Cancer is not just one disease. It is a group of more than 100 different and distinctive diseases. Bringing together data, related to cancer, in an organized manner, is the task of ONCOWIKIA.

Wednesday, December 29, 2010

Pazopanib (Votrient) Approved By The National Institute for Health and Clinical Excellence (NICE) For Treatment Of Advanced Renal Cell Carcinoma

The National Institute for Health and Clinical Excellence (NICE) is recommending Pazopanib (Votrient) as a first-line treatment option for people with advanced renal cell carcinoma (RCC) who have not previously received cytokine therapy and who are of Eastern Cooperative Oncology Group (ECOG) performance status 0-1, on the basis that GSK provided that an agreed patient access scheme agreed. The patient access scheme will offer straight discount of 12.5% (which will bring the price in par with Sunitinib) and makes provision for a possible partial rebate to the NHS in the future. The rebate  is conditional upon the outcome of a head-to-head trial with current standard of care treatment sunitinib (Sutent).
The study, COMPARZ, which started in 2008 will end in May 2011 and the results will be out in Mid 2012.
Usually NICE recommendations are accepted by UK National Health Service and this time NICE has recommended that NHS takes the deal.

Votrient is a type of medicine called a tyrosine kinase inhibitor (TKI) and it has been shown to effectively slow down the progression of advanced RCC whilst maintaining QoL compared with placebo; a significant consideration for patients at an advanced stage of disease.2,3 Votrient has an acceptable and manageable toxicity profile. The most frequent adverse events related to Votrient treatment were diarrhoea, hair colour change, hypertension, nausea, anorexia and increased liver enzymes.

Advanced RCC is an aggressive form of kidney cancer with a poor prognosis, due in part to its resistance to chemotherapy, radiotherapy and hormone therapy. Over 8,000 people in the UK are diagnosed with kidney cancer each year and around one third show signs of advanced RCC at the time of diagnosis.7-9 The introduction of targeted cancer therapies has transformed the management of advanced RCC. However, despite improvements in efficacy, side effects observed with available treatments to date can affect patients’ quality of life and their ability to carry out normal daily activities.12-17 This was acknowledged by the NICE Appraisal Committee in their evaluation of evidence from the patient experts and clinicians. With only one targeted treatment option (sunitinib) recommended by NICE as a first-line treatment until now,18 the NICE recommendation of Votrient will offer patients and clinicians a choice of effective treatment options with different side-effect profiles.

NICE statement

Saturday, December 18, 2010

Tumor-Specific Imaging Through Progression Elevated Gene- 3 Promoter, (PEG-Prom) Driven Gene Expression

PEG-Prom mediated reporter expression systems
Researchers may be a step closer to improving the detection of metastatic tumors in an organism — in real time — using a noninvasive approach that pairs an imaging agent with a genetic element that only expresses itself when it is in cancer cells.

The work, a collaborative effort between Virginia Commonwealth University and Johns Hopkins University, could lead to improved and earlier detection of tumors and metastases in patients and allow clinicians to monitor the cancer's response to therapy. The research builds upon a genetic element previously discovered and characterized by a VCU researcher Paul B. Fisher, M.Ph., Ph.D.

In the new study, published online in the December issue of the journal Nature Medicine, VCU researchers, together with researchers from the Johns Hopkins Medical Institutions, have shown how the genetic element, known as progression elevated gene-3 promoter, or PEG-Prom, can be used to image metastases in multiple animal models of human melanoma and human breast metastasis. The system can be used to measure gene expression, protein interaction or track gene-tagged cells in vivo. This approach offers significant advantages in sensitivity and accuracy over currently used imaging strategies.

PEG-Prom, which has been shown to have unique cancer specificity, was originally cloned in Fisher’s laboratory during his time at Columbia University. Fisher is VCU’s principal investigator on the study, and the first incumbent of the Thelma Newmeyer Corman Endowed Chair in Cancer Research with the VCU Massey Cancer Center.

“The PEG-Prom is the unique aspect of this innovative imaging approach. It is a cancer-specific region of the PEG-3 gene that selectively expresses when in cancer cells. It has minimal expression in normal tissue or animals without cancer,” said Fisher, who also is professor and chair of the Department of Human and Molecular Genetics, and director of the VCU Institute of Molecular Medicine in the VCU School of Medicine.

“This new, non-invasive imaging approach will allow researchers to test chemoprevention strategies and to use repeat applications to follow the course of therapy over time and more accurately define therapeutic outcome and response to therapy than using current methodologies,” he said.

“The potential for this approach to translate into a more effective mode of imaging in humans is extremely high. The benefits to patients would be enormous. One could diagnose tumor formation and cancer that has spread earlier and therefore allow testing of effective therapies. When combined with a therapeutic agent — a radiation emitting compound, a chemotherapeutic agent, or a cytokine such as mda-7/IL-24 — it could in the future permit both imaging and therapy of cancers and metastases (“theranostics”),” Fisher said.

According to Fisher, specific aspects of this technology are patented or in the process of being patented.

This work was supported by grants from the Society of Nuclear Medicine and the Korea Science and Engineering Foundation Fellowship Program, the National Institutes of Health and the National Foundation for Cancer Research.

The senior author was Martin G. Pomper, M.D., Ph.D., professor at Johns Hopkins Medical Institutions. The bulk of the studies described in this paper represent a long-term collaboration between research programs directed by Pomper at Johns Hopkins Medical Institutions and Fisher. The studies were performed by Carrie Bhang, Ph.D., a postdoctoral research scientist in Pomper’s laboratory.

EDITOR’S NOTE: A copy of the study is available for reporters by email request from
Virginia Commonwealth University
VCU researcher Paul B. Fisher, M.Ph., Ph.D.

Sathya Achia Abraham
VCU Communications and Public Relations
(804) 827-0890

Molecular-genetic imaging is advancing from a valuable preclinical tool to a guide for patient management. The strategy involves pairing an imaging reporter gene with a complementary imaging agent in a system that can be used to measure gene expression or protein interaction or track gene-tagged cells in vivo. Tissue-specific promoters can be used to delineate gene expression in certain tissues, particularly when coupled with an appropriate amplification mechanism. Here we show that the progression elevated gene-3 (PEG-3) promoter, derived from a rodent gene mediating tumor progression and metastatic phenotypes, can be used to drive imaging reporters selectively to enable detection of micrometastatic disease in mouse models of human melanoma and breast cancer using bioluminescence and radionuclide-based molecular imaging techniques. Because of its strong promoter activity, tumor specificity and capacity for clinical translation, PEG-3 promoter–driven gene expression may represent a practical, new system for facilitating cancer imaging and therapy.

Thursday, December 9, 2010

Aromasin, Arimidex and Femera, Breast Cancer Drugs Increase The Risk Of Heart Diseases.

Breast-cancer drug Aromasin from Pfizer Inc.,  and similar drugs from (Arimidex) AstraZeneca Plc and (Femara) Novartis AG seem to be making women prone to heart diseases. Women taking these drugs are 26 percent more likely to develop heart disease than an older therapy, a study presented today at the San Antonio Breast Cancer Symposium in Texas, found.  All these drugs belong to a family of treatments known as aromatase inhibitors and these halts the production of estrogen, which fuels cancer growth.
Tamoxifen a generic alternative, in use since 1977, proved to be better alternative during the same study.
“It appears that aromatase inhibitors have a significant increase in cardiotoxic side effects, such as heart attack, angina and heart failure, Switching drugs may reduce the side effects.” said Eitan Amir, a senior fellow in oncology and hematology at the Princess Margaret Hospital in Toronto, in a statement. 
via Bloomberg

Monday, December 6, 2010

Scientists Test Histone-modification Antibody Quality.

Scientists all over the world have been busy figuring out how DNA is packaged in cells, because a stretched out DNA strand would be as long as sic feet. But it fits nicely packaged inside a nucleus of one of our cells.   The packaging comprise an amino acid molecule called a histone, mostly and influences the on and off switches of different genes that regulate cellular function and play a role in human diseases ranging from cancer to genetic disorders.

Scientists study histones by using antibodies to specific “flavors” of histones that are only very slightly different from one another. The antibodies help to pinpoint what DNA is being packaged by a certain kind of “flavor” of histone, and how that affects gene regulation. Different flavors affect genes differently.

In a paper published today in the journal Nature Structural and Molecular Biology, Jason Lieb, PhD and his colleagues from across the country describe how they tested more than 200 antibodies against 57 histone  flavors in three different organisms, using three different tests commonly used in this kind of genetic analysis.  They found that about 25 percent of antibodies currently sold have a problem with specificity – targeting the anticipated histone – in a given test.  They believe that this proportion is likely to remain steady over time.

“And this is where it gets complicated, many companies make these antibodies that we scientists use in our labs – but there are so many different kinds of histones and types of tests we do that it’s just not feasible for the companies to anticipate every single way that a given antibody can be used. Histones are essentially the key to the DNA library.  They tell you which ‘shelves’ of that library – or areas of the genome – are open or closed to information moving in and out.  But since the differences between the different ‘flavors’ of histones are often extremely small, and it’s likely that an antibody may react with more than one histone or in different ways depending on the type of test being used in the lab.  It makes scientific precision very difficult. So we thought, OK, we need to help ourselves as scientists.  We set up a web-based searchable database at  Our results are there and other scientists can also post their results so that we have a self-sustaining, up-to-date source of information that is really important to scientists working to understand a broad range of genetic phenomena,” says Jason Lieb, PhD, ho is a professor of biology at the University of North Carolina at Chapel Hill and member of UNC Lineberger Comprehensive Cancer Center, and who led the project testing common antibodies.
The research was funded by the National Human Genome Research Institute (part of the United States National Institutes of Health) and included researchers from the Universities of California at Santa Cruz, Berkeley, and San Diego, the Lawrence Berkeley National Laboratory, the Ludwig Institute for Cancer Research, Harvard Medical School, the University of Cambridge (UK), Washington University in St. Louis, Ontario Institute for Cancer Research (Canada) and Rutgers University.
UNC Press Release

Monday, November 29, 2010

Clinical Staging For Prostate Cancer May Not Be Effective

A widely used Pinchot CS test aiding the prediction of outcome of most prostate cancer by doctors and patients seems to be worthless according to a new study by a group of researchers which was published in the journal CANCER..
CS is called “clinical stage” since it does not involve the findings of pathologic examination, which is usually the result of microscopic evaluation.
According to the results of research,
Clinical stage was assigned incorrectly in 1370 of 3875 men (35.4%). Errors more commonly resulted in patient downstaging than upstaging (55.1% vs 44.9%; P < .001). Patients with TRUS lesions were more likely to be staged incorrectly than those with abnormal DRE findings (65.8% vs 38.2%; P < .001). Biopsy laterality was found to strongly influence stage assignment. Even after correction of staging errors, there was no association noted between clinical stage and biochemical disease recurrence after radical prostatectomy. 
The researchers conclude that;
Errors in applying clinical staging criteria for localized prostate cancer are common. TRUS findings are frequently disregarded, and practitioners incorrectly incorporate biopsy results when assigning stage. However, staging errors do not appear to account for the inconsistent reliability of clinical stage in predicting prostate cancer outcomes. These findings further challenge the utility of a DRE‐based and/or TRUS‐based staging system for risk assessment of localized prostate cancer.Cancer 2010. © 2010 American Cancer Society.
The complete study is published online ahead of the print edition of the journal Cancer.

Monday, November 22, 2010

Cancer Care In The Developing World, A Pod Cast.

Of all the cancers deaths, as much as three-quarters of the deaths occur in developing countries. These places severely lack the resources needed to prevent, diagnose and treat cancer. As a result WHO and the International Atomic Energy Agency (IAEA) have created a Joint Programme on Cancer Control focusing on the needs of developing countries.
Following is the WHO Podcast by Veronica Riemer where she looks at cancer care in the developing world. She speaks with Dr Margaret Chan, WHO's Director-General, who explains what the IAEA brings to this program and others:
Listen to this episode - duration 07:37 min [mp3 4.4Mb] 

Saturday, November 20, 2010

A significant reduction in tumor volumes when different regimens of systemic PI-103 delivery are combined with NSC-derived S-TRAIL

The resistance of glioma cells to a number of anti-tumor agents and the highly invasive nature of glioma cells that escape the primary tumor mass are key impediments to the eradication of tumors in glioma patients. In this study, we evaluated the therapeutic efficacy of a novel PI3-kinase/mTOR inhibitor, PI-103, in established glioma lines and primary CD133+ glioma initiating cells and explored the potential of combining PI-103 with stem cell delivered secretable tumor necrosis factor apoptosis inducing ligand (S-TRAIL) both in vitro and in orthotopic mouse models of gliomas. We show that PI-103 inhibits proliferation and invasion, causes G0-G1 arrest in cell cycle, and results in significant attenuation of orthotopic tumor growth in vivo. Establishing co-cultures of neural stem cells (NSCs) and glioma cells, we show that PI-103 augments the response of glioma cells to stem cell delivered S-TRAIL. Using bi-modal optical imaging, we show that when different regimens of systemic PI-103 delivery are combined with NSC-derived S-TRAIL, a significant reduction in tumor volumes is observed compared to PI-103 treatment alone. To our knowledge this is the first study that reveals the anti-tumor effect of PI-103 in intracranial gliomas. Our findings offer a preclinical rationale for application of novel stem cell-based apoptotic therapies to improve treatment of malignant gliomas.


Friday, November 19, 2010

Amgen's XGEVA™ (denosumab), Gets FDA Approval for Fractures in Cancer Treatment

THOUSAND OAKS, Calif., (Nov. 18, 2010) /PRNewswire/ — Amgen Inc. (NASDAQ: AMGN) today announced that the U.S. Food and Drug Administration (FDA) has approved XGEVA™ (denosumab), the first and only RANK Ligand inhibitor for the prevention of skeletal-related events (SREs) in patients with bone metastases from solid tumors. XGEVA was approved following a 6 month priority review by the FDA, a designation reserved for drugs that offer major advances in treatment or provide a treatment where no adequate therapy exists. XGEVA is not indicated for the prevention of SREs in patients with multiple myeloma.
“Today’s approval of XGEVA illustrates what is possible when scientific innovation, commitment and investment come together to advance medicine,” said Kevin Sharer, chairman and chief executive officer of Amgen. “A diagnosis of bone metastases is a major event for patients living with cancer, and the consequences can be devastating. We are pleased to offer this new advance to patients and their healthcare providers.”
Bone metastases, the spread of cancer to the bones, are a serious concern for patients with advanced cancer and present a considerable burden to the healthcare system. Weakened bones due to metastases can lead to fractures and compression of the spinal cord and necessitate procedures like major surgery and radiation, designed to prevent or manage bone complications. The primary goal of treatment for bone metastases is to prevent the occurrence of debilitating and costly bone complications, which can disrupt a patient’s life and cause disability, pain and hospitalization.
“As many as 3 out of 4 patients with advanced prostate, lung, and breast cancer will experience spread to their bones. Despite the availability of current treatments, a significant proportion of these patients still experience bone complications or are not candidates for existing treatment,” said David H. Henry, M.D., clinical professor of medicine, and vice chair, Department of Medicine, Pennsylvania Hospital, University of Pennsylvania Healthcare System. “Based on the compelling science and robust clinical evidence seen with XGEVA, I expect this new option to quickly become a mainstay of cancer care and to play an important role in reducing the incidence of debilitating bone complications in patients with advanced cancer.”
The RANK Ligand pathway, first discovered by Amgen scientists in the mid-1990s, is believed to play a central role in cancer-induced bone destruction, regardless of cancer type. XGEVA is a fully human monoclonal antibody that binds to RANK Ligand, a protein essential for the formation, function and survival of osteoclasts (the cells that break down bone). XGEVA prevents RANK Ligand from activating its receptor, RANK on the surface of osteoclasts, thereby decreasing bone destruction.

XGEVA Clinical Trial Experience

The FDA approval of XGEVA is based on the results of three pivotal, Phase 3 head-to-head trials that evaluated XGEVA delivered every four weeks as a 120 mg subcutaneous injection versus Zometa® (zoledronic acid) delivered every four weeks via a 15-minute intravenous infusion, adjusted for kidney function per the labeled instructions. The clinical program for XGEVA spanned more than 50 tumor types in over 5,700 patients. In the Phase 3 trials, XGEVA demonstrated a clinically meaningful improvement in preventing SREs compared to Zometa. Specifically, in patients with breast or prostate cancer and bone metastases, XGEVA was superior to Zometa in reducing the risk of SREs. In patients with bone metastasis due to other solid tumors or bone lesions due to multiple myeloma, XGEVA was noninferior (trending towards superiority) to Zometa in reducing the risk of SREs. Superiority was also seen in the integrated analysis of the Phase 3 studies.
Overall rates of adverse events and serious adverse events were generally similar between XGEVA and Zometa. Osteonecrosis of the jaw (ONJ) was infrequent, with no statistically significant difference between treatment arms. Hypocalcemia was more frequent in the XGEVA arm. Overall survival and progression-free survival were similar between arms in all three trials.
“As many as 70 percent of patients with prostate cancer that have metastasized to the bone are not currently receiving therapy to prevent complications from these bone metastases. This may be secondary to urologists lacking comfort or facilities to provide infusion treatment,” said Neal D. Shore, M.D., FACS, medical director, Carolina Urologic Research Center. “XGEVA could provide increased treatment care options and accessibility for urologist’s who treat advanced prostate cancer; as XGEVA is administered as a subcutaneous injection on a monthly basis. Also, XGEVA does not require dose adjustment for changes in renal function.”


The total economic burden of patients with bone metastases in the U.S. alone estimated to be $12.6 billion annually.i Patients who experience an SRE as a result of bone metastases incur significantly higher medical costs compared with those who do not experience such events.ii iii iv In addition, once patients experience an SRE, the risk of a subsequent SRE is increased. The costs of SREs vary by type and severity, ranging from relatively low costs for minor fractures to high cost events like spinal cord compression associated with hospitalization. Studies have shown that the costs of treating SREs are a significant cost burden.
XGEVA is an innovative therapy that significantly reduces debilitating and costly SREs. This can result in cost offsets due to the reduced incidence of SREs and related medical costs. XGEVA will cost $1,650 monthly based on wholesale acquisition cost.


Amgen is committed to supporting patient access to important medicines through innovative programs including our newly established commercial co-pay program for XGEVA, financial support to independent third party co-pay foundations, and the Safety Net Foundation, which provides free products to uninsured patients who qualify. The XGEVA FIRST STEP™ Coupon Program is a landmark program among oncology commercial co-pay programs, as it is the first program under the medical benefit with no income eligibility requirement. The program is intended to provide assistance to eligible patients who need help meeting their deductible, co-insurance, and/or co-payment requirements under the medical benefit for XGEVA. Under this program, eligible patients will incur no out of pocket costs for their initial XGEVA injection and pay a maximum of $25 for subsequent injections.

XGEVA Regulatory Status

Amgen has also submitted marketing applications for XGEVA in the European Union, Australia, Canada and Switzerland. In Japan, Amgen is working with its licensing partner, Daiichi-Sankyo Company, Limited and a marketing application was submitted in August.

XGEVA Important Safety Information

XGEVA can cause severe hypocalcemia. Correct pre-existing hypocalcemia prior to XGEVA treatment. Monitor calcium levels and administer calcium, magnesium, and vitamin D as necessary. Advise patients to contact a healthcare professional for symptoms of hypocalcemia.
Osteonecrosis of the jaw can occur in patients receiving XGEVA. Patients who are suspected of having or who develop ONJ while on XGEVA should receive care by a dentist or an oral surgeon. In these patients, extensive dental surgery to treat ONJ may exacerbate the condition.
The most common adverse reactions in patients receiving XGEVA were fatigue/asthenia, hypophosphatemia, and nausea. The most common serious adverse reaction in patients receiving XGEVA was dyspnea. The most common adverse reactions resulting in discontinuation of XGEVA were osteonecrosis and hypocalcemia. Please visit for full prescribing information.
Denosumab is also marketed as Prolia™ in other indications.

Bone Metastases and SREs: Prevalence and Impact

Bone metastases occur in more than 1.5 million patients with cancer worldwide and are most commonly associated with cancers of the prostate, lung, and breast, with incidence rates as high as 75 percent of patients with metastatic disease.v
Approximately 50-70 percent of cancer patients with bone metastases will experience debilitating vii viii Events considered to be SREs include fractures, spinal cord compression, and severe bone pain that may require surgery or radiation.ix Such events can profoundly disrupt a patient’s life and can cause disability and pain.x xi xii

Denosumab and Amgen's Research in Bone Biology

The denosumab development program demonstrates Amgen's commitment to researching and delivering pioneering medicines to patients with unmet medical needs. Amgen is studying denosumab in numerous tumor types across the spectrum of cancer-related bone diseases. Over 11,000 patients have been enrolled in the denosumab oncology clinical trials. In addition to this newly approved indication, XGEVA is also being investigated for its potential to delay bone metastases in prostate and breast cancer.

Saturday, November 13, 2010

Medicare Open Enrollment Open From November 15 To December 31 2010

Every Year Medicare in the fall, offers new prescription drug and health plan coverage choices and everyone is encouraged to review their plans.
This year the open enrollment is open from November 15 to December 31st 2010. This year there are many differences offered with the new health care law, there are new benefits available including lower prescription costs, wellness check-ups, and additional preventive care services. has many resources to help you with choices during this Open Enrollment.
Follow the links after the jump (video) for resources to help you with Medicare Open Enrollment.

Where do I start?
How do I choose a Medicare plan?
How can I save money on my medical and drug costs?
How does the new health care law affect my Medicare?
Where can I get personalized help?

Thursday, November 11, 2010

Triple-Negative Breast Cancer A Review On Current Concepts.

Tripple Negative Breast Cancer appeared on PubMed, (A medical document archive) somewhere in 2006 and since then it has grown to be about 600 articles. This also shows the interest by oncologists, pathologists, and geneticists, and certainly by the approximately 12 to 17% of women with breast cancer who have triple-negative breast cancer. Triple breast cancer is generally diagnosed based upon the presence, or lack of, three "receptors" known to fuel most breast cancers: estrogen receptors, progesterone receptors and human epidermal growth factor receptor 2 (HER2). The most successful treatments for breast cancer target these receptors.
A triple negative breast cancer diagnosis means that the offending tumor is estrogen receptor-negative, progesterone receptor-negative and HER2-negative, thus giving rise to the name established as "triple negative breast cancer."
There is a Foundation, TNBF (Tripple Negative Breast Cancer Foundation) which  is devoted to finding targeted treatment for triple negative breast cancer. You too can help them as well as download PDF of the Guide to Understanding Triple Negative Breast Cancer,
A team of experts, including Dr. Foulkes at the Program in Cancer Genetics, Departments of Oncology and Human Genetics, Gerald Bronfman Centre for Clinical Research in Oncology, McGill University, have written an article on current concepts on Tripple Negative Breast Cancer with concluded with the following conclusion.
The article is available at NEJM, New England Journal of Medicine and from McGill University.
Histologic and Immunohistochemical
Features of Triple-Negative and Core Basallike
Breast Cancers.
Taken in their entirety, triple-negative and basal like breast cancers show aggressive clinical behavior, but a subgroup of these cancers is markedly sensitive to chemotherapy and is associated with a good prognosis when treated with conventional chemotherapy regimens. Furthermore, some triple-negative and basal-like cancers may harbor a dysfunctional BRCA1 pathway and thus may be sensitive to agents such as platinum salts and inhibitors of the PARP enzyme that selectively target cells deficient in homologous recombination DNA repair. It seems very likely that neither triple-negative nor basal-like breast cancers are single entities but rather are a collection of different diseases. Hence, studies that address the molecular underpinning of this heterogeneity and attempt to identify the drivers of therapeutically relevant subgroups of triple-negative and basal-like breast cancers are warranted.
A diagnosis of triple-negative disease has currently important implications for the choice of systemic therapies. Given the lack of an internationally accepted definition of basal-like breast cancer, it is not surprising that this diagnosis has no clinical implications — especially since a substantive portion of these cancers may be ER-positive or may over express HER2. It could be argued that instead of identifying descriptive and prognostic molecular subgroups (e.g., basal-like and claudin-low) within the triple-negative group, it would be more clinically relevant to identify those patients whose triple-negative tumors are sensitive to specific chemotherapy agents (or combinations thereof) and targeted therapies. The expressions “triple-negative” and “basal-like” are essentially operational rather than diagnostic. In time, they will probably be replaced by other, more specific terminology.

Novartis Discontinues Investigational Lung Cancer Drug Vadimezan (ASA404) Development.

Novartis announced that it has halted late-stage development of a new drug for lung cancer, Vadimezan (ASA404) citing Interim results from Phase III trial showed that the drug failed to meet primary endpoint of extending survival for the second-line treatment of non-small cell lung cancer.
Novartis had licensed the drug also known as vadimezan from Britain's Antisoma PLC in 2007.

Following is the press release from Novartis;

Basel, November 11, 2010 - Novartis announced today that the clinical trial program for the investigational cancer treatment ASA404 (vadimezan) will be discontinued and resources will be reallocated to other compounds in the oncology pipeline. The decision was made after interim results from a Phase III trial showed that ASA404 would not likely meet the primary endpoint of significantly extending overall survival when used in combination with chemotherapy for the second-line treatment of patients with advanced non-small cell lung cancer (NSCLC).

The study, called ATTRACT-2 (Antivascular Targeted Therapy: Researching ASA404 in Cancer Treatment), included patients with advanced (stage IIIb/IV) NSCLC of squamous or nonsquamous histology who experienced disease progression on or following an initial chemotherapy regimen. The trial has been stopped early based on a recommendation from an independent data monitoring committee. Investigators involved in the study and regulatory agencies have been notified of the decision to stop the trial. Novartis does not plan to proceed with regulatory filings based on these data.

An intangible asset impairment charge of approximately USD 120 million will be taken in the fourth quarter of 2010 in the Novartis Pharmaceuticals division.

About ASA404
ASA404 (vadimezan) is a tumor-vascular disrupting agent (tumor-VDA). Novartis signed an exclusive licensing agreement with Antisoma plc for the worldwide rights to ASA404 in April 2007. In March 2010, ASA404 also failed to meet the primary endpoint in the ATTRACT-1 trial, which evaluated ASA404 in combination with paclitaxel and carboplatin as first-line treatment for advanced (stage IIIb/IV) NSCLC of squamous or nonsquamous histology. 

Wednesday, November 10, 2010

Cancer Research Matters, Because It Saves Lives.

Each year cancer kill more people globally than HIV, TB and Malaria Combined. Watch the Video for fact-filled accomplishments and possibilities of cancer research or Oncology Research.

Tuesday, November 9, 2010

Tumor Suppression Protein p53 and TRF2, Telomere-capping Complex Shelterin Exchange Positive Feedback During Telomere-damage Signalling and Cellular Senescence

NCI scientists have linked p53, a protein that can suppress tumor formation and influence cellular aging, with TRF2, a protein that forms a complex that protects the ends of chromosomes from undergoing erosion. The ends of chromosomes are known as telomeres, and these end-pieces have been shown to influence cell longevity as well as cancer.  While activated p53 can be an indicator of DNA damage due to telomere malfunction, this study is the first to show that p53 also functions by negatively regulating the telomere-binding protein TRF2, thus suggesting the presence of a novel feedback loop. The study, lead by Curtis C. Harris, M.D., with coworkers Kaori Fujita, Ph.D., and Izumi Horikawa, M.D., of the Laboratory of Human Carcinogenesis, Center for Cancer Research, appeared online in Nature Cell Biology on Nov. 7, 2010.
Telomeres are capped at each end to protect them from degrading and from being recognized as damaged DNA. At the end of their lifespan, telomeres lose this protection and DNA-damage signaling pathways are triggered that activate p53. Harris and his team found that p53 controls TRF2 levels, through an intermediary component known as Siah-1. In this experiment, TRF2 was found to be repressed and Siah-1 was induced in normal human tissue cells when p53 was activated. The scientists also found that p53 affects DNA damage signaling from uncapped telomeres, as well as regulating the telomere-capping complex. This suggests that the p53-Siah-1-TRF2 pathway plays an integral part in orchestrating the DNA damage response of telomeres. Both p53 and telomeres have therapeutic significance in cancer. This discovery, therefore, provides not only a new mechanistic insight into p53- and telomere-based cancer therapeutics currently used or tested, but also the experimental basis for the development of new therapies, according to the scientists.

Nature Cell Biology  via

Monday, November 8, 2010

Annual Spiral Computed Tomography (CT) Screening Can Detect Lung Cancer That Is Curable.

An Annual screening using spiral computed tomography (CT) may aid people with stage 1 lung cancer according to findings by a team of researchers. They set out to find the outcome among patients with clinical stage I cancer that is detected on annual screening using spiral computed tomography (CT) as it is is unknown previously.

The team study set in a large collaborative study, screened 31,567 asymptomatic persons at risk for lung cancer using low-dose CT from 1993 through 2005, and from 1994 through 2005, 27,456 repeated screenings were performed 7 to 18 months after the previous screening.
The team estimated the 10-year lung-cancer–specific survival rate among participants with clinical stage I lung cancer that was detected on CT screening and diagnosed by biopsy, regardless of the type of treatment received.
Screening resulted in a diagnosis of lung cancer in 484 participants. Of these participants, 412 (85%) had clinical stage I lung cancer, and the estimated 10-year survival rate was 88% in this subgroup (95% confidence interval [CI], 84 to 91).
Those among those who underwent surgical resection of clinical stage I cancer within 1 month, had a survival rate of 92% (95% CI, 88 to 95).he 8 participants with clinical stage I cancer who did not receive treatment died within 5 years after diagnosis.
New England Journal of Medicine (PDF)

Contrast-enhanced CT angiography provides 3D datasets with excellent isotropic spatial resolution (sub-millimeter with current multidetector scanners) in very short scanning times. The lung parenchyma can be simultaneously evaluated and electrocardiographic gating allows for the study of cardiac function. 
On the other hand, CT offers only limited functional information (ie, flow) and requires iodinated contrast and ionizing radiation.(Source)

Thursday, November 4, 2010

Medicare Reimbursement Policy Change Significantly Reduces ADT Therapy For Prostate Cancer Treatment Claims.

According to a group of researchers deducted from their observations, that the Medicare Modernization Act led to moderate reductions in reimbursement for androgen-deprivation therapy (ADT) for prostate cancer, starting in 2004 and followed by substantial changes in 2005.
In order to conduct the research the team used the Surveillance, Epidemiology, and End Results (SEER) Medicare database, and found 54,925 men who received a diagnosis of incident prostate cancer from 2003 through 2005. Then the team divided these men into groups according to the strength of the indication for ADT use.
The use of ADT was deemed to be inappropriate as primary therapy for men with localized cancers of a low-to-moderate grade (for whom a survival benefit of such therapy was improbable), appropriate as adjuvant therapy with radiation therapy for men with locally advanced cancers (for whom a survival benefit was established), and discretionary for men receiving either primary or adjuvant therapy for localized but high-grade tumors. The proportion of men receiving ADT was calculated according to the year of diagnosis for each group. The team used modified Poisson regression models to calculate the effect of the year of diagnosis on the use of ADT.

The outcome of the research indicates that the rate of inappropriate use of ADT declined substantially during the study period, from 38.7% in 2003 to 30.6% in 2004 to 25.7% in 2005. There was no decrease in the appropriate use of adjuvant ADT (odds ratio, 1.01; 95% CI, 0.86 to 1.19). In cases involving discretionary use, there was a significant decline in use in 2005 but not in 2004.


Tuesday, November 2, 2010

Pathway That Drives Spread of Pediatric Bone Cancer Identified in Pre-Clinical Studies

Researchers have identified an important signaling pathway that, when blocked, significantly decreases the spread of pediatric bone cancer.

In their study, researchers at The University of Texas MD Anderson Children's Cancer Hospital in Houston found that blocking the Notch pathway in mice decreased metastases in the lungs 15-fold. The results of a series of pre-clinical studies were reported Sunday in an oral presentation at the 42nd Congress of the International Society of Pediatric Oncology.

Their research showed that the Notch pathway and Hes1 gene play a key role in promoting the metastasis of osteosarcoma, the most common form of bone cancer in children.

Approximately 400 children and teens under the age of 20 are diagnosed with osteosarcoma annually, and the majority present with cancer that has already metastasized. The primary destination for the cancer to spread is to the lungs, which accounts for more than 35 percent of pediatric patients dying from osteosarcoma.

"Knowing the initial results from blocking Notch in mice, we are encouraged to keep investigating the entire metastasis process, so we can find additional therapies and targets to prevent cancer from spreading and growing. By defining vital signaling pathways in bone sarcomas, we hope small molecule inhibitors can be applied, leading to longer survival and reducing morbidity and late effects from intensive chemotherapy, We also hope these new findings may apply to other solid tumors such as breast, prostate, colon and more, but we'll need additional research to determine whether or not that is the case" said Dennis Hughes, M.D., Ph.D., lead investigator and assistant professor at MD Anderson Children's Cancer Hospital.

In addition to Notch and Hes1's role in metastasis, Hughes believes that their expression can be correlated with a patient's prognosis. Hughes conducted a small retrospective study looking at patient samples, and 39 percent of patients with high expression levels of Hes1 survived 10 years versus the 60 percent survival rate for patients who had lower levels.


Sunday, October 31, 2010

Heterocyclic Amines In Well-done (Charred) Meat May Lead To Increased Risk Of Pancreatic Cancer.

Even though the summer is over, and grilling is mostly done with, there is some news that is timely if you want to avoid or lesson the risk of pancreatic cancer.
According to findings from a University of Minnesota study presented this week at the annual American Association of Cancer Research (AACR) meeting in Denver, eating charred meat on regular basis increase the risk of pancreatic cancer by up to 60%.
It was know that meat cooked at very high temperatures creates Heterocyclic Amines or HAs that increases the cancer risk. HAs are created when  amino acids and other substances in meats cooked at particularly high temperatures and that are particularly well-done or worse charred. HAs turn up in grilled and barbecued meat as well as broiled and pan-fried meat.
The University of Minnesota study study investigates the association of HAs and Pancreatic cancer on a larger scale. The team of researchers, led by Kristin Anderson, PhD, associate professor and cancer epidemiologist with the University of Minnesota's School of Public Health and Masonic Cancer Center, surveyed the eating habits of more than 62,000 people, noting meat intake, preferred cooking methods, and doneness preferences. The study participants were then followed for average of 9 years as part of the PLCO (Prostate, Lung, Colorectal and Ovarian) screening trial.
Over the study period, the team found that people who asked for well-done meat, be they bacon, sausage, hamburger, or steak had a higher risk of getting pancreatic cancer.
"We found that those who preferred very well-done steak were almost 60% more likely to get pancreatic cancer as those who ate steak less well-done or did not eat steak, furthermore, when we looked at amount of consumption with doneness preferences, we found that those with the highest intake of very well-done meat had a 70% higher risk for pancreatic cancer over those with lowest consumption. Our findings in this study are further evidence that turning down the heat when grilling, frying, and barbecuing to avoid excess burning or charring of the meat may be a sensible way for some people to lower their risk for getting pancreatic cancer," Kristin Anderson, PhD, associate professor and cancer epidemiologist with the University of Minnesota's School of Public Health and Masonic Cancer Center, said.
So in the future, when grilling or cooking meat;
  • Choose lean cuts of meat and trim any excess fat. Fat dripping onto hot coals causes smoke that contains potential carcinogens. Less fat means less smoke.
  • Line the grill with foil and poke small holes in it so the fat can still drip off, but the amount of smoke coming back onto the meat is lower.
  • Avoid charring meat or eating parts that are especially burned and black – they have the highest concentrations of HAs.
  • Add colorful vegetables and fruit to the grill. Many of the chemicals that are created when meat is grilled are not formed during the grilling of vegetables or fruits, so you can enjoy grilled flavor worry-free. Red, yellow, and green peppers, yellow squash, mushrooms, red onions, and pineapple all grill well and make healthy additions to your plate.
 Cancer Org

Friday, October 29, 2010

Experimental Lung Cancer Drug Crizotinib Meets Some Resistance From Tumors

Pfizer (Nasdaq: PFE) Inc's xperimental Lung Cancer Drug Crizotinib ( PF-02341066) said to be helping as much as 5% of lung cancer patients, while seems to be promising, might meet some resistance from some mutations of lung cancer.
Lung cancer affects 1.61 million people world wide, every year and 1.2 million succumb tot he illness. So any drug that effective against lung cancer will help to save that many people.
Crizotinib said to have shrunk tumors in 57% of the patients introduced to the drug. Another 33% of patients had the the cancer stabilized according to a study published in the New England Journal of Medicine.
"While this is a Phase 1 study, the high response rates  observed in patients with ALK-positive (lung cancer) who received crizotinib suggest that we may be one step closer to the development of 'precision' or 'personalized' cancer treatments that target specific genetic factors that drive certain tumors," said Pfizer's Dr. Mace Rothenberg.
Doctors of the University of Tokyo found a patient who developed two mutations that were resistant to Crizotinib. But the doctors were positive about the drug and also about being able to isolate the resistive mutations. Because a new drug could be developed to target these tumors.
The Pfizer's drug, Crizotinib works against cells that have turned cancerous when two genes fuse to form a new gene called EML4-ALK. Although only about 3 percent to 5 percent of people with non-small-cell lung cancer fall into this category, that translates into nearly 10,000 cancer patients in the United States alone.
AstraZeneca's Iressa and Roche's Tarceva are already known to be effective against cancer in patients with a mutation activating the epidermal growth factor receptor (EGFR).
Pfizer plans to submit the drug for approval early next year.

Pfizer press release;

Oct 27, 2010
NEW YORK, Oct. 27-- Pfizer Inc. (NYSE: PFE) announced today the publication of data showing that 57 percent of ALK-positive advanced non-small cell lung cancer (NSCLC) patients treated with crizotinib (PF-02341066), an investigational oral anaplastic lymphoma kinase (ALK) inhibitor, had either a complete (one patient) or partial (46 patients) response to treatment.  Data from 82 patients in this Part 2 expansion cohort of the Phase 1 study were published in the October 28 issue of the New England Journal of Medicine.(1)

"It is gratifying to learn of responses like those seen in our study of crizotinib (PF-02341066), especially when you consider that most patients had already received two or more therapies by the time they entered the trial," said Dr. Eunice Kwak, MD, Ph.D., department of medicine, Harvard Medical School, assistant in medicine, hematology/oncology, Massachusetts General Hospital and lead author of the study.  "As we're discovering more about lung cancer, we have confirmed the fundamental need to test tumors for molecular changes, like the ALK fusion gene, so we can better identify the patients who may benefit from certain treatments."
Updated results from this study were also recently presented at the 35th Congress of the European Society for Medical Oncology (ESMO) in Milan, Italy, reporting on 113 patients and preliminary median progression-free survival (PFS) data of 9.2 months.(2)
Study A8081001 is a 2-part Phase 1 open-label, multi-center study evaluating crizotinib (PF-02341066), in patients with solid tumors.(3)  The Part 2 expansion cohort from study A8081001 is evaluating the safety and response of crizotinib (PF-02341066) in patients with ALK-positive advanced NSCLC treated with a dose of 250 mg twice daily.(1)
Crizotinib (PF-02341066) is a first-in-class compound that inhibits the anaplastic lymphoma kinase, or ALK.(4)  ALK is believed to be a tumor-exclusive target that is a key driver of oncogenesis, or tumor development.(5)  Approximately 3-5 percent of NSCLC tumors are ALK-positive.(4)
"The development of crizotinib is a testament to the benefits of collaboration and partnership, between industry and academia, with investigators from all over the world, including the United States, Japan, Korea and Australia, working together with the goal of discovering a more effective treatment for advanced NSCLC patients with few other options," said Dr. Mace Rothenberg, senior vice president of clinical development and medical affairs for Pfizer's Oncology Business Unit.  "While this is a Phase 1 study, the high response rates observed in patients with ALK+ NSCLC who received crizotinib suggest that we may be one step closer to the development of "precision" or "personalized" cancer treatments that target specific genetic factors that drive certain tumors."
Pfizer is continuing to study crizotinib (PF-02341066) in an ongoing clinical development program,(6,7) and plans to submit crizotinib (PF-02341066) data in the first half of next year to the U.S. Food and Drug Administration (FDA) for regulatory review.
Additional trials of crizotinib (PF-02341066) include a randomized, Phase 3 open-label study, PROFILE 1007 (A8081007), evaluating the safety and anti-tumor activity of crizotinib (PF-02341066) versus standard of care chemotherapy in patients with previously treated ALK-positive advanced NSCLC.(5)  PROFILE 1005 (A8081005) is a Phase 2 open-label, single-arm study of efficacy and safety of crizotinib (PF-02341066) in patients with ALK-positive advanced NSCLC who have received more than one line of prior chemotherapy.(6)
For more information on these clinical trials, please contact the Pfizer Oncology Clinical Trial Information Service at 1-877-369-9753 (US/Canada) or 1-646-277-4066 (international), via email at or visit
Study Results Published in the New England Journal of Medicine
In the Part 2 expansion cohort study which included 82 patients with ALK-positive advanced NSCLC, 57 percent (n=47)(95% CI 46%, 68%) of patients treated with crizotinib (PF-02341066) at a dose of 250 mg twice daily had either a complete or partial response to treatment.  An additional 33 percent (n=27) met criteria for stable disease, including five unconfirmed partial responses.  At eight weeks, the disease control rate (complete response (n=1) + partial response (n=46) + stable disease (n=24)) was 87 percent (n=71).  Three patients with stable disease were not included in the disease control rate because their evaluation for response was outside a pre-specified timeframe.(1)
At the time of the analysis, 77 percent of patients (n=63) continued to receive treatment with crizotinib (PF-02341066).  The median duration of treatment was 6.4 months, and follow-up is ongoing.
The most commonly reported all-grade adverse events associated with crizotinib included nausea (n=44), diarrhea (n=39), vomiting (n=36), and mild visual disturbances (n=34).  Grade 3 ALT (alanine aminotransferase) and AST (aspartate aminotransferase) elevations occurred in four patients.  One patient experienced a Grade 4 elevation in ALT and one patient discontinued treatment due to Grade 3 ALT increases. Tumors in the analysis were primarily of adenocarcinoma histology, and patients tended to be young, and were never or former light smokers.  Ninety-three percent of patients (n=76) had received at least one prior therapy and five patients were treated in the first-line setting.(1)  This Part 2 expansion cohort study of patients with ALK-positive advanced NSCLC, independent of the number of previous chemotherapies, followed the completion of the dose-escalation study which enrolled 37 advanced cancer patients with various tumors, including NSCLC, colorectal, pancreatic and inflammatory myofibroblastic tumor (IMT) tumors.(8)
These data were previously presented at the 2010 American Society of Clinical Oncology Annual Meeting.(7)
About Crizotinib (PF-02341066)
Crizotinib (PF-02341066) is a first-in-class compound that inhibits the anaplastic lymphoma kinase, or ALK,(3) and is representative of Pfizer's personalized medicine approach to cancer treatment.  By inhibiting ALK, crizotinib (PF-02341066) blocks signaling in a number of cell pathways that may be critical for the growth and survival of tumor cells.(4)  Crizotinib (PF-02341066) is also an inhibitor of c-MET (mesenchymal endothelial transition factor).(3)
About Non-Small Cell Lung Cancer
Lung cancer is one of the most common cancers worldwide.(9)  NSCLC accounts for about 85 percent of lung cancer cases and remains difficult to treat, particularly in the metastatic setting. Approximately 75 percent of NSCLC patients are diagnosed late with metastatic, or advanced, disease, where the five-year survival rate is only 6 percent.(10,11)  In addition, the current standard of care for advanced NSCLC demonstrates a response rate of only about 15 percent.(12)  Approximately 3-5 percent of NSCLC tumors are ALK-positive.(4)

Wednesday, October 13, 2010

Puma Project Pink, Tweet #projectpink To Win Gear

Retweet #projectpink for the chance to win WPS gear!
On Twitter for a week from Tuesday 12th October, @PUMAfootball will be joining the cause to raise breast cancer awareness by tweeting a fact about breast cancer and we want you to get involved.  All you have to do is show your support with a retweet including the #projectpink hashtag to your Twitter community, friends and followers.

What’s more, if you can get your friends to retweet your tweet, we’d like to thank you by giving you a chance to win some prizes.

The first person to get 5 retweets of their retweet each day will win autographed #projectpink WPS gear, with the 5 people who retweeted them also getting a little something to say thanks.

Click here for terms and conditions and get tweeting to support the fight against breast cancer.
And don't forget that for each tweet with the #projectpink hashtag through October 18th, PUMA will donate $1 to the winning Project Pink charity, up to a maximum of $25,000. Check out the Project Pink site for more details.

Breast Cancer Recurrence And Alcohol Consumption: The Life After Breast Cancer Epidemiology study.

Relationship between alcohol consumption and the increased risk of breast cancer has always been assumed, discussed and digested,  but now there is solid data behind this theory. In a study conducted by researchers, Kwan et al*, from the Division of Research, Kaiser Permanente, Oakland, CA; and the University of Utah, Salt Lake City, UT, confirms that;

Consuming three to four alcoholic drinks or more per week after a breast cancer diagnosis may increase risk of breast cancer recurrence, particularly among postmenopausal and overweight/obese women, yet the cardioprotective effects of alcohol on non–breast cancer death were suggested.
The study included 1,897 LACE study participants diagnosed with early-stage breast cancer between 1997 and 2000 and recruited on average 2 years post diagnosis, primarily from the Kaiser Permanente Northern California Cancer Registry. Alcohol consumption (ie, wine, beer, and liquor) was assessed at cohort entry using a food frequency questionnaire. Cox proportional hazards models were used to estimate hazard ratios (HR) and 95% CI with adjustment for known prognostic factors.
The complete article could be found here.
Editorial on the subject of Breast Cancer and Alcohol

* Marilyn L. Kwan,, Lawrence H. Kushi,Erin Weltzien, Emily K. Tam, Adrienne Castillo,Carol Sweeney and Bette J. Caan
Alcohol Consumption and Breast Cancer Recurrence and Survival Among Women With Early-Stage Breast Cancer: The Life After Cancer Epidemiology Study

    Tuesday, October 12, 2010

    OncoSemantic, A Portal, Database And A Social Hub Fro Oncology Information.

    We are in the process of preparing the OncoSemantic, a site focusing on oncology (cancer) information, chemotherapy protocols, oncology research, cancer treatment regimens and even individual drugs. The site is mainly meant for Healthcare providers in the field of Oncology but we are confident, that everyone will find, valuable information.
    Bringing together all the data together via semantic technologies will aid all users since thay do not need to traverse, hundreds of sites, just to get information on, just say, breast cancer.

    Why Google Rock, BING, YAHOO Suck

    I created the Oncowikia blog yesterday and posted an article on Meddesktop regarding the inception of OncoWikia and OncoSemantic. Both sites related to upcoming sites of namesakes.
    I just wanted to see how the leading search engines will see the sites. (Of course I had just registered and created the sites and I did not expect to see OncoWikia blog on search engines.) Google also helped me to find Cancer And You.
    Google gave following results;
     Google managed to find the original article in a search for "oncowikia" followed by two spam sites who archive blogs or articles related to cancer.

     Bing managed to find a Spam site and only that.

    Yahoo follows Bing, and it only found what Bing found, a spam site. You may say that my site is not important. Yes it may not be important to you, but search engines, are supposed to index and rank and if you only find spam sites, search engine fail.
    Both Bing and Yahoo had it wrong about the search itself, both said they could not find "oncowikia" and only found "onco Wikia" but the results show, as you can see from above, "oncowikia".

    Cancer And You, Source For Cancer Related Keywords

     I was checking on ONCOWIKIA on search engines, I found that Cancer and You site listed just below my post on Meddesktop, ONCOWIKIA and ONCOSEMANTIC, Will Be Caring For Cancer. A little examination found that Cancer and you is very good at collecting keywords related to cancer on it's blog. It only selects right words and gets very high search engine visibility for cancer. The way the posts are made, looks like a spam site. The admin has installed the Semper Fi Web Design's "All In One SEO Pack", (By the way SFWD is a good resource for Wordpress related stuff and run by U.S. Combat Veterans.) Good idea for ONCOWIKIA blog, yes I like Wordpress better for SEO work than Blogger.
    Last few entries visible on the blog are centered on Mesothelioma and since all those article sites are filled with posts about Mesothelioma, Cancer and you, is getting a good collection.
    But if you are really looking for info Cancer and You.

    Monday, October 11, 2010

    How Cells Grow and Divide To Be Cancer

    This NOVA: video segment from "Battle in the War on Cancer: Breast Cancer" describes the role of oncogenes in uncontrolled cancerous growth. The video describes the journey of cancer cells from their origin, travel into the circulatory system, and then on to other parts of the body. Cancer never stops.
    How Cancer Grow! (Click here for the video)

     You can read more at Nova Beta. Articles like these will appear on ONCOSEMANTIC

    ONCOWIKIA, A Place Where All Information About Cancer And You Come Together.

    People, will seek information on cancer, even if they are not cancer patients themselves. But in the world of information overload, it is difficult to locate proper and trustable information., will bring just that with OncoSemantic while OncoMeme will be the center of all news related to the cancer working as a knowledge sharing portal, for all involved or interested. Please wish us good luck and join us in combating cancer.
    ONCOWIKIA.COM, If It Is About Cancer, We Will Have It Here.