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Petrylak D.P.,Yale Cancer Center
American Journal of Managed Care | Year: 2013

Prostate cancer (PrCa) is the most common cancer found among men in the United States, and is the second-leading cause of death for these individuals. Although most patients with prostate cancer experience disease control after primary therapy, approximately 20% to 40% of these patients will eventually encounter recurrent disease. While androgen deprivation therapy may achieve temporary tumor control or regression in the majority of patients with advanced disease, virtually all patients with metastatic disease will experience progressive PrCa. Consequently, their disease may no longer respond to primary androgen blockade and may then spread to distant sites, most commonly to the bones and/or regional lymph nodes. This state of disease, termed castration-resistant prostate cancer (CRPC), is heterogeneous, has a variety of clinical symptoms which may include biochemical progression, progression in bone, or soft tissue, and may present with or without symptoms from cancer. While treatments were previously somewhat limited, there has been a substantial increase in the understanding of the biological and genetic basis for PrCa progression. The mechanisms of androgen independence in CRPC include, but are not limited to, autocrine production of androgen by the prostate cancer cell, as well as androgen receptor activity despite low testosterone levels, through a variety of different mechanisms. These findings have led to more targeted therapies for CRPC, improved clinical outcomes, and increased survival. Further understanding of the mechanisms that cause castration resistance potentially could improve therapeutic efficacy. Source

Strout M.P.,Yale Cancer Center
Blood | Year: 2015

In this issue of Blood, complementary studies by Amin et al and Linley et al demonstrate that sugar moieties linked to surface immunoglobulin (sIg) of follicular lymphoma (FL) cells directly interact with endogenous lectins within the lymphoma niche and lead to activation of downstream B-cell receptor (BCR) signaling pathways. In addition to providing further insight into the role of the microenvironment in lymphomagenesis, these findings expose a unique molecular interaction that may represent a viable target for therapeutic intervention.1,2. © 2015 by The American Society of Hematology. Source

Mehnert J.M.,Cancer Institute of New Jersey | Kluger H.M.,Yale Cancer Center
Current Oncology Reports | Year: 2012

The identification of somatic driver mutations in human samples has allowed for the development of a molecular classification for melanoma. Recent breakthroughs in the treatment of metastatic melanoma have arisen as a result of these significant new insights into the molecular biology of the disease, particularly the development of inhibitors of activating BRAFV600E mutations. In this article the roles of several mutations known to be involved in the malignant transformation of melanocytes are reviewed including BRAF, PTEN, NRAS, ckit, and p16 as well as some of the emerging mutations in cutaneous and uveal melanoma. The bench to bedside collaborations that resulted in these discoveries are summarized, and potential therapeutic strategies to target driver mutations in specific patient subsets are discussed. © Springer Science+Business Media, LLC 2012. Source

Petrylak D.P.,Yale Cancer Center
American Journal of Managed Care | Year: 2013

Castration-resistant prostate cancer (CRPC) has historically presented significant challenges to both clinicians and patients in regard to disease progression and consequent management. The first advances in the treatment of this state of prostate cancer with docetaxel chemotherapy demonstrated a survival benefit over the palliative standard of care, mitoxantrone combined with prednisone. The recognition that these patients still maintained active androgen receptor access identified new therapeutic agents for CRPC that aimed to further deplete testosterone levels or directly interact with the androgen receptor (ie, enzalutamide). Other therapeutic targets that have established efficacy in randomized phase 3 trials include bone metastases (ie, radium 223 dichloride), the immune system (ie, sipuleucel-T), and tubulin (ie, cabazitaxel). These new and evolving agents are positioned to substantially alter the therapeutic environment for CRPC and to improve patient outcomes and quality of life. Source

Foss F.M.,Yale Cancer Center
Seminars in Hematology | Year: 2010

The National Comprehensive Cancer Network (NCCN) practice guidelines for peripheral T-cell lymphoma (PTCL) accentuate the lack of standard treatment options for this disease. Outcomes with conventional therapies, many of which are borrowed from B-cell lymphoma, are poor. Strategies to enhance existing approaches include creating a new platform for first-line therapy and adding novel agents, such as denileukin diftitox, to existing chemotherapy platforms. Furthermore, to improve outcomes, patients must reach transplant through effective first-line therapies. Additionally, treatment should be individualized based on histopathologic subtype, as all PTCL patients will not respond to the same treatment regimen. © 2010. Source

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