The Role Of HER2 Overexpression In Cancers

Its locus is particularly amplified in these noted tumours leading to the progression of these cancers, it can be suppressed by p53 (tumour/ proliferation suppressor) which represses the EZH2 promoter, resulting inhibition of cell proliferation and invasion (Bracken, 2003; Xiao, 2011).

Optimal management of NSCLC now requires that tumours be screened for a certain range of predictive and prognostic biomarkers that help to predict sensitivity to targeted therapy and estimate prognosis respectively . For NSCLC, much of the work in the past years has been focussed on mutations of the epidermal growth factor receptor (EGFR) and on the abnormal fusion of the anaplastic lymphoma kinase (ALK) being inhibited successfully with EGFR tyrosine kinase inhibitors (TKI) and crizotinib respectively. Targeted agents are now being rationally designed to inhibit particular mutations leading to a more streamlined clinical trial process. In this review, we will examine the major subtypes of driver mutations that have been identified in NSCLC and relevant targeted therapies available both now, and in the foreseeable future.

Results showed that VeriStrat® testing was able to identify a group of patients who have worse progression free survival (PFS) when treated with Femara alone, independent of Her2 status.

Breast Cancer is a type of cancer where in the breast cells growth are uncontrolled. To enhance our understanding of breast cancer, knowing how any cancer can develop is crucial. Cancer develops as a result of the alteration of the genes, or abnormal changes in the genes accountable for managing the growth of the cells and maintaining their health. In each nucleus, the genes operates as the “control room.” The cells in our bodies replace themselves through a process called cell growth in which the

The aim of this report is to provide primary evidence which supports and explains the reasons why Herceptin is used in the treatment of HER2+ cancers.

CDK7 inhibition was a highly selective and potent means to disrupt expression of a key cluster of genes. This study demonstrates that inhibition of transcription is an effective strategy to target highly aggressive breast cancers such as TNBC with high genetic heterogeneity and lacking obvious ‘driver’ oncogenes. Further studies will be required to determine whether these observations will translate to clinical treatment of

In vitro: Co-treatment with BEZ235 (10 μM) enhanced the tumor cell-killing effect of olaparib in BRCA1-negative breast cancer cells [4]. BEZ235 (25 - 800 nM) significantly inhibited the proliferation of HER2-postive gastric cancer cells and induced

Ceritinib is a potent inhibitor of anaplastic lymphoma kinase (ALK), a tyrosine kinase involved in the pathogenesis of nonsmall cell lung cancer (NSCLC). ALK gene abnormalities due to mutations or translocations may result in expression of oncogenic fusion proteins, that alter signaling, and expression and result in increased cellular proliferation and survival in tumors. The primary mechanism of

To hear you have breast cancer can be a very shocking thing. “Besides skin cancer, breast cancer is the most common cancer diagnosed among women in America as of 2015” (breastcancer,2015). First step is to know what you are dealing with when your doctor believes you have cancer, you will want to know what cancer is and how your doctor can detect it. Next your doctor will go over different stages of breast cancer that will help come to a conclusion on your next step. Lastly you and your doctor will go over the different treatment plan that best fits you. This journey a women or man will take when being diagnosed with cancer is a long and hard one but, with the help from your doctors and the knowledge you can get through this.

Nusrat Epsi, MBA is a PhD student working at the Rutgers University, School of Healthcare Professional with Dr. Antonina Mitrafanova. Prior to beginning the PhD program, Nusrat worked in the Pharmaceutical Industry. She consulted on a variety of projects which involved both qualitative and quantitative analysis to achieve strategic realignments within large pharmaceutical systems. From this work she developed an interest in drug discovery and drug structure. She is currently working on designing possible targeted cancer therapy to interfere with specific AR genes for tumor growth and progression. She also had a primary interest in the invasion of bladder cancer. She is also interested studying other Hormonal carcinogenesis. For her doctoral

Eotaxin-2, also called MPIF2 & Ckb6, is a novel CC chemokine produced by activated monocytes and T lymphocytes. Eotaxin-2 can selectively chemoattract cells expressing CCR3 including basophils, eosinophils, Th2 T cells, mast cells, as well as certain subgroups of dendritic cells. In addition, Eotaxin-2 is able to inhibit the proliferation of multipotential hematopoietic progenitor cells. The mature protein of Eotaxin-2 consists of 78 amino acids (92 amino acids for the mouse homolog, without C-terminal truncation). Eotaxin-2 is encoded by the CCL24 gene. This gene is located on human chromosome 7 in humans.

Herceptin works by binding to the extra HER2 receptors on the cell, so that hormones cannot bind and produce signals to divide. In the absence of Herceptin, HER2 receptors undergo dimerisation (the pairing of receptors), however, in the presence of Herceptin, trastuzumab interferes with dimerisation and inhibits HER2 activation by blocking downstream signalling to inhibit division of cells, see figure 1 (Vu & Claret, 2012). As an antibody, one of the

Cancer is one of the leading causes of death worldwide as it can develop in almost any organ or tissue. Significant advances in understanding the cellular basis of cancer and the underlying biological mechanisms of tumour has been vastly improved in the recent years (Jiang et al. 1994). Cancer is a genetic disease which requires a series of mutation during mitosis to develop, its characteristics can be associated with their ability to grow and divide abnormal cells uncontrollable while in the mean time invade and cause nearby blood vessels to serve its need. Even though many people are affected by cancer today, the abilities which cancer cells have make it hard to find a single effective treatment for cancer. The focus of research now lies

Cancer is the uncontrollable division and growth of abnormal cells resulting in formation of an aggressive tumour. In some forms of Breast cancer, the cells proliferate uncontrollably due to over-expression of the protein HER2 (Human Epidermal Growth Factor Receptor 2); a receptor embedded within the membrane of cells, allowing for the transfer of signals outside to inside the cell. Trastuzumab is a monoclonal antibody administered through intravenous infusion, to be taken on its own or in combination with one or more chemotherapy regimens. It reduces risk of the cancer reoccurring or spreading by inhibiting the effects of HER2, and enhancing the body’s immune system.

Background: The pathological response to trastuzumab-based neoadjuvant therapy (TNT) has an important prognostic role, but is extremely variable among patients and still not fully understood. Although, previous studies have supported the correlation between TNT response and both HER2 amplification and immunohistochemistry (IHC), as yet reliable predictive factors of TNT response are missing. Therefore, this study aims to identify the contribution of different clinico-pathological features to TNT pathologic response in a consecutive series of HER2-positive BCs based on frontline dual-color HER2 FISH.