Bora Gurel

Kocaeli University, School of Medicine, Faculty Member

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Supervisors: Angelo De Marzo, M.D., Ph.D.

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Vivekanand Jha

Fortis Escorts Heart Institute

Dr. K.R.Mulla

Visvesvaraya Technological University

Vinod K K

INDIAN AGRICULTURAL RESEARCH INSTITUTE, NEW DELHI, INDIA

Anna M. Czarnecka

Medical University of Warsaw

Tugba Mehmetoglu Gurbuz

Texas Tech University El Paso

David Seamon

Kansas State University

Dr.Mahmoud Lotfy

Minufiya University

Armando Marques-Guedes

UNL - New University of Lisbon

Jon R Sayers

The University of Sheffield

Prof. Mohamed Labib Salem

Tanta University

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Books by Bora Gurel

Molecular Pathology of Prostate Cancer

Prostatic adenocarcinoma is the most common noncutaneous malignancy in men and the second leading... more Prostatic adenocarcinoma is the most common noncutaneous malignancy in men and the second leading cause of cancer death in Western populations. Despite its prevalence, an understanding of the molecular alterations affecting the development, progression, and treatment of the disease was largely lacking until recently. Rapid advances in molecular techniques in the past decade have seen a dramatic increase in our understanding of the role molecular alterations play in prostate cancer. Though still early, these developments have provided insight into distinct subsets of prostate cancer that promise to change how the disease is both diagnosed and managed. The molecular alterations discovered have shown that prostate cancer development involves multiple genetic abnormalities and that detection or targeting of a single genetic event is unlikely to impact all cases of prostate cancer. Of the ones that have shown the most promise to changing diagnostic and treatment paradigms are the gene fusion of TMPRSS2 and members of the ETS family of transcription factors, primarily ERG, as well as the inactivation of the tumor suppressor PTEN. A greater understanding of the molecular alterations present in prostate cancer will lead to further improvements in diagnosis, prediction of prognosis, stratification for specific therapies, and ultimately better outcomes for patients.

Papers by Bora Gurel

Data from PTEN Protein Loss by Immunostaining: Analytic Validation and Prognostic Indicator for a High Risk Surgical Cohort of Prostate Cancer Patients

Purpose: Analytically validated assays to interrogate biomarker status in clinical samples are cr... more Purpose: Analytically validated assays to interrogate biomarker status in clinical samples are crucial for personalized medicine. PTEN is a tumor suppressor commonly inactivated in prostate cancer that has been mechanistically linked to disease aggressiveness. Though deletion of PTEN, as detected by cumbersome FISH spot counting assays, is associated with poor prognosis, few studies have validated immunohistochemistry (IHC) assays to determine whether loss of PTEN protein is associated with unfavorable disease.Experimental Design: PTEN IHC was validated by employing formalin fixed and paraffin-embedded isogenic human cell lines containing or lacking intact PTEN alleles. PTEN IHC was 100% sensitive and 97.8% specific for detecting genomic alterations in 58 additional cell lines. PTEN protein loss was then assessed on 376 prostate tumor samples, and PTEN FISH or high resolution single nucleotide polymorphism microarray analysis was done on a subset of these cases.Results: PTEN protein...

Association of PTEN loss with outcome of patients (pts) with early high-risk prostate cancer (CaP) treated with adjuvant docetaxel following radical prostatectomy (RP)

Journal of Clinical Oncology, 2011

43 Background: Loss of the PTEN tumor suppressor and subsequent activation of the PI3K pathway is... more 43 Background: Loss of the PTEN tumor suppressor and subsequent activation of the PI3K pathway is common and has potential clinical and therapeutic value in CaP. We examined the PTEN status of primary tumors in pts who underwent adjuvant docetaxel tx in a prospective clinical trial. Methods: Of the 77 pts enrolled in a prospective multi-institutional adjuvant docetaxel trial (TAX 2501, J Urol 2007), we prospectively collected 56 primary tumor pathology specimens suitable for analysis of PTEN status by immunoreactivity (IHC) and/or fluorescence in situ hybridisation (FISH) assay. Protocol defined progression included a PSA of ≥ 0.4 ng/mL, radiological/pathological evidence of recurrent disease or death from any cause. Univariate and multivariable analyses based on the Cox proportional hazards regression model were used to analyze the independent association of PTEN and other known prognostic factors with progression free survival (PFS). Results: PTEN loss was observed in 37/56 pts (6...

Cell-autonomous intracellular androgen receptor signaling drives the growth of human prostate cancer initiating cells

The Prostate, 2010

The lethality of prostate cancer is due to the continuous growth of cancer initiating cells (CICs... more The lethality of prostate cancer is due to the continuous growth of cancer initiating cells (CICs) which are often stimulated by Androgen Receptor (AR) signaling. However, the underlying molecular mechanism(s) for such AR-mediated growth stimulation are not fully understood. Such mechanisms may involve cancer cell-dependent induction of tumor stromal cells to produce paracrine growth factors or could involve cancer cell autonomous autocrine and/or intracellular AR signaling pathways. The present studies document that stromal AR expression is not required for prostate cancer growth, since tumor stroma surrounding AR-positive human prostate cancer metastases (N=127) are characteristically AR-negative. This lack of a requirement for AR expression in tumor stromal cells is also documented by the fact that prostate cancers derived from 5 independent patients grow equally well when xenografted in wild-type vs. AR-null nude mice. Using a series of AR-positive human prostate cancer cell lines, AR-dependent growth stimulation was documented to involve secretion, extracellular binding, and signaling by autocrine growth factors. Orthotopic xenograft animal studies documented that the cell autonomous autocrine growth factors which stimulate prostate CIC growth are not the andromedins secreted by normal prostate stromal cells. Such cell autonomous and extracellular autocrine signaling is necessary but not sufficient for the optimal growth of prostate CICs based upon the response to anti-androgen plus/or minus pre-conditioned media. Thus, AR-induced growth stimulation of human prostate CICs requires AR-dependent intracellular pathways. The identification of such AR-dependent intracellular pathways offers new leads for the development of effective therapies for prostate cancer.

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