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Potential Clue Associated with Aggressive Prostate Cancer Identified by Rutgers Investigators

Prostate cancer is one of the most common forms of cancer in men and the leading cause of cancer deaths in white, African-American and Hispanic men, according to the Centers for Disease Control. Current treatment of prostate cancer targets androgens, hormones which promote the growth and spread of cancer cells. However, it remains unclear why, despite treatment, some prostate cancers progress and may become fatal. Researchers at Robert Wood Johnson Medical School, part of Rutgers, The State University of New Jersey, who are studying the underlying mechanisms that cause invasive tumor growth have identified a key transcription factor, a protein which regulates the flow of information from DNA, that is over-produced in treatment-resistant prostate cancer, as well as the two protein kinases that trigger the process. This finding, published and highlighted on the cover of the July issue of Molecular Cancer Research, a journal of the American Association for Cancer Research (AACR) could be utilized to develop treatments for prostate cancer that is resistant to current therapies.

The research team, led by Joseph Fondell, PhD, associate professor of pharmacology, found that in clinically localized human prostate cancer — cancer that is confined to the prostate and pelvic area — the key transcription factor termed MED1 is overexpressed, meaning that significantly more MED1 is produced than is typical. According to Fondell, the finding potentially could be used as a biomarker in cancer screenings, indicating to oncologists that the prostate cancer has become aggressive. “As MED1 is a known co-activator of androgen receptors, the overexpression of MED1 is thought to facilitate alternative gene expression patterns that drive treatment-resistant cancer cell growth in the prostate,” Fondell said.

“Our study showed for the first time that MED1 expression is elevated in malignant cells of a statistically significant number of patients with clinical prostate cancer and that this overexpression correlates with an increase in cancer cell growth and invasiveness,” said Feng Jin, PhD, a former graduate student in Fondell’s lab and first author on the study. “In addition to accelerated tumor growth, our study showed that overexpression of MED1 may also be involved with inflammation of the prostate.”

Further study of the process using mouse models that mimic human prostate cancer, showed that two protein kinases, ERK and PI3K/AKT, were overactive and responsible for MED1 overproduction, ultimately accelerating the progression and spread of prostate cancer.

“Whereas the current treatment approach for prostate cancer is to prohibit androgen production and signaling, our findings indicate that MED1 could represent a novel target for new therapies that stop the process at the molecular level, before prostate cancer can progress to an advanced stage,” added Fondell, who also is a member of Rutgers Cancer Institute of New Jersey.

Study: ERK and AKT Signaling Drive MED1 Overexpression in Prostate Cancer in Association with Elevated Proliferation and Tumorigenicity [Molecular Cancer Research]

Source: Robert Wood Johnson Medical School

QIAGEN’s KRAS Companion Diagnostic for Colorectal Cancer Adopted by Clarient, a Leading U.S. Oncology Service Lab

QIAGEN N.V. (NASDAQ: QGEN; Frankfurt Prime Standard: QIA) recently announced that Clarient – a GE Healthcare Company and leading provider of cancer laboratory testing services in the United States – has adopted the use of the therascreen® KRAS RGQ PCR Kit (therascreen KRAS test) as a companion diagnostic to guide the use of Erbitux® (cetuximab) as a treatment in patients with metastatic colorectal cancer. Clarient, with a customer base of more than 2,000 pathologists, oncologists, clinical laboratories and hospitals, selected QIAGEN’s therascreen KRAS test and QIAGEN’s Rotor-Gene Q MDx instrument following the Food and Drug Administration (FDA) approval of the test in July 2012. Clarient joins a rapidly growing number of laboratories switching from laboratory-developed tests (LDTs) to the FDA-approved therascreen KRAS test for diagnostic testing for late stage colorectal cancer.

“We are very pleased to partner with Clarient, a leading laboratory with a strong reputation among pathologists, oncologists and hospitals, to offer the therascreen KRAS test. Together, we will help bring our shared vision of the value of personalized healthcare to reality and transform outcomes by delivering personalized information to guide physicians and patients in the treatment of late-stage colorectal cancer,” said Dr. Helge Lubenow, Senior Vice President, Molecular Diagnostics Business Area and member of the Executive Committee of QIAGEN. “The future of Personalized Healthcare will be shaped by standardized tests like the therascreen KRAS test, backed by scientific rigor and regulatory review. Our growing portfolio of innovative diagnostics and efficient automation platforms is making healthcare more effective, saving money for payers and improving life for patients.”

“We believe precision medicine is the new direction in diagnosing and treating cancer and Clarient uses state-of-the-art diagnostic technologies like the therascreen KRAS test to bring clarity and precision to physicians to assist them in making better treatment decisions for their patients,” said Carrie Eglinton Manner, CEO, Clarient.”Clarient’s comprehensive offering and fast turnaround time coupled with our experience with the therascreen KRAS test permits us to provide a higher level of performance. Also, the fact that it is FDA approved provides Clarient with additional assurance of its quality and reliability.”

The U.S. launch of the therascreen KRAS test system including the Rotor-Gene Q MDx instrument, approved by the FDA in July 2012, is progressing well. To drive adoption, QIAGEN supports partners like Clarient with co-marketing programs, reimbursement service, on-site validation and communication with pathologists and oncologists. For an updated list of U.S. laboratories now offering the therascreen KRAS test, please visit http://www.qiagen.com/mc/therascreenkrastest/patient/labfinder.aspx.

Approximately 110,000 metastatic colorectal cancer patients each year in the U.S. could benefit from KRAS testing, according to QIAGEN estimates. In patients for whom standalone surgery and chemotherapy are insufficient, treatment with an epidermal growth factor receptor (EGFR) inhibitor such as Erbitux has been shown to improve overall survival. However, determining the presence or absence of KRAS mutations in tumors affects outcomes. Approximately 60% of patients, whose tumors have mutation-negative (wild-type) KRAS genes, may benefit from anti-EGFR therapy. Approximately 40%, whose tumors have KRAS mutations, may not benefit.

QIAGEN’s FDA-approved therascreen KRAS test offers a fast, consistent and reliable process to determine optimal treatment for colorectal cancer patients who are candidates for EGFR-inhibitor therapy. QIAGEN’s therascreen KRAS test has been shown to have a high sensitivity (low limit of detection) for KRAS mutations, a critical factor in ensuring high-quality data for treatment decisions.

The U.S. healthcare system could save more than $600 million a year by determining KRAS status in colorectal cancer patients and avoiding unnecessary use of medicines, studies show.

QIAGEN is actively expanding its global portfolio of Personalized Healthcare technologies and intends to submit several companion diagnostics for U.S. regulatory approval. Earlier this month the Company announced submission of its therascreen® EGFR RGQ PCR Kit to the FDA as a proposed companion diagnostic to guide treatment with afatinib, a new investigational oncology compound developed by Boehringer Ingelheim. More than 15 projects are under way to co-develop and market companion diagnostics with other leading pharmaceutical and biotech companies such as Amgen, AstraZeneca, Bayer and Pfizer.

The U.S. rollout of the therascreen KRAS test builds on success in Europe, where QIAGEN offers 10 CE-marked assays based on real-time PCR technology or on Pyrosequencing. QIAGEN currently markets therascreen assays in Europe for biomarkers including KRAS, EGFR, NRAS, BRAF, PI3K, JAK2, MGMT and UGT1A1. In Japan, regulators approved the therascreen KRAS and EGFR kits in 2011, solidifying QIAGEN’s leadership in that market. QIAGEN also offers technologies for research use in the development of new medicines and companion diagnostics.

Source: Qiagen

Qiagen Submits Companion Diagnostic To Fda To Guide Treatment Decisions For New Investigational Lung Cancer Compound

QIAGEN N.V. (NASDAQ: QGEN; Frankfurt Prime Standard: QIA) recently announced submission of its therascreen® EGFR RGQ PCR Kit (therascreen EGFR test) to the U.S. Food and Drug Administration (FDA) as a proposed companion diagnostic to guide treatment with afatinib, a new investigational oncology compound developed by Boehringer Ingelheim. Afatinib has been accepted for filing and granted Priority Review by the FDA as a proposed treatment for patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) with an epidermal growth factor receptor (EGFR) mutation detected by an FDA-approved test.

Gene Mutation Identifies Colorectal Cancer Patients Who Live Longer with Aspirin Therapy, Study Finds

Aspirin therapy can extend the life of colorectal cancer patients whose tumors carry a mutation in a key gene, but has no effect on patients who lack the mutation, Dana-Farber Cancer Institute scientists report in the Oct. 25 issue of the New England Journal of Medicine.

TCGA Study Brings Ovarian Cancer Patients Closer to Personalized Medicine

In the June 30 issue of Nature, researchers from The Cancer Genome Atlas (TCGA) Research Network provide a large-scale integrative report on genetic mutations and pathways that distinguish the most common and aggressive type of ovarian cancer from other types of ovarian cancer as well as from other solid tumors. The disease is not defined by one or few cancer-driving genes but rather numerous mutations that individually occur in only a small number of cases. Given the degree of genomic disarray, the study results suggest that genomic structural variation is the driver of ovarian cancer. The findings may be helpful in guiding physicians to choose experimental treatments that are most likely to target molecular alterations effectively in patients with high-grade serous ovarian adenocarcinoma.