172ptriple Negative Breast Cancer: Clinicopathologic Characteristics and Fatty Acid Synthase (fasn) Expression as a Potential Target.

نویسندگان

  • F Holguin Flores
  • G Vinas
  • G Oliveras
  • A Giro-Perafita
  • F Perez-Bueno
  • A Roque
  • J Brunet
  • T Puig
چکیده

Aim: Triple negative breast cancer (TNBC) is defined by the lack of estrogen and progesterone receptors expression and the absence of human epidermal growth factor receptor 2 amplification. TNBC has specific clinical/pathological features and molecular biology. The absence of effective targeted therapies requires new biomarkers to develop therapeutic strategies. FASN, the sole mammalian enzyme capable of de novo fatty acid synthesis, is highly expressed in several carcinomas. FASN is associated with poor prognosis and its inhibition is selectively cytotoxic to breast cancer cells. Therefore, lipogenesis mediated by FASN represents a potential target. The aim of our study was to evaluate the clinical and histopathologic features of a large population of TNBC patients and to analyze FASN expression in vitro and in vivo.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Fatty acid synthase is a primary target of MiR-15a and MiR-16-1 in breast cancer

Fatty acid synthase (FASN) is upregulated in breast cancer and correlates with poor prognosis. FASN contributes to mammary oncogenesis and serves as a bona fide target in cancer therapies. MicroRNAs inhibit gene expression through blocking mRNA translation or promoting mRNA degradation by targeting their 3'-UTRs. We identified four microRNAs in two microRNA clusters miR-15a-16-1 and miR-497-195...

متن کامل

A new mechanism of drug resistance in breast cancer cells: fatty acid synthase overexpression-mediated palmitate overproduction.

Multidrug resistance is a major problem in successful cancer chemotherapy. Various mechanisms of resistance, such as ABC transporter-mediated drug efflux, have been discovered using established model cancer cell lines. While characterizing a drug-resistant breast cancer cell line, MCF7/AdVp3000, we found that fatty acid synthase (FASN) is overexpressed. In this study, we showed that ectopic ove...

متن کامل

Preclinical Evaluation of Fatty Acid Synthase and EGFR Inhibition in Triple-Negative Breast Cancer.

PURPOSE Triple-negative breast cancer (TNBC) lacks an approved targeted therapy. Despite initial good response to chemotherapy, 30% of the patients relapse within 5 years after treatment. EGFR overexpression is a common marker in TNBC, and its expression has been correlated with poor outcome. Inhibition of fatty acid synthase (FASN) activity leads to apoptosis of human carcinoma cells overexpre...

متن کامل

Targeting FASN in Breast Cancer and the Discovery of Promising Inhibitors from Natural Products Derived from Traditional Chinese Medicine

Molecular targeted therapy has been developed for cancer chemoprevention and treatment. Cancer cells process a fundamental change in its bioenergetic metabolism from normal cells on an altered lipid metabolism, also known as the de novo fatty acid synthesis, for sustaining their high proliferation rates. Fatty acid synthesis is now associated with clinically aggressive tumor behavior and tumor ...

متن کامل

The metastasis inducer CCN1 (CYR61) activates the fatty acid synthase (FASN)-driven lipogenic phenotype in breast cancer cells

The angiogenic inducer CCN1 (Cysteine-rich 61, CYR61) is differentially activated in metastatic breast carcinomas. However, little is known about the precise mechanisms that underlie the pro-metastatic actions of CCN1. Here, we investigated the impact of CCN1 expression on fatty acid synthase (FASN), a metabolic oncogene thought to provide cancer cells with proliferative and survival advantages...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:
  • Annals of oncology : official journal of the European Society for Medical Oncology

دوره 25 suppl_4  شماره 

صفحات  -

تاریخ انتشار 2014