Tuesday, October 4, 2011
HPV which is responsible for cervical cancer now appear to be responsible for throat cancer. A Research team tested tumor samples from 271 patients with throat cancer diagnosed from 1984 to 2004. The Human papilloma virus was found in only 16% of the samples that were from the 1980s and increased to 72% of the samples collected during 2000s.
The researchers estimated that over all, throat cancers caused by the virus have increased to 2.6 per 100,000 people in 2004 from 0.8 cases per 100,000 people in 1988. If the trend continues, by 2020 the virus will be causing more throat cancer than cervical cancer, the study concluded.
There are two vaccines Gardasil and Cervarix, targetting HPV Type 16 and other strains of the HPV but they are only for girls, to protect them from cervical cancer. Now doctors say it might be a good idea to administer the vaccines to boys as well.
See th editorial doi: 10.1200/JCO.2011.37.8893; listen to the podcast by Dr Gillison at www.jco.org/podcast
Monday, October 3, 2011
BURLINGTON, N.C.-Laboratory Corporation of America® Holdings (LabCorp®) (NYSE: LH) announced today the nationwide availability of a new FDA-approved companion diagnostic for lung cancer patients.
The drug XALKORI®, available from Pfizer, and Abbott Molecular’s Vysis ALK Break Apart FISH Probe companion diagnostic test were simultaneously approved by the FDA on August 26, 2011 for use in patients with advanced ALK-positive non-small cell lung cancer (NSCLC). The Vysis ALK Break Apart FISH Probe test detects all ALK gene rearrangements and is the only available diagnostic assay that has been clinically validated to predict response to the targeted therapy XALKORI. An estimated 6,500-11,000 individual will develop advanced ALK-positive NSCLC in the United States in 2011.
“2011 has been an important year for personalized medicine,” indicated Dr. Mark Brecher, LabCorp's Chief Medical Officer. “The recent approval of XALKORI for NSCLC and its companion test demonstrates how laboratory diagnostics will play an even larger role in cancer care, assisting physicians in administering the treatments best suited to the disease.”
Approximately 3% to 5% of NSCLC tumors are characterized by genetic rearrangements in a gene called ALK. The ALK gene encodes a key cell signaling protein, and when altered by a rearrangement that combines ALK with other gene sequences, the pathway becomes constitutively active and drives cell proliferation and uncontrolled growth. The drug XALKORI inhibits the mutant ALK protein, and thereby diminishes the ability of the cancer cells to grow and divide. There is limited efficacy data in patients that lack the ALK rearrangement and a clinically validated companion diagnostic is essential for identifying which patients will benefit from therapy. The new FDA-approved Vysis ALK Break Apart FISH Probe Kit for XALKORI detects a specific rearrangement in the ALK gene using a technique called fluorescence in-situ hybridization (FISH). The Vysis ALK Break Apart FISH Probe Kit has been optimized only for identifying and quantifying rearrangements of the ALK gene from formalin-fixed, paraffin-embedded human NSCLC tissue specimens.
LabCorp’s Center for Molecular Biology and Pathology (CMBP), was instrumental in the studies supporting the approval of this new companion diagnostic. CMBP collaborated with Abbott Molecular in the analytical validation of the ALK companion diagnostic. LabCorp’s Esoterix Clinical Trials Services provided testing for tumor samples in these studies that supported FDA approval.
The Vysis ALK Break Apart FISH Probe test is now available for patient testing nation-wide through LabCorp.
Laboratory Corporation of America® Holdings, an S&P 500 company, is a pioneer in commercializing new diagnostic technologies and the first in its industry to embrace genomic testing. With annual revenues of $5.0 billion in 2010, over 31,000 employees worldwide, and more than 220,000 clients, LabCorp offers a broad test menu ranging from routine blood analyses to reproductive genetics to DNA sequencing. LabCorp furthers its scientific expertise and innovative clinical testing technology with its Centers of Excellence: The Center for Molecular Biology and Pathology, National Genetics Institute, ViroMed Laboratories, Inc., The Center for Esoteric Testing, Litholink Corporation, Genzyme GeneticsSM*, DIANON Systems, Inc., US LABS, Monogram Biosciences, Inc., and Esoterix and its Colorado Coagulation, Endocrine Sciences, and Cytometry Associates laboratories. LabCorp conducts clinical trials testing through its Esoterix Clinical Trials Services division. LabCorp clients include physicians, government agencies, managed care organizations, hospitals, clinical labs, and pharmaceutical companies. To learn more about our organization, visit our Web site at: www.labcorp.com.
*Genzyme Genetics and its logo are trademarks of Genzyme Corporation and used by Esoterix Genetic Laboratories, LLC, a wholly-owned subsidiary of LabCorp, under license. Esoterix Genetic Laboratories and LabCorp are operated independently from Genzyme Corporation.
XALKORI is a trademark of Pfizer.
This press release contains forward-looking statements. Each of the forward-looking statements is subject to change based on various important factors, including without limitation, competitive actions in the marketplace and adverse actions of governmental and other third-party payors. Actual results could differ materially from those suggested by these forward-looking statements. Further information on potential factors that could affect LabCorp’s financial results is included in the Company’s Form 10-K for the year ended December 31, 2010, and subsequent SEC filings.
Monday, September 12, 2011
Two doses of the Cervarix vaccine for human papilloma virus (HPV) is as effective as multiple dozes.
Thursday, September 8, 2011
Kimio Yonesaka, MD, PhD, formerly of Dana-Farber and now at Kinki University School of Medicine, in Osaka, Japan, together with other scientists including Pasi Jänne, MD, PhD, of Dana-Farber , have discovered a pair of backup circuits in cancer cells that enable the cells to bypass the effect of a widely used cancer drug cetuximab, an antibody that interferes with cancer cell growth by blocking a structure known as the epidermal growth factor receptor (EGFR).
Their research found out that interfering the said backup circuits ERBB2 with targeted therapies may heighten or restore the cetuximab’s potency. The paper covering the study is published in the Sept. 7 issue of Science Translational Medicine.
"ERBB2 activates a critical signaling pathway that is not normally blocked by cetuximab, and in this way subverts cetuximab’s function, Because ERBB2 isn’t affected by cetuximab, this is an easy way for cancers to become resistant to the drug."" says Jänne, the study's co-senior author with Kazuhiko Nakagawa, MD, PhD, of Kinki University.
"We hope the findings of our study will inspire the development of clinical trials aimed at overcoming cetuximab resistance, We've identified biomarkers that can be used to select cetuximab-resistant patients who may benefit from a combination of cetuximab and ERBB2 inhibitors."" Yonesaka remarks.
Abstract from Science Translational Medicine.
Cetuximab, an antibody directed against the epidermal growth factor receptor, is an effective clinical therapy for patients with colorectal, head and neck, and non–small cell lung cancer, particularly for those with KRAS and BRAF wild-type cancers. Treatment in all patients is limited eventually by the development of acquired resistance, but little is known about the underlying mechanism. Here, we show that activation of ERBB2 signaling in cell lines, either through ERBB2 amplification or through heregulin up-regulation, leads to persistent extracellular signal–regulated kinase 1/2 signaling and consequently to cetuximab resistance. Inhibition of ERBB2 or disruption of ERBB2/ERBB3 heterodimerization restores cetuximab sensitivity in vitro and in vivo. A subset of colorectal cancer patients who exhibit either de novo or acquired resistance to cetuximab-based therapy has ERBB2 amplification or high levels of circulating heregulin. Collectively, these findings identify two distinct resistance mechanisms, both of which promote aberrant ERBB2 signaling, that mediate cetuximab resistance. Moreover, these results suggest that ERBB2 inhibitors, in combination with cetuximab, represent a rational therapeutic strategy that should be assessed in patients with cetuximab-resistant cancers.
Dana-Farber Press Release;
September 07, 2011 Scientists at Dana-Farber Cancer Institute and colleagues overseas have discovered a pair of backup circuits in cancer cells that enable the cells to dodge the effect of a widely used cancer drug. Jamming those circuits with targeted therapies may heighten or restore the drug’s potency, according to a study published in the Sept. 7 issue of Science Translational Medicine.cetuximab (From NCI Drug Dictionary)The research focused on the drug cetuximab, an antibody that interferes with cancer cell growth by blocking a structure known as the epidermal growth factor receptor (EGFR). Cetuximab is effective in many patients with colorectal cancer or squamous cell cancer of the head and neck, but the benefits rarely last longer than a year, and some patients receive no benefit from the drug.Until now, scientists haven't known why cancers that initially respond to cetuximab become resistant to it, or how to overcome such resistance.
In the new study, researchers led by Pasi Jänne, MD, PhD, of Dana-Farber and Kimio Yonesaka, MD, PhD, formerly of Dana-Farber and now at Kinki University School of Medicine, in Osaka, Japan, found that in some cetuximab-resistant cancer cells, a protein known as ERBB2 was actively sending "grow" signals, circumventing the "stop growing" signals triggered by cetuximab. The researchers discovered that ERBB2's activity sprang from an oversupply of the protein’s parent gene, Her2/neu, or by a related protein, ERBB3, when prompted by high levels of the protein heregulin. In both cases, the new growth messages are unaffected by cetuximab."ERBB2 activates a critical signaling pathway that is not normally blocked by cetuximab, and in this way subverts cetuximab’s function," says Jänne, the study's co-senior author with Kazuhiko Nakagawa, MD, PhD, of Kinki University. "Because ERBB2 isn’t affected by cetuximab, this is an easy way for cancers to become resistant to the drug."
The findings suggest that combining cetuximab with ERBB2-inhibiting drugs could be an effective therapy for cancers that are cetuximab-resistant from the start or for those that become resistant over time, the study authors say. Several such inhibitors have already been approved, while others are undergoing clinical study."We hope the findings of our study will inspire the development of clinical trials aimed at overcoming cetuximab resistance," Yonesaka remarks. "We've identified biomarkers that can be used to select cetuximab-resistant patients who may benefit from a combination of cetuximab and ERBB2 inhibitors."Jänne estimates that up to 40 percent of colorectal cancers are cetuximab-resistant when first diagnosed. He notes that although the ERBB2 pathway may be responsible for many cases of cetuximab resistance, there are undoubtedly other pathways, yet to be discovered, that play a similar role. Further research is needed to confirm ERBB2's role in cetuximab resistance and to develop strategies for testing ERBB2 inhibitors and cetuximab in clinical trials.Funding for the study was provided by grants from the National Institutes of Health, the American Cancer Society, the William Randolph Hearst Foundation, and the Hazel and Samuel Bellin research fund.Co-authors of the paper include Kreshnik Zejnullahu, Dalia Ercan, Andrew Rogers, Juliet Philips, MS, Jason Sun, Takafumi Okabe, MD, PhD, Jeffrey Swanson, MD, and Ramesh Shivdasani, MD, PhD, Dana-Farber; Isamu Okamoto, MD, PhD, Taroh Satoh, MD, Masayuki Takeda, MD, PhD, Yasuhito Fujisaka, MD, Toshio Shimizu, MD, PhD, Osamu Maenishi, Hiroyuki Itoh, MD, Kiyotaka Okuno, MD, Minoru Takada, MD, Masahiro Fukuoka, MD, and Kazuto Nishio, MD, PhD, Kinki University, Osaka, Japan; Federico Cappuzzo, MD, Massimo Roncalli, MD, and Annarita Destro, PhD, Instituto Clinico Humanitas, Rozzano, Italy; John Souglakos, MD, PhD, University of Crete, Heraklion, Greece; Yonggon Cho, and Marileila Varella-Garcia, University of Colorado Cancer Center, Denver; Koichi Taira, MD, and Koji Takeda, MD, Osaka City General Hospital, Japan; and Eugene Lifshits and Jeffrey Engelman, MD, PhD, Massachusetts General Hospital.
A recombinant, chimeric monoclonal antibody directed against the epidermal growth factor (EGFR) with antineoplastic activity. Cetuximab binds to the extracellular domain of the EGFR, thereby preventing the activation and subsequent dimerization of the receptor; the decrease in receptor activation and dimerization may result in an inhibition in signal transduction and anti-proliferative effects. This agent may inhibit EGFR-dependent primary tumor growth and metastasis. EGFR is overexpressed on the cell surfaces of various solid tumors. Check for active clinical trials or closed clinical trials using this agent. (NCI Thesaurus)
|Synonyms:||Anti-EGFR Monoclonal Antibody|
Anti-Epidermal Growth Factor Receptor Monoclonal Antibody
C225 monoclonal antibody
Chimeric Anti-EGFR Monoclonal Antibody
Chimeric Monoclonal Antibody C225
Immunoglobulin G1, anti-(human epidermal growth factor receptor) (human-mouse monoclonal C225 gamma1-chain), disulfide with human-mouse monoclonal C225 kappa-chain, dimer
monoclonal antibody C225
|US brand name:||Erbitux|
|Abbreviations:||Chimeric MoAb C225|
Wednesday, August 24, 2011
Now, a Cornell-led study identifies for the first time the mechanisms by which p53 controls cell movement and invasion into other areas of the body.
Using cultures of ovarian surface epithelium cells, where ovarian cancer originates, the researchers found that when they inactivated the p53 gene, the cells began to move and invade the underlying gelatinous protein mixture used in the lab that resembles an extracellular tissue environment.
"People thought that cell motility and invasion were part of later stages of cancer, but we show that this characteristic can be found in cells at the very beginning of cancer formation," said Chang-Il Hwang, lead author of the paper recently published in the Proceedings of the National Academy of Sciences and a graduate student in the lab of Cornell biomedical sciences professor and senior author Alexander Nikitin.
Under normal circumstances, p53 regulates the expression of a receptor protein called MET. But when p53 mutates, MET overexpresses, leading to cell movement and invasive growth. The researchers found two distinct pathways by which p53 regulates and suppresses MET.
"One of the next steps is to study ways to inhibit MET," said Hwang. "Our findings support the idea that suppression of MET could be a particularly reasonable and effective approach to controlling cancer carrying p53 mutations. We hope our findings can be generalized into other types of cancer as well."
In tests, the researchers found the p53 and MET network were consistent in both lung and colon cancer.
Mutations of p53 take many forms, with the most common mutation affecting one of the pathways that regulates MET but not the other pathway. By understanding how different p53 mutations affect each of the two pathways, researchers may one day develop individualized cancer therapies by suppressing MET, said Hwang.
"Different p53 mutations may affect the cancer from different angles," he added.
The study was funded by the National Institutes of Health, the Marsha Rivkin Center for Ovarian Cancer, Cornell's College of Veterinary Medicine and the Ovarian Cancer Research Fund.
Wednesday, August 10, 2011
FDA Rejection Of Exelbine For Treating Non-small Cell Lung Cancer Affects ADVENTRX Pharmaceuticals Share Prices
Conference Call and Webcast
ADVENTRX will hold a conference call on Wednesday, August 10, 2011 beginning at 8:30 a.m. Eastern time to review the developments discussed in this news release and answer questions. Individuals interested in listening to the conference call may do so by dialing (800) 860-2442 for domestic callers, (412) 858-4600 for international callers and requesting the ADVENTRX Pharmaceuticals Update Call, or, from the webcast on the investor relations section of the Company's Web site at www.adventrx.com. A telephone replay will be available for five days approximately one hour after the conclusion of the call by dialing (877) 344-7529 for domestic callers, or (412) 317-0088 for international callers, and entering conference number 10003222. The webcast will be available on the Company's Web site for 30 days following the completion of the call.
Friday, August 5, 2011
These findings were only possible due to the advancement of science and technology.
"The team used whole genome sequencing technology so that no genes would be excluded, and we found to our surprise that one gene, on chromosome 19, was mutated in six out of the seven initial tumor specimens we sequenced,A mutation frequency of 85 percent is very high." said Hai Yan, MD, PhD, Duke associate professor of pathology and co-corresponding author of the study.
Press release by John Hopkins (the Press release by Duke University is here);
Release Date: 08/04/2011
--Findings reveal cause of the tumors
Johns Hopkins Kimmel Cancer Center scientists have completed a comprehensive map of genetic mutations occurring in the second-most common form of brain cancer, oligodendroglioma. The findings, reported in the Aug. 4 issue of Science, also appear to reveal the biological cause of the tumors, they say.
To create the map, the scientists sequenced protein-coding genes in seven oligodendroglioma tissue samples, and focused attention on recurring mutations in two genes not previously associated with these tumors – CIC and FUBP1. The investigators say that CIC and FUBP1 are known to regulate cell-signaling processes, and CIC mutations have been rarely linked to sarcoma, breast and prostate cancers.
More mutations in the two genes were found in an additional 27 oligodendroglioma samples. In all, two-thirds of the samples studied had CIC and FUBP1 mutations.
“Whenever we find genes mutated in a majority of tumors, it is likely that the pathway regulated by that gene is critical for the development and biology of the tumor,” says Nickolas Papadopoulos, Ph.D., associate professor of oncology at the Johns Hopkins Kimmel Cancer Center.
In brain cancer, the Johns Hopkins investigators say CIC and FUBP1 mutations may be the “missing link” in what scientists describe as a “two-hit” theory of cancer development. The theory is based on the fact that each cell in the human body has two copies of 23 chromosomes containing thousands of protein-producing genes. If a gene on one chromosome is damaged or deleted, the other copy makes up for the loss of protein. But if the second copy fails as well, the cell cannot make the proper protein and may become cancerous.
In oligodendrogliomas, the “first hit” has long been known to occur in regions of chromosome 1 and 19, which fuse together resulting in a loss of many genes on both chromosomes. Up to 70 percent of oligodendroglioma patients have these DNA fusions, and most of them respond better to chemotherapy and radiation than those who lack the deletions in the chromosomes. For more than a decade, researchers have been looking for evidence of a “second hit” in specific mutated genes that allow oligodendrogliomas to develop.
In the current study, the Johns Hopkins investigators found mutations in the remaining copies of the CIC and FUBP1 genes on chromosomes 1 and 19, suggesting that these mutations represent the second hit needed to create cancer.
“Thanks to the Human Genome Project and advances in cancer genome sequencing, a single study can now resolve decade-old questions and reveal the genetics of this brain cancer,” says Kenneth Kinzler, Ph.D., professor and co-director of the Ludwig Center at Johns Hopkins. “Knowing the genetic roadmap of a cancer is the key to attacking it.”
Oligodendrogliomas account for up to 20 percent of brain cancers and more commonly occur in younger people aged 30 to 45. The cancer forms most often in the frontal lobe of the brain in cells that coat neurons. Median survival of 10 years is considered far better than other brain cancers. Oligodendrogliomas are treated initially with surgery, followed by chemotherapy and radiation.
The research team says its next step will be to test whether patients with CIC and FUBP1 mutations have the same favorable prognosis as those who have the chromosome 1 and 19 fusion, says Chetan Bettegowda, M.D., Ph.D., chief resident in the Department of Neurosurgery at Johns Hopkins.
“We can focus now on when these mutations develop during tumor formation, whether they can guide prognosis, and how they might form targets for therapy,” says Bettegowda.
Bettegowda says the gene map uncovered mutations in other genes, such as PIK3CA, which have been well-studied in cancer. It is possible, he says, that oligodendroglioma patients with mutations in PIK3CA or other genes could be enrolled in current clinical trials using experimental therapies that target these mutations.
Funding for the research was provided by the Virginia and D.K. Ludwig Fund for Cancer Research, the Pediatric Brain Tumor Foundation, the Duke Comprehensive Cancer Center Core, the Burroughs Wellcome Fund, the James S. McDonnell Foundation, state funding from Sao Paulo (FAPESP), the National Cancer Institute and National Institutes of Health.
Contributors to the research include Nishant Agrawal, Yuchen Jiao, Mark Sausen, Laura D. Wood, Ralph H. Hruban, Fausto J. Rodriguez, Daniel P. Cahill, Gregory Riggins, Victor Velculescu and Bert Vogelstein of Johns Hopkins; Roger McLendon, Darell Bigner and Hai Yan of Duke University; and Sueli Mieko Oba-Shinjo and Suely Kazue Nagahashi Marie of the University of Sao Paulo, Brazil.
Under agreements between the Johns Hopkins University, Genzyme, Exact Sciences, Inostics, Qiagen, Invitrogen and Personal Genome Diagnostics, Papadopoulos, Vogelstein, Kinzler and Velculescu are entitled to a share of the royalties received by the university on sales of products related to genes and technologies described in this manuscript. Papadopoulos, Vogelstein, Kinzler, and Velculescu are co-founders of Inostics and Personal Genome Diagnostics, are members of their Scientific Advisory Boards, and own Inostics and Personal Genome Diagnostics stock, which is subject to certain restrictions under Johns Hopkins University policy.
Monday, August 1, 2011
If you ever wondered where all the money you donated to Stand Up To Cancer go. Please watch the above video. And if you have not donated yet or want to learn more about Stand Up To Cancer PI3K Pathway, follow the link below.
"Rarely do you see responses with investigational drugs in phase one but with these compounds some very dramatic responses are being seen." - Dr. Lewis C. Cantley SU2C PI3K Dream Team Leader
SU2C, Stand Up To Cancer
Wednesday, July 13, 2011
Sarilumab Succeeds In Treating Rheumatoid Arthritis But Fails In Addressing Ankylosing Spondylitis in Phase 2b Trial
Sarilumab Succeeded in treating Rheumatoid Arthritis but failed in addressing Ankylosing Spondylitis, a long-term disease that causes inflammation of the joints between the spinal bones, and the joints between the spine and pelvis in Phase 2b Trial.
"Following these encouraging Phase 2b results in rheumatoid arthritis, the companies are currently discussing the dose(s) of sarilumab to advance into the Phase 3 portion of the MOBILITY trial," said Elias Zerhouni, President, Global Research & Development, Sanofi.
Further details about the MOBILITY trial are available at http://clinicaltrials.gov/ct2/results?term=SAR+153191+mobility.
Friday, July 8, 2011
Asbestosis, or scarring of the lungs that makes it hard to breathe
Mesothelioma, a rare cancer that affects the lining of the lungs or abdomen
Lung diseases associated with asbestos usually develop over many years. Smoking cigarettes increases the risk.
Exposure to asbestos may increase the risk of asbestosis, other nonmalignant lung and pleural disorders, lung cancer, mesothelioma, and other cancers.
Smokers who are also exposed to asbestos have a greatly increased risk of lung cancer.
Individuals who have been exposed (or suspect they have been exposed) to asbestos on the job, through the environment, or at home through a family contact should inform their physician and report any symptoms.
Government agencies can provide additional information on asbestos exposure.
Learn more at National Cancer Institute
Thursday, June 16, 2011
Wednesday, June 8, 2011
Learn first-hand how oncologists are using Cisco TelePresence to:
•Review patient cases with top specialists irrespective of
distance or location
•Accelerate discussions about treatment options and facilitate
•Enable immersive, high-quality consultations
If your organization is looking for a better way to enable clinician collaboration beyond your hospital’s four walls, or you want to learn how oncologists employ video conferencing together with data sharing, this is one session you don’t want to miss. You can register at Cisco by following the link below.