Sunday, November 17, 2013

Cancer Drugs Losing Out: Pruning the Branches, Not Cutting the Trees

An oncologist puts the cancer patient on a targeted therapy, the cancer goes away, patient goes home. But, 6 months later, the cancer is back (relapsed) and is aggressive stage IV. Biologically, the cancer cells have mutated to bypass/ignore the expensive targeted therapy.

At the molecular level, the cancer cells are constantly mutating, evolving, and generating diversity. This phenomenon of cancer evolution is central to cancer relapse, tumor escape and therapeutic failure.

New research from the Institute of Cancer Research, UK, shows extreme diversity of cancer cell types in leukemia patients: multiple cancers within a cancer. 

Saturday, November 16, 2013

Using canSAR Database to Learn About Cancer Drugs and Targets

Imagine that you heard about a groundbreaking hot new cancer drug on the evening news. And you are curious, and you want to find more about this drug. Where would you turn to? Google? 

Among the search engine hits will be a press release from the company and a multitude of news commentaries and blogposts, all various incarnations of the press release itself. These sources will have a summary of the best results from the Phase 3 clinical trial, promising (maybe self-congratulatory) statements from the CEO or CMO of the company, a paragraph on safety signals and usual disclaimers.

But what if you actually want to know more about the drug target, its biology, chemistry, structural biology, pharmacology, bioactivity (and experimental models) and all kinds of apparently boring (to the investment community) scientific data. 

This "mundane" data is generally scattered in journal articles, conferences abstracts and posters, and patent filings. Now there is an easier way to get a snapshot of this data: via a public database canSAR.

Sunday, October 20, 2013

Common Mutations Drive 12 Different Cancer Types

Cancer types from leukemia to breast cancer, and bladder cancer to lung cancer are all driven by a common set of genes containing driver mutations. Researchers from The Cancer Genome Network (TCGN) sequenced and analyzed genomes of 3,281 tumors from 12 different cancer types and discovered 127 genes that were involved in the initiation or progression of these cancers. This research appears in the October 17, 2013, issue of the journal Nature

Saturday, October 19, 2013

Cancer Meetings and Conferences 2013 (Archived)

Archived list below.
***For upcoming meetings list, go to page 

How does ARIAD's Ponatinib (Iclusig) Work

Mechanism of Action Series: Ponatinib

Ariad Pharmaceuticals' leukemia drug ponatinib has been in the news lately for major toxicity fears that can potentially derail its further clinical development. While these issues will be sorted out in coming months, it's a good time to review how does this drug work.

Ponatinib is a pan-inhibitor of native and T315I mutant forms of BCR-ABL kinase.

Tuesday, October 1, 2013

The Effect of US Congressional Tantrums on Science

Here is one snapshot of what their childish behavior can do. (Let's hope the next generation of congressmen and congresswomen are smarter than this bunch.)



Tuesday, September 24, 2013

How Does AR Antagonist ARN-509 Work

Mechanism of Action Series: ARN 509

ARN-509 is an androgen receptor signaling inhibitor currently in phase 2 clinical trial for castration-resistant prostate cancer (CRPC).  How does ARN-509 work to block prostate cancer cells is described below.

Friday, September 6, 2013

FDA Approves Abraxane for Pancreatic Cancer

ABRAXANE® (generic name: nab-paclitaxel) was approved by the FDA as first-line therapy for the metastatic adenocarcinoma of the pancreas when used in combination with gemcitabine. The approval of ABRAXANE is a major development in pancreatic cancer care and is expected to replace gemcitabine alone as a new standard of care for pancreatic cancer. 

Wednesday, June 19, 2013

List of Inspirational Cancer Blogs at "Navigating Cancer" Website

Cancer can affect any organ but the underlying biology and signaling may have strong similarities. Thus one drug targeting a particular signaling pathway may work in multiple cancers.

But patients and their family often seek experiences that relate specifically to them. Someone who has kidney cancer would want to know how another kidney cancer patient is coping with such unexpected and unwanted diagnosis. They may be less interested in the experiences of those with stomach or colon cancer even though the molecular drivers may be similar.

Thursday, June 13, 2013

BRCA Freed from Myriad's Patents, Supreme Court Rules

The Supreme Court in a 9-0 ruling invalidated Myriad's patents on BRCA opening up the field for cheaper testing for the breast cancer risk genes BRCA1 and BRCA2. Myriad was criticized for selling $3000 tests and blocking mon-n-pop University labs to run similar tests at fraction of the cost.

Sunday, June 2, 2013

GSK Receives FDA Approval for Melanoma Drugs Dabrafenib and Trametinib

The approval of two new melanoma drugs TAFINLAR® (dabrafenib) and MEKINIST™ (trametinib) by the FDA this week is timely for melanoma patients whose tumors often develop resistance to other targeted therapies, such as Zelboraf. 

Dabrafenib is indicated for patients with BRAF V600E mutation. Another drug, vemurafenib (aka ZELBORAF) by Genentech which was approved in January 2011 also targets the same protein. BRAF V600E is an always-on signaling protein found in majority of melanomas. (Read more about vemurafenib or BRAF V600E here.)

The second drug, trametinib is the first MEK inhibitor to be approved for melanoma.  Unlike dabrafenib or vemurafenib, this drug's target is downstream of BRAF kinase and, thus trametinib can complement the other two drugs in clinical practice. Both drugs will be available by prescription in Fall 2013.

Sunday, May 19, 2013

Antiangiogenic Agent Thalidomide No Good in Mesothelioma

Malignant pleural or peritoneal mesothelioma is invariably fatal cancer with options that are largely supportive in nature. The current first-line chemotherapy regimens including pemetrexed with or without cisplatin or carboplatin do not provide long-term survival. This cancer is highly angiogenic and thus preclinical and early data supported the use of anti-angiogenic agent thalidomide.

However, a recent clinical trial published in this month's issue of the journal Lancet Oncology shows that thalidomide when added to chemotherapy does not provide any additional benefit.  

Thursday, May 2, 2013

The Specter of Rising Cancer Deaths in Latin America and Caribbean

Latin America and the Caribbean are the next hotspots of cancer-related deaths in the world and countries in this region are woefully ill-prepared to face this growing epidemic. A report by Latin American Cooperative Oncology Group (LACOG) presented at the LACOG Conference 2013 on April 26-27, 2013, at Sao Paulo, Brazil, put these facts in depressing hard numbers: currently 13 people of 22 diagnosed with cancer die in Latin America and the Caribbean in contrast to 13 of 37 in US or 13 of 30 in Europe. This translates to 59% of cancer patients dying of cancer in Latin America and the Caribbean compared to 35% in US or 43% in EU.


Wednesday, May 1, 2013

Upcoming meeting: Tumor Models, Boston, July 23-25, 2013


Better Preclinical Models. Better Predictions. Better Patient Response.

Tumor Models gives you the tools to develop and utilize the very best preclinical oncology models. 
This is a meeting for drug developers who are looking for answers to the difficulties faced with preclinical oncology models that are currently being used to test new cancer drugs. This is a forum to learn what you really need to know about the models pharma are using that are superior in predicting efficacy and mimicking tumor activity in patients. It’s also the best way to identify what preclinical questions need to be answered and make the best possible translational decisions. Decisions that will lead to more effective drug performance in the clinic. 

Sunday, April 14, 2013

Three Decades of SEER Data Confirms That Mammogram Screening Does More Harm Than Good

Nearly one-third or 1.3 million women over the past 30 years were overdiagnosed with breast cancer (ie, their tumors would have never led to clinical symptoms in their lifetimes) in the United States,  according to the research published in the November 22, 2012 issue of the New England Journal of Medicine. 

Saturday, April 13, 2013

Serious Doubts on Biosimilars Ability to Rise Over the Cancer Biologics' Patent Cliffs

The year 2012 saw conversation on the pricing structure and affordability of oncology drugs taking a center stage with commentaries, such as, "The Truly Staggering Cost Of Inventing New Drugs," by Mathew Herper in Forbes pegging the cost of inventing and developing these drugs at $1-$4 Billion, to news about Sloan-Kettering Cancer Center saying "NO" to Zaltrap (Sanofi's drug for colon cancer, then priced at $11,000 per month) for providing a marginal 1.4 month survival benefit. (Sanofi has since cut the price by 50%.) 

What will rein in these Aston Martin-like price tags. At least Herceptin will lose its patent protection soon. Right? And biosimilars will force the price down. Wrong! Those banking on biosimilars to bring the cost down to earth are in for a rude shock.

Tuesday, February 19, 2013

Pexa-Vec Doubles Survival of Advanced Hepatocellular Carcinoma Patients

An oncolytic virus-based drug JX-594 (also called Pexa-Vec) is highly effective in patients with advanced hepatocellular carcinoma. According to the results of a Phase II clinical trial published online at Nature Medicine journal's website on February 10, 2013, the patients who were given higher (more effective) dose of JX-594 had a median survival of 14.1 months which was twice that seen in the low dose group (6.7 months).