Microvascular and lymphovascular tumour invasion are associated with poor prognosis and metastatic spread in renal cell carcinoma: a validation study in clinical practice

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Abstract

To validate microvascular (MVI) and lymphovascular (LVI) invasion as prognostic factors in patients with renal cell carcinoma (RCC).

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Prognostic significance of morphologic parameters in renal cell carcinoma.

Susan A. Fuhrman, Larry C Lasky, Catherine Limas (1982)

The prognostic significance of morphologic parameters was evaluated in 103 patients with renal cell carcinoma diagnosed during 1961--1974. Pathologic material was classified as to pathologic stage, tumor size, cell arrangement, cell type and nuclear grade. Four nuclear grades (1--4) were defined in order of increasing nuclear size, irregularity and nucleolar prominence. Nuclear grade was more effective than each of the other parameters in predicting development of distant metastasis following nephrectomy. Among 45 patients who presented in Stage I, tumors classified as nuclear grade 1 did not metastasize for at least 5 years, whereas 50% of the higher grade tumors did so. Moreover, among Stage I tumors there was a significant difference in subsequent metastatic rate between nuclear grades 1 and 2. There was an apparent positive relationship between cell type and metastatic rate; clear cell tumors were less aggressive than predominantly granular cell tumors (metastatic rate 38% versus 71%). This relationship in part a function of the nuclear grade: only 5% of grade 3 and 4 tumors consisted of clear cells, whereas such high grades were seen in 57% of granular cell tumors. The size of the primary correlated well with the stage at the time of surgery. However, with the exception of extremely large and small tumors, the size was not useful in predicting the subsequent course of patients treated for Stage I tumors. Nuclear grade was the most significant prognostic criterion for the outcome of Stage I renal cell carcinoma.

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The genetic basis of kidney cancer: a metabolic disease.

W Linehan, Ramaprasad Srinivasan, Laura Schmidt (2010)

Kidney cancer is not a single disease but comprises a number of different types of cancer that occur in the kidney, each caused by a different gene with a different histology and clinical course that responds differently to therapy. Each of the seven known kidney cancer genes, VHL, MET, FLCN, TSC1, TSC2, FH and SDH, is involved in pathways that respond to metabolic stress or nutrient stimulation. The VHL protein is a component of the oxygen and iron sensing pathway that regulates hypoxia-inducible factor (HIF) levels in the cell. HGF-MET signaling affects the LKB1-AMPK energy sensing cascade. The FLCN-FNIP1-FNIP2 complex binds AMPK and, therefore, might interact with the cellular energy and nutrient sensing pathways AMPK-TSC1/2-mTOR and PI3K-Akt-mTOR. TSC1-TSC2 is downstream of AMPK and negatively regulates mTOR in response to cellular energy deficit. FH and SDH have a central role in the mitochondrial tricarboxylic acid cycle, which is coupled to energy production through oxidative phosphorylation. Mutations in each of these kidney cancer genes result in dysregulation of metabolic pathways involved in oxygen, iron, energy or nutrient sensing, suggesting that kidney cancer is a disease of cell metabolism. Targeting the fundamental metabolic abnormalities in kidney cancer provides a unique opportunity for the development of more-effective forms of therapy for this disease.

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Guidelines for the development and incorporation of biomarker studies in early clinical trials of novel agents.

L Shankar, Maria Koehler, RALPH E. PARCHMENT … (2010)

The National Cancer Institute (NCI) Investigational Drug Steering Committee (IDSC) charged the Biomarker Task Force to develop recommendations to improve the decisions about incorporation of biomarker studies in early investigational drug trials. The Task Force members reviewed biomarker trials, the peer-reviewed literature, NCI and U.S. Food and Drug Administration (FDA) guidance documents, and conducted a survey of investigators to determine practices and challenges to executing biomarker studies in clinical trials of new drugs in early development. This document provides standard definitions and categories of biomarkers, and lists recommendations to sponsors and investigators for biomarker incorporation into such trials. Our recommendations for sponsors focus on the identification and prioritization of biomarkers and assays, the coordination of activities for the development and use of assays, and for operational activities. We also provide recommendations for investigators developing clinical trials with biomarker studies for scientific rationale, assay criteria, trial design, and analysis. The incorporation of biomarker studies into early drug trials is complex. Thus the decision to proceed with studies of biomarkers should be based on balancing the strength of science, assay robustness, feasibility, and resources with the burden of proper sample collection on the patient and potential impact of the results on drug development. The Task Force provides these guidelines in the hopes that improvements in biomarker studies will enhance the efficiency of investigational drug development.

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Author and article information

Journal

Title: BJU International

Abbreviated Title: BJU Int

Publisher: Wiley

ISSN: 14644096

Publication date Created: January 2018

Publication date (Print): January 2018

Publication date (Electronic): September 10 2017

Volume: 121

Issue: 1

Pages: 84-92

Affiliations

[1 ]Department of Urology; Eberhard Karls University Tübingen; Tübingen Germany

[2 ]Department of Urology; Ernst-Moritz Arndt University of Greifswald; Greifswald Germany

[3 ]Institute of Pathology; Ernst-Moritz Arndt University of Greifswald; Greifswald Germany

[4 ]Department of Urology; Medical University of Vienna; Vienna Austria

[5 ]Institute of Pathology; Eberhard Karls University Tübingen; Tübingen Germany

[6 ]Clinical Institute of Pathology; Medical University of Vienna; Vienna Austria

[7 ]Department of Urology; Addenbrooke's Hospital; Cambridge UK

Article

DOI: 10.1111/bju.13984

PubMed ID: 28803448

SO-VID: 02ff4e6b-0d09-4b8d-a4a6-3f3cf2391112

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http://doi.wiley.com/10.1002/tdm_license_1.1

http://onlinelibrary.wiley.com/termsAndConditions#vor

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