FDA Approves New Lung Cancer Diagnostic "Cobas EGFR Mutation Test"

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Main Category: Lung Cancer
Also Included In: Cancer / Oncology;??Medical Devices / Diagnostics
Article Date: 15 May 2013 - 2:00 PDT Current ratings for:
FDA Approves New Lung Cancer Diagnostic "Cobas EGFR Mutation Test"

The U.S. Food and Drug Administration (FDA) has approved the cobas EGFR Mutation Test, a companion diagnostic for the cancer drug Tarceva (erlotinib). This is the first FDA-approved companion diagnostic that detects epidermal growth factor receptor (EGFR) gene mutations, which are present in approximately 10 percent of non-small cell lung cancers (NSCLC).

Patients with such genetic mutations generally benefit from treatment with an anti-EGFR tyrosine kinase inhibitor, such as Roche's Tarceva (erlotinib).

The diagnostic test, manufactured by the Roche Molecular Systems in Pleasanton, California, will be used as a companion diagnostic for drug Tarceva, as a form of first-line treatment for patients with NSCLC whose cancers have spread to other parts of the body.

Tarceva (erlotinib), an oral lung cancer treatment, was officially licensed as first-line monotherapy for the treatment of patients with advanced forms of non-small cell lung cancer (NSCLC) with a certain mutation, saving them from up-front chemotherapy.

According to the National Cancer Institute, lung cancer is currently one of the leading causes of cancer-related deaths, with an anticipated 228,190 new cases of the cancer this year alone (and approximately 159,480 deaths). Each year in the U.S., lung cancer kills more individuals than prostate, colon, and breast cancers combined.

NSCLC is the most common form of lung cancer, accounting for about 85 percent of cases.

Alberto Gutierrez, Ph.D., director of the Office of In Vitro Diagnostics and Radiological Health in the FDA's Center for Devices and Radiological Health, said:

"The approval of the cobas EGFR Mutation Test will allow physicians to identify non-small cell lung cancer patients who are candidates for receiving Tarceva as first line therapy. Companion diagnostics play an important role in determining which therapies are the safest and most effective for a particular patient."

Clinical studies demonstrated the effectiveness of the cobas EGFR Mutation Test. Patients with a specific type of EGFR mutation who received Tarceva treatment lived for 10.4 months without their disease progressing, as opposed to only 5.4 months for those who were only treated with standard two-drug chemotherapy regimen.

Those with the mutation were identified with the new diagnostic test.

On April 16, 2010, the drug Tarceva was approved by the FDA for patients suffering from locally advanced or metastatic NSCLC. It was originally approved, in 2004, for the treatment of locally advanced NSCLC following the failure of a chemotherapy regiment.

Written by Joseph Nordqvist

Copyright: Medical News Today
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20 May. 2013. APA

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'FDA Approves New Lung Cancer Diagnostic "Cobas EGFR Mutation Test"'

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Inostics' Blood-Based Mutation Testing Receives CLIA Certification

Main Category: Cancer / Oncology
Also Included In: Regulatory Affairs / Drug Approvals;??Blood / Hematology
Article Date: 04 Jun 2013 - 2:00 PDT Current ratings for:
Inostics' Blood-Based Mutation Testing Receives CLIA Certification

Inostics, a molecular diagnostics company that provides blood-based mutation testing, received CLIA (Clinical Laboratory Improvement Amendments) licensure for its clinical laboratory located in Baltimore, MD. This marks a critical milestone for the clinical adoption of this non-invasive molecular approach for the analysis of tumor biomarkers.

"Due to the non-invasiveness and real-time reflection of tumor genetics, the OncoBEAM blood test represents a valuable tool to complement clinical decision making. We are extremely excited to be able to bring this solution to cancer patients as OncoBEAM tests offer a significant enhancement to clinical care over traditional tissue-based molecular testing," Dr. Frank Diehl, CSO of Inostics, said.

The OncoBEAM blood test is based on BEAMing technology which combines emulsion based digital PCR with flow cytometry. This technology enables the molecular analysis of tumor DNA shed from primary and metastatic tumors, found circulating in the blood of patients.

Due to its non-invasiveness, OncoBEAM blood tests introduce new possibilities for the management of various cancers like skin, colorectal, breast, and lung cancer. Now a simple blood draw can support clinical decision making in the context of therapy selection, assessment of drug response, resistance and recurrence monitoring, and detection of minimal residual disease (MRD).

Article adapted by Medical News Today from original press release. Source: Source: Inostics
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Splicing Process Hijacked By Oncogene Mutation To Promote Growth And Survival

Main Category: Cancer / Oncology
Also Included In: Genetics
Article Date: 04 Jun 2013 - 1:00 PDT Current ratings for:
Splicing Process Hijacked By Oncogene Mutation To Promote Growth And Survival

An international team of researchers - led by principal investigator Paul S. Mischel, MD, a member of the Ludwig Institute for Cancer Research and professor in the Department of Pathology at the University of California, San Diego School of Medicine - has found that a singular gene mutation helps brain cancer cells to not just survive, but grow tumors rapidly by altering the splicing of genes that control cellular metabolism.

The findings are published online in the journal Cell Metabolism.

Mischel, who heads the Ludwig Institute's molecular pathology laboratory based at UC San Diego, and colleagues focused upon a process called alternative splicing, in which a single gene encodes for multiple proteins by including or excluding different, specific regions of DNA.

Alternative splicing is a tightly regulated and normal activity in healthy cells. For Mischel and colleagues in Los Angeles, Ohio and Japan, the question was whether mutations of a gene called EGFRvIII caused differential alternative splicing in glioblastoma multiformes (GBMs), the most common and aggressive type of malignant brain tumor. Median survival after GBM diagnosis is just 15 months with standard-of care radiation and chemotherapy. Without treatment, it is less than five months.

The scientists were particularly interested in whether the EGFRvIII mutation induced alternative splicing events that resulted in deregulation of normal cellular metabolism. "We focused on the 'Warburg Effect,' a common metabolic derangement in cancer that enables tumor cells to metabolize glucose in a way that provides both a sufficient supply of energy and a source of building blocks that can be used for growth," Mischel said.

They discovered a complex but compelling series of consequential events: The EGFRvIII mutation controls expression of a splicing factor called HNRNPA1, which initiates an alternatively spliced form of a regulatory protein called Max. The alternative form is called Delta Max.

Max is associated with MYC, a gene that drives tumor growth and the Warburg Effect in cancer. "Unlike the regular form of Max," said Mischel, "Delta Max actually enhances c-MYC activity, specifically by promoting the glycolytic phenotype of the tumor cells." In other words, the EGFRvIII mutation and subsequent alternative splicing commandeer the cell's metabolic machinery in a way that lets it take up and use glucose to promote rapid tumor growth.

Mischel noted that the findings are specific to the EGFRvIII mutation and GBMs. It's not known whether other oncogenes are able to exploit alternative splicing in similar fashion.

The findings, according to Mischel, provide two clear insights. First, they highlight the central role of EGFRvIII in GBM pathogenesis and its critical role in altering cellular metabolism in tumors. Second, they show that oncogenes can regulate cell metabolism through alternative splicing, which may provide a new set of targets for oncogene-specific drug development.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our cancer / oncology section for the latest news on this subject. Co-authors are Ivan Babic, Kenta Masui and Beatrice Gini, Ludwig Institute for Cancer Research, UCSD; Erik S. Anderson, Department of Microbiology, Immunology and Molecular Genetics, UCLA; Kazuhiro Tanaka, Department of Neurosurgery, Kobe University, Japan; Deliang Guo, Department of Radiation Oncology, Ohio State University Medical Center; Bing Li and Siavash K. Kurdistani, Department of Biological Chemistry, UCLA; Shaojun Zhu, David Nathanson and Rui Li, Carolina Espindola Camacho and Heather R. Christofk, Department of Molecular and Medical Pharmacology, UCLA; Yuchao Gu, Ludwig Institute for Cancer Research, UCSD and Department of Molecular and Medical Pharmacology, UCLA; Genaro R. Villa, Ludwig Institute for Cancer Research, UCSD and Department of Molecular and Medical Pharmacology, UCLA; David Akhavan, Department of Molecular and Medical Pharmacology, UCLA; Sergey Mareninov, Department of Pathology and Laboratory Medicine, UCLA; Ascia Eskin and Stanley F. Nelson, Department of Human genetics, David Geffen School of Medicine, UCLA; William H. Yong, Department of Pathology and Laboratory Medicine, UCLA; Webster K. Cavenee, Ludwig Institute for Cancer Research, UCSD and UCSD Moores Cancer Center; Timothy F. Cloughesy, Department of Neurology, David Geffen School of Medicine, UCLA; and Douglas L. Black, Howard Hughes Medical Institute and Department of Microbiology, Immunology and Molecular Genetics, UCLA.

Funding for this research came, in part, from National Institutes of Health grants CA119347, NS73831, R01 GM084317 and P01 CA95616, the Ben and Catherine Ivy Foundation, Art of the Brain Fund, Accelerate brain Cancer Cure, the Fred Miller Family, the John W. Carson Foundation, the Ziering Family Foundation, the Henry Singleton Brain Cancer Fund and National Cancer Institute grant P30CA23100.

University of California - San Diego

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Screening Radiation Exposure May Increase Breast Cancer Risk in Some BRCA Mutation Carriers

Radiation exposure from x-rays, mammograms, and other diagnostic tests prior to age 30 may increase the risk of breast cancer in women who carry BRCA1 or BRCA2 mutations, according to the results of a large, retrospective cohort study published in the British Medical Journal. ?

Inherited mutations in two genes—BRCA1 and BRCA2—have been found to greatly increase the lifetime risk of developing breast and ovarian cancer. Mutations in these genes can be passed down through either the mother’s or the father’s side of the family.?

A mammogram is an X-ray of the breast. Screening mammography is performed in a woman without breast symptoms in order to detect breast cancer at an early stage when it is most easily treated. Currently, mammography is the most reliable tool for screening the general population for breast cancer and may even reduce the risk of death from breast cancer (due to early detection). Mammograms are most often used in women over the age of 40; however, women who carry BRCA mutations are considered high-risk and may benefit from earlier and more frequent screening. This earlier screening can come with the added risk of increased radiation exposure—and exposure to ionizing radiation, especially when it occurs at an early age, is an established risk factor for breast cancer.? ?

To examine the relationship between radiation exposure and breast cancer risk among BRCA1/2 mutation carriers, researchers from Europe followed nearly 2,000 women over age 18 with a BRCA1 or BRCA2 mutation. The women reported their history of procedures—such as x-rays or mammograms—that involved radiation to the chest or shoulders. The researchers then used this information to estimate the cumulative dose of radiation to the breast for each woman and compared this against confirmed breast cancer diagnoses among the women. ?

When compared with no exposure, any exposure to chest radiation prior to age 30 was associated with almost double the risk of breast cancer in BRCA1/2 mutation carriers. Exposure prior to age 20 was associated with a 62 percent increased risk. Women who received the highest doses or radiation prior to age 30 had almost four times the increased risk. In contrast, there was no evidence of an increased risk of breast cancer associated with exposure after age 30. ?

The researchers concluded that exposure to diagnostic radiation before age 30 among carriers of BRCA1/2 mutations was associated with an increased risk of breast cancer. What’s more—the increased risk of breast cancer was observed at radiation doses considerably lower than those associated with an increased risk among other populations. ?

Because women with BRCA1/2 mutations have an increased risk of developing breast cancer, some guidelines recommend earlier screening; however, the results of this study may indicate that BRCA1/2 carriers under age 30 might benefit from surveillance that uses non-ionizing radiation imaging, such as magnetic resonance imaging (MRI).?

Reference:?

Pijpe A, Andrieu N, Easton DF, et al. Exposure to diagnostic radiation and risk of breast cancer among carriers of BRCA1/2 mutations: retrospective cohort study (GENE-RAD-RISK). British Medical Journal. 2012; 2012;345:e5660?

Posted October 2, 2012

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A BRCA Gene Mutation in the Family Does Not Increase Cancer Risk for Those Without the Mutation

For women who do not have a BRCA1 or BRCA2 gene mutation, having a close relative with one of these mutations does not increase breast cancer risk. These results were published in the Journal of Clinical Oncology.?

Inherited mutations in two genes—BRCA1 and BRCA2—have been found to greatly increase the lifetime risk of developing breast and ovarian cancer. Mutations in these genes can be passed down through either the mother’s or the father’s side of the family.????

Women who test negative for a BRCA gene mutation—but who have family members with a mutation—are generally thought to have a risk of breast cancer that’s similar to that of women in the general population. A study published in 2007, however, raised concerns that relatives of BRCA mutation carriers may have a substantially increased risk of breast cancer even if they test negative for their family’s mutation.[1]?

To further explore cancer risk among close relatives of people with BRCA mutations, researchers conducted a study among more than 3,000 families with at least one case of breast cancer; 160 families had a BRCA1 mutation and 132 families had a BRCA2 mutation.[2]?

For women without a BRCA mutation, breast cancer risk was similar whether or not the woman’s family had a BRCA mutation. These results suggest that coming from a family with a BRCA1 or BRCA2 gene mutation does not increase cancer risk for those who test negative for the mutation.?????

Although this is reassuring news, women who test negative for their family’s gene mutation should continue to follow cancer screening guidelines. These women do not have the very elevated cancer risk that their affected relatives have, but they can still get cancer.???

References:?

Posted November 9, 2011

[1] Smith A, Moran A, Boyd MC et al. Phenocopies in BRCA1 and BRCA2 families: evidence for modifier genes and implications for screening. Journal of Medical Genetics. 2007;44:10-15.?

[2] Kurian AW, Gong GD, John EM et al. Breast cancer risk for noncarriers of family-specific BRCA1 and BRCA2 mutations: findings from the Breast Cancer Family Study. Journal of Clinical Oncology. Early online publication October 31, 2011.?

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