Archive for the ‘Targeted Cancer Therapy’ Category

Targeted Cancer Therapies Doomed to Fail?

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Posted 15 Jun 2012 — by James Street
Category Targeted Cancer Therapy


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By Michael Smith, North American Correspondent, MedPage Today

Published: June 13, 2012

Reviewed by Dori F. Zaleznik, MD; Associate Clinical Professor of Medicine, Harvard Medical School, Boston and Dorothy Caputo, MA, BSN, RN, Nurse Planner



Resistance to targeted cancer therapies may be almost inevitable, at least if they are used alone, two groups of researchers reported online in Nature.

Mathematical modeling, based on genetic testing of colorectal cancer patients, suggests that resistance already exists even before targeted therapy begins, according to Luis Diaz, MD, of Johns Hopkins Kimmel Cancer Center, and colleagues.

One effect of single-agent targeted therapy, they noted, is to allow tumor cells containing resistance mutations to grow and prosper, leading to disease progression.

A second group, led by Alberto Bardelli, PhD, of the Institute for Cancer Research and Treatment in Turin, Italy, found some evidence of preexisting resistance, but added that resistance could also emerge as a result of single-agent targeted treatment.

The solution, both groups argued, may be to use combination therapies to delay or prevent progression.

Molecules that block the epidermal growth factor receptor (EGFR) often have a dramatic initial effect on cancers driven by the receptor, Diaz and colleagues noted.

But resistance almost always arises within a few months of starting therapy, leading to relapse, although the exact mechanisms of the resistance have been unclear.

To help clarify the situation, they studied 28 patients with metastatic colorectal cancer, a disease in which patients whose tumors have a wild-type KRAS gene are often sensitive to EGFR blockade.

Four of the patients already had KRAS mutations at the start of monotherapy with panitumumab (Vectibix), a monoclonal antibody aimed at EGFR. But nine of the remaining 24 with normal KRAS developed mutations about 5 or 6 months after starting treatment.

Mathematical modeling, Diaz and colleagues wrote, showed that the parent cells of those with KRAS mutations must have been present before the panitumumab treatment started.

“These resistance mutations develop by chance as cancer cells divide so that tumors always contain thousands of resistance cells,” Diaz said in a statement, adding that the findings likely apply to any targeted cancer therapy.

Co-author Bert Vogelstein, MD, also of Johns Hopkins, added that the finding means that “long-term remissions of advanced cancers will be nearly impossible with single targeted agents.”

The research team also noted that their method – testing tumor DNA found in the blood – is noninvasive and was able to detect changes in KRAS long before those changes translated into renewed tumor growth.

That should allow physicians the opportunity to alter the treatment, perhaps by adding agents to the regimen.

“The good news is that there is a limited number of pathways that go awry in cancer, so it should be possible to develop a small number of agents that can be used in a large number of patients,” Vogelstein said in a statement.

Bardelli and colleagues reached similar conclusions after studying colorectal tumor cell lines and a group of 10 patients with metastatic disease who were being treated with cetuximab (Erbitux), a chimeric antibody aimed at EGFR.

They found that preexisting KRAS mutations were amplified in one patient and emerged after treatment in six others.

The resistance mutations were detectable in blood samples as early as 10 months before radiological assessment confirmed that the disease had progressed, Bardelli and colleagues said.

“Our results suggest that blood-based noninvasive monitoring of patients undergoing treatment with anti-EGFR therapies … could allow for the early initiation of combination therapies that may delay or prevent disease progression,” they concluded.

The study by Diaz and colleagues was supported by The Virginia and D. K. Ludwig Fund for Cancer Research, the National Colorectal Cancer Research Alliance, the NIH, the National Cancer Institute, the European Research Council, the Austrian Science Fund, and the John Templeton Foundation.

The authors declared competing financial interests, including affiliations with Personal Genome Diagnostics and Inostics.

The study by Bardelli and colleagues had support from the European Union Seventh Framework Programme, the Associazione Italiana per la Ricerca sul Cancro, the Regione Piemonte, the Fondazione Piemontese per la Ricerca sul Cancro, Oncologia Ca’ Granda ONLUS, Mr William H. Goodwin and Mrs Alice Goodwin and the Commonwealth Foundation for Cancer Research, the Experimental Therapeutics Center of Memorial Sloan-Kettering Cancer Center, the Society of MSKCC, the NIH, the Beene Foundation, and the Regione Lombardia and Ministerio Salute.

The authors declared they had no competing financial interests

New Patent Promises to Accelerate Cancer Trials

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Posted 21 Feb 2012 — by James Street
Category Clinical Trials, Individualized treatment, Moffitt Cancer Center, Personalized, Targeted Cancer Therapy

Computer system IDs suitable patients, helps new drugs reach market faster

TAMPA, Fla., Feb. 14, 2012 /PRNewswire/ – A new patent has been issued to Moffitt Cancer Center for a computerized system that efficiently selects the right patient for the right clinical trial. The newly patented system matches the registered patient’s own molecular profile – warehoused in a database of thousands of patient-donated biological tissue or tumor samples – to the molecular design of the drug aimed at targeting their disease at the molecular level, and do it quickly. The system promises to accelerate clinical trials and help shorten the time that it takes to get critically needed new drugs into the market.

Getting new drugs to market to fight cancer and other serious diseases requires, on average, 15 years. The drug development process is long and complex, but the three-phase clinical trials process – estimated to take up to half of those 15 years – is often the bottleneck in getting innovative drugs to the patients who need them.

Clinical trials, increasingly becoming more expensive, are also multifaceted. While patients may qualify for a clinical trial based on their age or stage of disease, they may not be, over the long term of the trial, the best candidates to test a drug. Adverse events, changes in a patient’s health status and the potential for a drug not being effective for them slow the process. Although patients may have met the trial protocol’s criteria, the drug may not be right for them because their molecular profile is not a good match for the chemical and molecular properties of the drug.

Because the concept of personalized medicine is selecting the right drug for the right patient, innovations have been needed to bring personalized medicine to reality. Personalizing the selection process for clinical trials is a vital step.

With the development of new and better ways to examine and understand a tumor’s molecular profile, matching the right patient to the right clinical trial becomes increasingly important. But handling the massive data evaluation necessary to accomplish this has been a stumbling block.

The newly patented computer system, Patent Number US 8,095,389 B2, or “Computer Systems and Methods for Selecting Patients for Clinical Trials,” is designed to surmount that problem.

The newly patented computer system is designed to:

  • Select patients to clinical trials matching an individual’s/drug’s molecular profile
  • Match patients to clinical trials by a patient’s disease/diagnosis
  • Match patients to clinical trials by their symptoms
  • Match patients to clinical trials by their demographic information and family history
  • Track a clinical trial participant’s disease progression compared to drug efficacy

The newly patented computer system and associated products, such as operating system, software, interfaces and data retrieval system, improve clinical trial selection efficacy by making the patient selection process less random and more selective. The technology has the potential to refine clinical trials by eliminating bottlenecks, overhauling the selection process and shortening the timeline, ultimately bringing new drugs to market more efficiently.

About Moffitt Cancer Center

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Located in Tampa, Moffitt Cancer Center is a National Cancer Institute-designated Comprehensive Cancer Center, a description that recognizes Moffitt’s excellence in research and contributions to clinical trials, prevention and cancer control. Moffitt is also a member of the National Comprehensive Cancer Network, a prestigious alliance of the country’s leading cancer centers, and is listed in U.S. News & World Report as one of “America’s Best Hospitals” for cancer.

Media release by Florida Science Communications:

SOURCE Moffitt Cancer Center

December 19, 2011 Monday – 11:50 am EST inShare 1 Text Size Smaller Normal Larger E-mail Print ‘Fantastic Potential’: Researchers Keep Cells Alive Away From Body

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Posted 20 Dec 2011 — by James Street
Category Diagnostic, Personalized, Stem Cell Research, Targeted Cancer Therapy

December 19, 2011 Monday – 11:50 am EST

By Adam Daley

Georgetown researchers say they have just significantly changed biomedical research.

Researchers know that normal cells don’t last long once removed from a human, dividing only a few times in a laboratory setting. Common cancers won’t grow in a lab.

That’s about to change.

Senior investigator, Richard Schlegel, M.D., Ph.D., and chairman of the department of pathology at Georgetown Lombardi Comprehensive Cancer Center, has discovered a way to keep normal cells as well as tumor cells taken from an individual cancer patient alive in the laboratory. The technique could be a critical advance, ushering in a new era of personalized cancer medicine, and has potential application in regenerative medicine.

“Because every tumor is unique, this advance will make it possible for an oncologist to find the right therapies that both kills a patient’s cancer and spares normal cells from toxicity,” said Dr. Schlegel. “We can test resistance as well chemosensitivity to single or combination therapies directly on the cancer cell itself.”

The research team found that inserting a Rho kinase (ROCK) inhibitor and fibroblast feeder cells to cancer and normal cells in a laboratory pushes them to morph into stem-like cells. The cells visibly changed their shape as they reverted to a stem-like state.

“In short, we discovered we can grow normal and tumor cells from the same patient forever, and nobody has been able to do that,” said Dr. Schlegel. “Normal cell cultures for most organ systems can’t be established in the lab, so it wasn’t possible previously to compare normal and tumor cells directly.”

“Today, pathologists don’t work with living tissue. They make a diagnosis from biopsies that are either frozen or fixed and embedded in wax,” added Dr. Schlegel. “In the future, pathologists will be able to establish live cultures of normal and cancerous cells from patients, and use this to diagnose tumors and screen treatments. That has fantastic potential.”

The study, which was funded by grants from the National Institutes of Health, Department of Defense fellowship funding, and an internal grant from Georgetown Lombardi’s Cancer Center Support Grant from the National Cancer Institute, is published online today in the American Journal of Pathology.

Expression Profiling Findings at 12th Annual International Congress of Human Genetics

press release

Oct. 18, 2011, 9:30 a.m. EDT

Caris Life Sciences Highlights Gene

Data Presented Shows Clinical Utility of Molecular Profiling Helping Physicians Select More Effective Therapeutic Treatments for Cancer Patients

IRVING, Texas, Oct 18, 2011 (GlobeNewswire via COMTEX) — Caris Life Sciences(TM), Inc., a leading biosciences company focused on enabling precise and personalized healthcare through the highest quality molecular profiling and blood-based diagnostic services, presented at the 12th International Congress of Human Genetics (ICHG). Caris presented clinical data that demonstrates microarray analysis is a reliable and robust method to perform gene expression profiling on routine solid tumor samples. The data provides further support for the quality and clinical utility of information generated by evidence-based molecular profiling services like Caris Target Now.

The study validated a commercially available microarray platform (Illumina whole genome DASL) with clinical tumor samples including FFPE, frozen tissues and RNA later preserved samples. Clinical laboratory findings based on gene expression profiling of 2,384 solid tumors showed that researchers were able to obtain relative gene expression profiles in patient tumor samples when compared to normal reference tissue samples. All sample types yielded quality expression profiling results with a wide variety of tumor types.

“Optimizing therapeutic selections for cancer patients using the molecular profile of their individual tumor is satisfying a large unmet need in oncology,” said Dr. Matthew J. McGinniss, Director of Molecular Diagnostics and lead author of the study. “At Caris, we are committed to advancing the current understanding of various biomarkers and the role of molecular diagnostics in cancer therapy. We are confident that the findings presented at the ICHG conference will continue to validate the clinical utility of the Caris Target Now Service which provides patient- and tumor-specific information for physicians to use in selecting the most effective cancer therapies for each patient.”

Caris Target Now is an evidence-based molecular profiling service that associates biomarker status in a patient’s tumor sample to proven therapeutic agents associated with specific tumor markers. The biomarker/drug associations are drawn from nearly 100,000 published clinical studies that are reviewed and graded by Caris’ evidence team of PhDs. Caris Target Now then provides a consolidated report outlining a personalized list of treatment options, including those that may be more likely to elicit a response, as well as those likely to be ineffective.

About Caris Life Sciences

Caris Life Sciences, a leading biosciences company, specializes in the development and commercialization of the highest quality molecular profiling and blood-based diagnostic technologies, in the fields of oncology, dermatopathology, hematopathology, gastrointestinal pathology and urologic pathology. The company provides academic-caliber consultations for thousands of patients a day, through its industry-leading team of expert, subspecialty pathologists. Caris also offers advanced molecular analyses of patient samples through prognostic testing services and genomic, transcriptomic, and proteomic profiling to assist physicians in their treatment of cancer. Currently, Caris is developing a series of blood tests utilizing the patented Carisome(TM) platform — a proprietary, blood-based testing technology for diagnosis, prognosis, and theranosis of cancer and other complex diseases. The company is headquartered in the Dallas metroplex, and operates laboratories at the headquarters, as well as in the Phoenix and Boston metro areas.

This news release was distributed by GlobeNewswire,

SOURCE: Caris Life Sciences

        CONTACT: Caris Life Sciences
        Media Inquiries:
        Holly Clark

EMCC Speakers Look Forward To Widespread Personalized Patient Care

By Anna Azvolinsky, PhD | September 28, 2011


The European Multidisciplinary Cancer Congress (EMCC), took place September 23–27 in Stockholm, brought together the European oncology community in a joint effort between the European Society for Medical Oncology (ESMO), the European Cancer Organisation (ECCO), and the European Society for Therapeutic Radiology and Oncology (ESTRO).

The multidisciplinary nature of the meeting is highlighted by the tagline of the congress—“Integrating basic and translational science, surgery, radiotherapy, medical oncology and care”—and, indeed, the meeting has emphasized the integration of these components and their important roles in driving cancer research toward providing better patient treatment and care. As clinical practice is becoming increasingly interdisciplinary with patients being treated in multidisciplinary teams, a multifaceted meeting such as this one is important for the continued dialogue, education, and communication among cancer clinicians and researchers.

The EMCC had 285 sessions and over 2,000 presentations from 707 experts in the field, with over 16,000 attendees from around the world.

A call to drive better personalized care deliverables for patients

The opening session of the EMCC emphasized that the field of oncology should continue to strive torward streamlined and personalized patient care. José Baselga, MD, PhD, the associate director and chair in hematology/oncology at the Massachusetts General Hospital Cancer Center gave a presentation, “New World of Cancer: Personalized Medicine for All Patients” that urged the cancer community to see molecular targeting of cancer as a new era. Dr. Baselga pointed out that he believes that classic approaches to cancer therapy such as radiation therapy and chemotherapy have achieved a plateau in terms of patient response. In this “classic therapy” era, only an empirical approach to clinical trial design was possible, where patient populations were unselected and large-scale trials were necessary in order to see any treatment benefit. These types of trials led to a high failure rate and minimal benefits. “The system can no longer tolerate an incremental benefit,” he stated as he transitioned to a discussion of what he calls the “new era of molecular targeting of cancer.”

As researchers and clinicians are beginning to understand the wiring of cancer and the underlying molecular causes, Baselga stated, “we are getting into an era of the right drug for the right tumor.” He went on to highlight that identifying the right molecular targets can result in the creation of specific molecules that act on these targets, and said, “chemistry is on our side, to design new treatments.” Dr. Baselga cited early success stories of targeted therapies that have resulted in dramatic patient benefits, including gefitinib (Iressa) and erlotinib (Tarceva), two selective inhibitors of EGFR for lung cancer, crizotinib (Xalkori) for lung cancer patients, which inhibits ALK in patients that harbor the EML4-ALK fusion; and vemurafenib (Zelboraf), the BRAF inhibitor that has recently been approved for metastatic melanoma.

“We will have an incremental number of genetic mutations identified in tumors and we will have an increased number of therapies to treat these tumors,” Baselga said, highlighting his optimism in the collaboration of bench-scientists and clinicians to develop new treatments, in conjunction with the increasing understanding of cancer mutations from patient tumor data.

“We have to realize that this is a watershed moment in cancer history. We have to make sure we match each drug with each individual tumor and we have to change the way we test these new drugs,” said Dr. Baselga.

Looking forward, Dr. Baselga spoke about the need for better, streamlined, and throughput methods to test these new agents for efficacy in a rational way that will provide meaningful data. After isolating compounds that have the potential to be efficacious, the ability to identify patients that will benefit is crucial. Baselga stated, “We have to embark on a comprehensive genetic characterization of tumors: chrosomomsal alterations, epigenetics, mutations, and proteomics.”

While the challenging tasks of platform and clinical validation, archiving quality specimens, improving turnaround time and informatics approaches, and looking for novel mutations is daunting, it is “far less than treating patients with expensive drugs that may not work unless they are targeted for the patient.” In this sense, the field has progressed significantly over the last decade, with the mutational landscapes for lung and breast cancers providing a categorization of subclassifications of these disease that facilitate tailored therapy treatments.

Baselga pointed out that one highly important point that, thus far, has not been widespread due to high cost and the inability to obtain appropriate patient sampling, is the serial monitoring of tumors during therapy. Looking at the genetic makeup of a tumor prior to and post-treatment will greatly facilitate the knowledge about how tumor genetic factors influence treatment response and resistance. Baselga cited the new research on circulating tumor cells (CTCs), and said that by applying novel therapies earlier in disease “you can identify very early on when a patient responds, which can help clinicians modulate therapy.”

He highlighted a particular example of the use of technology to predict response that was subsequently presented at EMCC (Gamez et al. “FDG-PET/CT for Early Prediction of Response to Neoadjuvant Lapatinib, Trastuzumab, and Their Combination in HER2-positive Breast Cancer Patients: the Neo-ALTTO Study Results, abstract #5013).

Dr. Baselga ended by listing his vision of novel clinical trial design in the new molecular era: 1) smaller smarter clinical trials without the need for 1000+ , expensive trials, 2) the importance of combination treatments 3) applying novel targeted agents earlier in the course of disease, and 4) the study of resistance to therapies. “Over the course of the next ten years,” he said, “we need good biomarker programs and facilities, the sharing of data, attracting the best pool of physician scientists into our culture of teamwork, and we need creativity and willingness in our clinical trial design.”

A pragmatic assessment of today’s personalized molecular medicine

Following Dr. Baselga’s talk, Gordon B. Mills, MD, PhD and chairman of the department of systems biology at the M.D. Anderson Cancer Center addressed what the cancer community needs to be doing to deliver personalized medicine outside of the research environment. “We have to determine to work with medicine and industry in a better manner. Drugs coming out of the pipeline must be linked to the right patient,” he stated.

Professor Mills defined personalized medicine as “the right treatment for the right person at the right and first time,” in contrast to the current practice of “trial and error.” He asked the audience to think about whether they are educating patients and physicians enough and whether they are overpromising on what the current treatments and care can deliver.

In the view of Professor Mills, there are still only subpopulations of patients that experience the biomarker benefit, calling the current phase “stratified and precision medicine.” He stated that he agreed with Dr. Baselga that breast cancer is leading the way in this. “Breast cancer is now a series of different diseases, at least eight of them. But the problem is that some of these subpopulations are too small to have clinical trials that will show good enough data. Rather than distinct diseases, currently, there are still only subpopulations,” he asserted.

Emphasizing that despite the latest positive results with targeted agents, “every single patient on [vemurafenib] has recurred.” His goal was for the oncology community to aim for higher achievements.

Finally, Professor Mills outlined the current landscape of challenges he sees that need to be overcome. In terms of patients, these include the need to identify a patient’s genetic makeup to determine whether a treatment will succeed, the need to assess individualized dosing and toxicity limits, and the issue of intra-tumoral heterogeneity and the evolution of the tumor from primary to recurrent stages of cancer.

As far as technology challenges, filtering passenger vs driver mutations is necessary, and Mills also cited the need to find actionable aberrations, as there are still a limited number of drugs for all of the mutations identified in tumors. He highlighted the fact that most tumor suppressors are still recalcitrant to treatments and that the cost of treatments is continually on the rise.

The issue of the accrual of large amounts of sequencing information is such that database storage costs outweigh the costs of generating sequencing data, and said that this is something that needs to be addressed. “The $1000 genome is now the $100,000 analysis cost,” he said. Lastly, he pointed to the expanded number of parties that are involved in treatment development and implementation. He stated that the ethics of telling patients about germ-line mutations that are discovered during genomic sequencing needs to be discussed thoroughly, and mentioned the need for participation by the U.S. Food and Drug Administration in the education of patients and physicians and the issue of reimbursement for testing and sequencing.

The communication, education, and open dialogue about these issues going forward among the global oncology community and other key stakeholders, as well as about novel treatment paradigms and progress, will be highly important for oncologists to be fully entrenched in this promising molecular therapy era.

Pfizer Wins U.S. Approval for Tumor-Fighting Medicine to Treat Lung Cancer

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Posted 26 Aug 2011 — by James Street
Category ALK, genetic research, Lung Cancer, Personalized, Targeted Cancer Therapy, Xalkori (crizotinib)
By Molly Peterson – Aug 27, 2011

Pfizer Inc. (PFE) won U.S. approval to sell a drug targeted at a form of lung cancer caused by a gene defect, as the world’s largest drugmaker seeks tumor-fighting medicines to replace sales expected to be lost to generics.

The treatment, crizotinib, was cleared five weeks ahead of schedule for patients with late-stage, non-small cell lung cancer with a rare genetic abnormality, the Food and Drug Administration said yesterday in a statement. Pfizer will sell the twice-a-day pill under the name Xalkori. The agency also approved a companion test made by a unit of Abbott Laboratories (ABT) to determine whether a patient has the abnormal ALK gene.

The drug is among more than 20 cancer medicines that may help New York-based Pfizer offset $11 billion in revenue at risk to generic copies of the best-selling Lipitor cholesterol pill. In a study presented at a conference last year, the drug reduced tumor size in 57 percent of patients and stopped progression of the disease in 87 percent.

“Xalkori represents a new chapter in personalized therapy for lung cancer, enabling physicians to provide the right treatment for the right patient,” said Mace Rothenberg, senior vice president of clinical development and medical affairs for Pfizer’s oncology business unit.

The treatment may generate sales of $540 million by the end of 2015, according to the average estimate of four analysts surveyed by Bloomberg.

The drug, the first new lung-cancer treatment approved by the FDA in more than six years, is available immediately through specialty pharmacies, Pfizer said in a statement. Xalkori also is the first lung-cancer treatment developed and approved with a diagnostic test, the company said.

‘Targeted Therapy’

“Targeted therapies such as Xalkori are important options for treating patients with this disease and may ultimately result in fewer side effects,” Richard Pazdur, director of the Office of Oncology Drug Products in the FDA’s Center for Drug Evaluation and Research, said in the statement.

About 221,000 cases of lung cancer will be diagnosed in the U.S. this year and the disease will kill about 157,000 people, according to the National Cancer Institute.

The ALK gene abnormality causes cancer development and growth and affects about 1 percent to 7 percent of those with the non-small lung cancer, the most common form of the disease, the FDA said in its statement.

‘Breakthrough’ Advance

“The Abbott-Pfizer collaboration marks a breakthrough in the advancement of personalized medicine — and companion diagnostics specifically — that will help a subset of lung- cancer patients get treatment tailored to their unique genetic profile,” said Stafford O’Kelly, head of Abbott’s molecular diagnostics business, in a company statement.

Pfizer’s drug is the second cancer therapy approved by the FDA this month in conjunction with a diagnostic test. Zelboraf, a skin-cancer drug from Roche Holding AG (ROG) and Daiichi Sankyo Co., won FDA clearance Aug. 17 with a Roche companion test that helps detect whether patients have the gene mutation the drug targets.

Xalkori is the third cancer drug this month to win FDA clearance ahead of schedule. The FDA had a Sept. 30 target decision date for Pfizer’s new treatment, and an Oct. 28 date for Zelboraf. The agency approved Seattle Genetics Inc. (SGEN)’s lymphoma drug Adcetris on Aug. 19, 11 days early.

All three drugs were evaluated under six-month priority reviews. While the FDA typically takes at least 10 months to rule on drug applications, it grants priority status to therapies that may provide major advances in treatment.

Lipitor, the world’s best-selling drug, will face generic competition in the U.S. starting Nov. 30 if Ranbaxy Laboratories Ltd. (RBXY) wins FDA approval to begin selling a copy of the medicine by then.

Watson Pharmaceuticals Inc. has an agreement with Pfizer to start selling a so-called authorized generic on Nov. 30. Pfizer will provide Lipitor to Watson to sell without the brand label as a generic in return for a share of the sales.

To contact the reporter on this story: Molly Peterson in Washington at

To contact the editor responsible for this story: Adriel Bettelheim at

New chemotherapy treatment targets cancer directly

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Posted 20 Aug 2011 — by James Street
Category Bladder Cancer, Hormone, Prostate Cancer, Targeted Cancer Therapy

MIAMI (WTVJ/NBC) – Researchers have developed new drugs that go directly to cancer cells.

Cancer patient Robert Chambers received the last of six treatments Tuesday with an experimental drug therapy designed to target his bladder cancer, which had spread to his liver and lymph nodes.

His wife, Alice, says before enrolling in this clinical trial he was in a lot of pain.

“He was in the bed all the time, exhausted, and he was ready to let go. We were pretty close to the edge of saying it can’t go on like this,” she said.

In the pharmacy at the Sylvester Comprehensive Cancer Center, they carefully mix the combination therapy designed by a Nobel Prize-wining researcher at the University of Miami.

AEZS 108 combines a traditional chemotherapy agent, adriamycin, with a synthetic version of a hormone produced by the brain.

It helps deliver the chemo right to the cancer cells, which are covered with receptors for that hormone.

That’s why this is called targeted therapy.

“It’s like a lock and key, and if you take a bomb and attach it to the key, you can deliver a bomb to the cancer cell. And that’s how the stuff works,” said Dr. Norman Block, UM researcher.

“That means that in theory the drug will internalize in the cancer cells not so much in the normal cells” said Dr. Gustavo Fernandez, Chambers’ oncologist.

Chambers is the first patient here to try this experimental targeted therapy, and he’s had promising results.

“I had a tumor that I could feel in my neck, and after two treatments I couldn’t feel it anymore. After two treatments I was off the pain medications,” he said.

In July, the Chambers were able to celebrate their 43rd anniversary.

“He’s back to vacuuming the pool and cooking and all those good things,” Alice Chambers said.

Doctors said his tumors are 70 percent smaller after four treatments. UM is one of only two sites in the country testing this new therapy.

“In California, one of our collaborators is using it for prostate cancer that’s become resistant to normal chemicals, and it’s working very well,” Block said.

UM Sylvester researchers hope to try the new therapy on pancreatic and breast cancer.

They hope to start before the end of the year.

Copyright 2011 WTVJ via NBC. All rights reserved.

Genetic differences distinguish stomach cancers, treatment response

Contact: Sarah Avery
Duke University Medical Center

SINGAPORE – Stomach cancer is actually two distinct disease variations based on its genetic makeup, and each responds differently to chemotherapy, according to an international team of scientists led by researchers at Duke-National University of Singapore Graduate Medical School.

The finding, published in the Aug. 1, 2011, edition of the journal Gastroenterology, is the first large-scale genomic analysis of gastric cancer to confirm the two discrete tumor types.

The researchers also found that a certain regimen of chemotherapy is more effective on one tumor type, while a different drug works best on the other, setting the groundwork for a more effective approach to treating gastric cancer patients.

“Our study is the first to show that a proposed molecular classification of gastric cancer can identify genomic subtypes that respond differently to therapies, which is crucial in efforts to customize treatments for patients,” said Patrick Tan, M.D., PhD, senior author of the study and associate professor in the Cancer and Stem Cell Biology Program at the Duke-NUS Graduate Medical School.

An estimated 21,000 people in the United States will be diagnosed with stomach cancer this year, and 10,570 will die of the disease, according to the National Cancer Institute. Worldwide, only lung cancer is more lethal.

Patients have long had markedly different responses to treatments, suggesting that their tumors may have underlying differences.

Hinting at those differences, a microscopic pathology test developed in the 1960s broadly described how well the tumor cells clumped together, typing them as either “intestinal” or “diffuse.” Known as the Lauren classification, after the doctor who first described the distinctions, the analysis fell short as a reliable prognostic tool.

“Most gastric cancer patients today are still being treated with a common one-size-fits-all regimen,” said Tan, who also serves as group leader at the Genome Institute of Singapore and a senior investigator at the Cancer Sciences Institute of Singapore.

“One reason for this is that the Lauren classification requires significant gastric cancer experience and there is considerable variation in classifying gastric cancers, even among qualified pathologists,” Tan said.

But the genetic findings by the Singapore-based researchers add greater specificity to the microscopic classifications and, for the first time, provide some guidance for doctors to prescribe effective treatments.

The team first analyzed 37 gastric cancer cell lines, which were pure cancer cells free of blood, tissue and other adulterations that could skew results.

Gene expression profiles yielded highly distinct patterns that indicated the two subtypes. In 64 percent of cases, the genetic subtypes validated the Lauren classifications – either intestinal or diffuse. In the other 36 percent of cases, the genomic process distinguished the subtypes where the pathology test could not.

Findings were confirmed using tumor samples from 521 cancer patients.

“It was quite reassuring to us that the genomic subtypes were associated with Lauren’s system,” Tan said. “There is a general assumption in the field that intestinal and diffuse gastric cancers (as classified by Lauren) represent two very different versions of gastric cancer, and now genomic data confirms this by demonstrating that the two genomic subtypes have very different molecular patterns.”

Establishing the highly accurate definition of tumor subtypes enabled the researchers to observe the different responses to chemotherapy. The intestinal-type tumors showed significantly better response to the chemotherapies 5-fluorouracil and oxaliplatin, and were more resistant to cisplatin than the diffuse tumors.

“The exact mechanistic reasons for this difference are currently unclear, and this is an area that we are actively working on,” Tan said, adding that the researchers are working to find subtype-specific molecular vulnerabilities to drugs.

The researchers have launched a prospective clinical trial, called the 3G study, where gastric cancer tumors will be genomically profiled, and treatments will be allocated on the basis of the tumor type.


In addition to Duke-NUS, research institutions included the National Cancer Centre Singapore; National University of Singapore; Singapore General Hospital; Genome Institute of Singapore; Yonsei Cancer Center, Seoul, South Korea; Peter MacCallum Cancer Centre, East Melbourne, Australia; National University Health System, Singapore; Kanagawa Cancer Center, Yokohama, Japan; Leeds Institute for Molecular Medicine, Leeds, England; Yonsei University College of Medicine, Seoul, South Korea; MD Anderson Cancer Center, Houston, Texas.

The study was funded by the Biomedical Research Council and National Medical Research Council of Singapore, Duke-NUS Graduate Medical School, and the Cancer Sciences Institute of Singapore. The researchers reported no conflicts of interest.

New Genetic Mutations Found for Non-Hodgkin Lymphoma

Dr. Lisa RimszaDr. Lisa Rimsza

By Sara Hammond, Arizona Cancer Center, July 27, 2011

Some tumor samples for the cancer-sequencing study came from the Arizona Lymphoma Repository housed in the UA College of Medicine.


Scientists at the BC Cancer Agency in British Columbia, Canada and their U.S. collaborators have identified a number of new genetic mutations involved in non-Hodgkin lymphoma, or NHL.

This massive cancer-sequencing study, published online in the journal Nature, will open a floodgate for researchers around the world to explore the significant number of newly discovered gene mutations and their role in the growth and development of lymphoma cells.

The work was performed at the BC Cancer Agency Genome Sciences Centre, which has received major support from several governmental and private sources, including the U.S. National Institutes of Health in Bethesda, Md.

In an extensive undertaking, researchers sequenced the entire genome of lymphoma cancer cells from 14 NHL patient samples and the “active” genes from 117 NHL patients to search for genetic mutations specific to cancer cells.

Tumor samples were collected from British Columbia scientists as well as their U.S. collaborators, including the Arizona Lymphoma Repository housed at the University of Arizona’s College of Medicine under the direction of Dr. Lisa Rimsza, a professor of pathology and Arizona Cancer Center member.

The magnitude of data revealed 109 genes with recurring mutations, from which 26 have been identified as contributors to NHL based on their mutation patterns. More than two-thirds of mutated genes had never been linked to lymphoma prior to this study.

Understanding tumors’ genetic signatures “tells us what makes the tumors tick and what might be their vulnerable spots to aim for with treatment. This information should provide better diagnoses, more accurate prognostic information and help to identify unique targets of therapy for each tumor type, therefore advancing personalized medicine for our patients,” Rimsza said.

“Based on the patterns of mutation in these 26 genes, we can see that these mutations enable tumor cells to grow and expand in non-Hodgkin lymphoma patients,” said Ryan Morin, the study’s lead author. “The mutated genes we’ve discovered, most of which were previously unknown to lymphoma or other cancers, should enable us to design new tests that allow us to recognize subtypes of lymphoma and may help us predict how each variation of this disease will react to different treatments.”

Non-Hodgkin lymphoma is the fifth most common form of cancer in Canada, and the fourth most common cause of cancer in the U.S.

“This new abundance of genetic information is thrilling. Researchers and clinicians can now collaborate to eventually create new drugs, or identify existing drugs, that inhibit these mutated genes directly and prevent the growth of non-Hodgkin lymphoma,” said Dr. Joseph Connors, a medical oncologist and distinguished scientist at the BC Cancer Agency and a clinical professor of medical oncology at the University of British Columbia.

The pattern of mutation observed in some of these genes is indicative of new tumor suppressors and oncogenes, the latter of which may be ideal targets for existing therapies.

Specifically, one of the novel lymphoma-related genes discovered in this study, MLL2, is mutated in 89 percent of Follicular lymphoma patients, suggesting it is the most commonly mutated gene in NHL. Mutation of MLL2, which appears to be a tumor suppressor, is suspected to provide cancer cells with the ability to grow rapidly in-spite of the body’s regulatory mechanisms.

A second novel gene discovery, MEF2B, bears a so-called “hot spot” mutation pattern reminiscent of other known cancer genes.

New Study Reports CancerTYPE ID Expands Tumor Type Coverage and Demonstrates Clinical Utility

CancerTYPE ID is Now a Covered Benefit for Medicare Part B Patients

Published Wednesday, Jul. 27, 2011

SAN DIEGO, July 27, 2011 — /PRNewswire/ bioTheranostics, a bioMerieux company that develops innovative oncology diagnostic tests to support targeted disease management, announced today study results published in the next issue of the Journal of Molecular Diagnostics related to the clinical validity and the clinical utility of CancerTYPE ID®, its 92-gene molecular classification test to aid in the determination of the origin of a tumor. The company also announced Medicare reimbursement coverage.

The study, Performance and Clinical Evaluation of the 92-Gene Real-time PCR Assay for Tumor Classification, demonstrates that CancerTYPE ID classifies 30 main tumor types and 54 histological subtypes, covering over 95% of all solid tumors. A database of 2206 specimens with a median of 62 samples per tumor type allowed for the increase in tissue coverage. The 92-gene classification algorithm demonstrated sensitivities of 87% for the 30 main tumor types and 85% for the 54 histological subtypes.

“Our study featured a 300 consecutive clinical case series in which CancerTYPE ID classified 22 types and 36 different subtypes, which included several rare tumors. This real-world clinical finding shows the importance of having a comprehensive scope of reportable tumor types to resolve differential diagnosis, to avoid the risk of misclassification and for overall clinical applicability,” said Richard Ding, Chief Executive Officer of bioTheranostics. “This study provides more evidence that CancerTYPE ID is establishing a new standard in the emerging field of molecular cancer classifiers.”

Additional highlights from the study showed that CancerTYPE ID can discriminate among tumor types that pose diagnostic dilemmas including neuroendocrine subtypes, squamous carcinomas (head and neck vs. lung), tumors present in the ovary (ovarian mucinous vs. GI tumor), and gynecological tumors (cervical vs. ovarian). “Thought leaders in the field and our physician customers have provided us valuable input regarding essential tumor types for molecular classifiers. We are pleased that CancerTYPE ID can address their diagnostic challenges,said Mark Erlander, PhD, Chief Scientific Officer of bioTheranostics. “Target therapies for metastatic cancers require precise knowledge of both tissue origin and underlying pathways. Our product provides critical information as a part of cancer management.”

bioTheranostics also announced that CancerTYPE ID is now a covered benefit for Medicare Part B patients following a coverage determination by Medicare’s administrative contractor Palmetto GBA. “This coverage decision was based on a review of the evidence supporting the analytical validity, clinical validity and clinical utility of CancerTYPE ID, making it one of the few molecular cancer tests supported by a Medicare coverage decision,” Ding said. “It’s another milestone in the history of bioTheranostics as we continue to improve existing products and bring additional high medical value products to market.”

About bioTheranostics

Advancing Molecular Diagnostics in Oncology

bioTheranostics discovers, develops and commercializes molecular diagnostic tests for cancer patients. Leveraging its unique expertise in expression profiling and algorithm development, bioTheranostics provides innovative tests to the oncology community to support targeted disease management. The company operates a CLIA-certified, CAP-accredited diagnostic service laboratory in San Diego, CA to perform its proprietary molecular diagnostic tests: Breast Cancer Index(SM), which provides risk stratification in patients with estrogen receptor (ER)-positive, lymph-node negative breast cancer; and CancerTYPE ID, a cancer classification assay that provides molecular classification of cancers with indeterminate, uncertain, or differential diagnoses to aid in the determination of the tumor site of origin. For more information call Client Services at 1-877-886-6739 or visit

For more information, including quotes and links, please visit the social media news release (SMNR) at

About bioMerieux

Advancing Diagnostics to Improve Public Health

A world leader in the field of in vitro diagnostics for over 45 years, bioMerieux is present in more than 150 countries through 39 subsidiaries and a large network of distributors. In 2009, revenues reached euro 1.223 billion with 85% of sales outside of France.

bioMerieux provides diagnostic solutions (reagents, instruments, software) which determine the source of disease and contamination to improve patient health and ensure consumer safety. Its products are used for diagnosing infectious diseases and providing high medical value results for cancer screening and monitoring and cardiovascular emergencies. They are also used for detecting microorganisms in agri-food, pharmaceutical and cosmetic products.

bioMerieux is listed on the NYSE Euronext Paris market (Symbol: BIM – ISIN: FR0010096479). Other information can be found at

bioTheranostics ContactsTim SchofieldTel: +1 858 587

bioMerieux ContactKoren Wolman-Tardy Tel: + 011 33 6 13 94 51 14

SOURCE bioTheranostics