and also included metastatic tumors, which previously have been shown to be enriched for TP53 aberrations irrespective of sarcomatoid features Similarly the finding of increased NF2 mutations occurring in sRCC may also be limited due to the diverse background of primary RCC histologies in this cohort. Our understanding of the molecular composition and the clinical implications of uRCC are both poorly defined and poorly understood.

The recognition that inherited forms of renal cancer exist, and that chromosomal abn- malities can be identified in these tumors, suggested a genetic basis for renal cell carcinoma.

http://leondumoulin.nl/language/short/seven-characteristic-pieces-op7.php The familial cancer syndrome, Von Hippel Lindau disease, provided the setting in which the genetic abnormalites associated with the development of renal cancer were first described. Currently the functions of the VHL protein are being investigated, and the biology of clear cell carcinoma of the kidney is under study. Additionally, papillary carcinomas of the kidney appear to express different molecular defects, and these are now being unraveled.

I firmly believe this is the most complete yet concise "monogram" on the subject of renal cancers. It is a high quality book that would be extremely useful for anyone who manages renal cell carcinomas on a regular basis. This book is the only one of its kind and hence cannot be compared.

Introduction

This book has many strengths. One is its organization. Each chapter is divided into clearly labeled, short subsections, making it highly readable and allowing the reader to locate information on a particular topic efficiently.

Renal cell carcinoma : molecular biology, immunology, and clinical management Renal cell carcinoma : molecular biology, immunology, and clinical management
Renal cell carcinoma : molecular biology, immunology, and clinical management Renal cell carcinoma : molecular biology, immunology, and clinical management
Renal cell carcinoma : molecular biology, immunology, and clinical management Renal cell carcinoma : molecular biology, immunology, and clinical management
Renal cell carcinoma : molecular biology, immunology, and clinical management Renal cell carcinoma : molecular biology, immunology, and clinical management
Renal cell carcinoma : molecular biology, immunology, and clinical management Renal cell carcinoma : molecular biology, immunology, and clinical management
Renal cell carcinoma : molecular biology, immunology, and clinical management Renal cell carcinoma : molecular biology, immunology, and clinical management
Renal cell carcinoma : molecular biology, immunology, and clinical management Renal cell carcinoma : molecular biology, immunology, and clinical management
Renal cell carcinoma : molecular biology, immunology, and clinical management Renal cell carcinoma : molecular biology, immunology, and clinical management

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