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.

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.

Thursday, November 25, 2010

Happy Thanksgiving Day! Let Us Look Forward To A Cancer Free World.

Happy Thanksgiving and enjoy the weekend.

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.