Tissue biomarkers in renal cell carcinoma: Issues and solutions

Napoli, Arianna Di; Signoretti, Sabina

doi:10.1002/cncr.24233

Cited by 38 publications

(31 citation statements)

References 77 publications

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“…This is performed by placing the sample as soon as possible into a sterile vial and DNase-free liquid under ice conditions; the temperature is extremely important, and storage must be at -80˚C after the sample has been frozen in liquid nitrogen. This ensures the transcription of genes and prevents the degradation of DNA and RNA (62).…”

Section: Discussionmentioning

confidence: 99%

Relative mRNA expression of prostate-derived E-twenty-six factor and E-twenty-six variant 4 transcription factors, and of uridine phosphorylase-1 and thymidine phosphorylase enzymes, in benign and malignant prostatic tissue

et al. 2015

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Abstract. Prostate cancer is the most frequent urological tumor, and the second most common cancer diagnosed in men. Incidence and mortality are variable and appear to depend on behavioral factors and genetic predisposition. The prostate-derived E-twenty-six factor (PDEF) and E-twenty-six variant 4 (ETV4) transcription factors, and the thymidine phosphorylase (TP) and uridine phosphorylase-1 (UP-1) enzymes, are reported to be components of the pathways leading to tumorigenesis and/or metastasis in a number of tumors. The present study aimed to analyze the mRNA expression levels of these proteins in prostatic cancerous and benign tissue, and their association with clinical and pathological variables. Using quantitative reverse transcription polymerase chain reaction, the mRNA expression levels of PDEF, ETV4, TP and UP-1 were studied in 52 tissue samples (31 of benign prostatic hyperplasia and 21 of prostate adenocarcinomas) obtained from patients treated by transurethral resection of the prostate or by radical prostatectomy. Relative expression was assessed using the ∆-CT method. Data was analyzed using Spearman's tests for correlation. P<0.05 was considered to indicate a statistically significant difference. The results revealed that PDEF, ETV4, UP-1 and TP were expressed in 85.7, 90.5, 95.2 and 100% of the prostate cancer samples, and in 90.3, 96.8, 90.3 and 96.8% of the benign samples, respectively. PDEF and ETV4 exhibited a significantly higher relative expression level in the tumor samples compared with their benign counterparts. The relative expression of TP and UP-1 did not differ significantly between benign and cancerous prostate tissues. The relative expression of TP was moderately and significantly correlated with the expression of ETV4 in the benign tissues. The relative expression of UP-1 was significantly lower in T3 compared with T1 and T2 cancers. These findings indicate that PDEF, ETV4, TP and UP-1 are typically expressed in benign and malignant prostatic tissues. Further studies are necessary to define the role of these proteins as therapeutic targets in prostate cancer.

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Section: Discussionmentioning

confidence: 99%

Relative mRNA expression of prostate-derived E-twenty-six factor and E-twenty-six variant 4 transcription factors, and of uridine phosphorylase-1 and thymidine phosphorylase enzymes, in benign and malignant prostatic tissue

et al. 2015

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“…It has been estimated that nearly 70% of somatic mutations present in RCC tissues are not detectable across all tumor sites. Another barrier to biomarker development is the inconsistency and variability in tissue preparation and biomarker evaluation, 97 which will affect accuracy of the biomarker data that are collected and interpreted. Efforts to define prognostic or predictive factors have largely shown that clinical features, including tumor grade, local extent of tumor, regional lymph node metastases and evidence of metastases at presentation remain the most consistent features associated with survival.…”

Section: Issues In Specific Tumor Typesmentioning

confidence: 99%

NCCN Working Group Report: Designing Clinical Trials in the Era of Multiple Biomarkers and Targeted Therapies

Venook¹,

Arcila²,

Benson³

et al. 2014

J Natl Compr Canc Netw

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Defining treatment susceptible or resistant populations of cancer patients through the use of genetically defined biomarkers has revolutionized cancer care in recent years for some disease/patient groups. Research continues to show that histologically defined diseases are diverse in their expression of unique mutations or other genetic alterations, however, which presents both opportunities for the development of personalized cancer treatments, but increased difficulty in testing these therapies because potential patient populations are divided into ever-smaller numbers. To address some of the growing challenges in biomarker development and clinical trial design, NCCN assembled a group of experts across specialties and solid tumor disease types to begin to define the problems and to consider alternate ways of designing clinical trials in the era of multiple biomarkers and targeted therapies. Results from that discussion are presented, focusing on issues of clinical trial design from the perspective of statisticians, clinical researchers, regulators, pathologists and information developers.

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“…For example, with MRI, it is now considered that by focusing on the intracellular lipid content, intratumoral hemosiderin deposition and enhancement patterns and by using profiles in different MRI sequences (e.g., chemical shift MRI), it is possible to obtain magnetic resonance phenotypes as a biological signature of tumors (e.g., to differentiate subtypes) [14,15]. One of the major advantages of imaging biological signatures compared with traditional tissue or blood biomarkers is that the tumor is in situ and metabolically active and so will not be subject to significant bias by the lack of standardization in tissue sample acquisition, storage and ana lysis [16,17]. Imaging may also be repeated at intervals and is noninvasive, allowing development of treatment and monitoring algorithms that are commonplace in oncology.…”

Section: Biomarkers and Functional Imagingmentioning

confidence: 99%