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Bayraktar S.,Mercy Cancer Center | Gluck S.,University of Miami
Breast Cancer Research and Treatment | Year: 2013

Triple-negative breast cancer (TNBC) refers to a heterogeneous group of tumors that do not express the estrogen/progesterone-receptor (ER/PR), and human epidermal growth factor receptor-2 (HER2). TNBC is an aggressive histological subtype with limited treatment options and very poor prognosis following progression after standard chemotherapy regimens. There have been significant improvements in the outcome of other subtypes of breast cancer, including ER-positive/HER2 overexpressed tumors, attributed to the addition of targeted therapy, including hormonal agents and trastuzumab. However, no specific targeted agents are currently available for the treatment of TNBC. This review aims to collate and describe the most recent data on targeted therapies that have demonstrated efficacy in the management of metastatic TNBC. Targeted agents that have been investigated in the treatment of metastatic TNBC include inhibitors of poly(ADP-ribose) polymerase, angiogenesis, mammalian target of rapamycin, epidermal growth factor receptor, HDAC, Jak2, and Src. Several of these agents have shown considerable promise. © 2013 Springer Science+Business Media New York.

Beach P.R.,Mercy Cancer Center | White B.E.,Mercy Childrens Hospital
Clinical Journal of Oncology Nursing | Year: 2012

Life-threatening diseases are being diagnosed at younger ages and successfully managed for longer periods of time. Adult patients increasingly will have parents who want to be present and help during treatment. Little is known about how best to include parents of adult children in the nursing plan of care. Healthcare professionals must balance the independence and privacy needs of adult patients with parents' desire to help and provide care.

Bayraktar S.,Mercy Cancer Center | Thompson P.A.,Arizona Cancer Center | Yoo S.-Y.,University of Houston | Do K.-A.,University of Houston | And 4 more authors.
Oncologist | Year: 2013

Background. Several single-nucleotide polymorphisms (SNPs) associated with breast cancer risk have been identified through genome-wide association studies (GWAS).Weinvestigated whether eight risk SNPs identified inGWASwere associated with breast cancer disease-free survival (DFS) and overall survival (OS) rates. Patients and Methods. A cohort of 739 white women with early-stage breast cancer was genotyped for eight GWASidentified SNPs (rs2981582, rs1219648 [FGFR2], rs3803662, rs12443621, rs8051542 [TOX3], rs999737 [RAD51L1], rs6504950 [17q23], and rs4973768 [3p24]). Relationships between SNPs and breast cancer outcomes were evaluated using Cox proportional hazard regression models. The cumulative effects of SNPs on breast cancer outcomes were assessed by computing the number of at-risk genotypes. Results. At a median follow-up of 121 months (range: 188 - 231 months) for survivors, 237 deaths (32%) and 186 breast cancer events (25%) were identified among the 739 patients. After adjusting for age, clinical stage, and treatment, rs12443621 (16q12; p =.03) and rs6504950 (17q23; p =.008) were prognostic for OS but not DFS. A higher risk for death was also found in the multivariable analysis of patients harboring three or four at-risk genotypes of the GWAS SNPs compared to patients carrying two or less atrisk genotypes (hazard ratio: 1.60, 95% confidence interval: 1.23-2.24; p=.0008). Conclusion. The study results suggest that previously identified breast cancer risk susceptibility loci, rs12443621 (16q12) and rs6504950 (17q23), may influence breast cancer prognosis or comorbid conditions associated with overall survival. The precise molecular mechanisms through which these risk SNPs, as well as others that were not included in the analysis, influence clinical outcomes remain to be determined. ©AlphaMed Press 2013.

Yan B.,University of Mississippi Medical Center | Yan B.,Mercy Cancer Center | Ouyang R.,Central South University | Huang C.,University of Mississippi Medical Center | And 5 more authors.
Biochemical and Biophysical Research Communications | Year: 2012

Background: Hyperthermia plays an important role in cancer therapy. However, as with radiation, it can cause DNA damage and therefore genetic instability. We studied whether hyperthermia can induce gene amplification in cancer cells and explored potential underlying molecular mechanisms. Materials and methods: (1) Hyperthermia: HCT116 colon cancer cells received water-submerged heating treatment at 42 or 44. °C for 30. min; (2) gene amplification assay using N-(phosphoacetyl)-l-aspartate (PALA) selection of cabamyl-P-synthetase, aspartate transcarbarmylase, dihydro-orotase (cad) gene amplified cells; (3) southern blotting for confirmation of increased cad gene copies in PALA-resistant cells; (4) γH2AX immunostaining to detect γH2AX foci as an indication for DNA double strand breaks. Results: (1) Heat exposure at 42 or 44. °C for 30. min induces gene amplification. The frequency of cad gene amplification increased by 2.8 and 6.5 folds respectively; (2) heat exposure at both 42 and 44. °C for 30. min induces DNA double strand breaks in HCT116 cells as shown by γH2AX immunostaining. Conclusion: This study shows that heat exposure can induce gene amplification in cancer cells, likely through the generation of DNA double strand breaks, which are believed to be required for the initiation of gene amplification. This process may be promoted by heat when cellular proteins that are responsible for checkpoints, DNA replication, DNA repair and telomere functions are denatured. To our knowledge, this is the first study to provide direct evidence of hyperthermia induced gene amplification. © 2012 Elsevier Inc.

Bayraktar S.,University of Miami | Lima C.M.R.,University of Miami | Lima C.M.R.,Mercy Cancer Center
Expert Opinion on Emerging Drugs | Year: 2012

Introduction: Patients with pancreatic cancer (PC) present with advanced disease that is lethal and notoriously difficult to treat. The research focused initially on combining cytotoxic therapies with gemcitabine, and over the past decade, a large number of studies have been published that aimed to target the molecular abnormalities implicated in pancreatic tumor growth. Areas covered: The cell cycle is a tightly regulated series of events that governs cell replication and division. Deregulation of cell cycle kinases have been implicated in PC tumorigenesis. In this review, we discuss the potential and limitations of current cyclin-kinase inhibitors. We also summarize progress in evaluating other mitotic kinase inhibitors and novel cell-cycle kinase inhibitors as potential therapeutic agents in PC. Expert opinion: While the successful development and approval of cell-cycle inhibitors for PC therapy remains unresolved, pre-clinical identification of resistant mechanisms would help design better early- phase clinical trials where relevant combinations may be evaluated prior to Phase II testing. The authors believe that cell-cycle kinases are important anti-cancer targets that operate in collaboration with other oncogenes intimately involved in uncontrolled tumor proliferation and by providing a unique, targeted, and complimentary anti-cancer mechanism, expand the available armamentarium against PC. © 2012 Informa UK, Ltd.

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