Recurrent head and neck tumors have gene mutations that could be vulnerable to cancer drug

April 4, 2014

An examination of the genetic landscape of head and neck cancers indicates that while metastatic and primary tumor cells share similar mutations, recurrent disease is associated with gene alterations that could be exquisitely sensitive to an existing cancer drug. Researchers from the University of Pittsburgh Cancer Institute (UPCI) and Yale University School of Medicine will share their findings during a mini-symposium Sunday at the American Association for Cancer Research Annual Meeting 2014.

About 50 percent of patients diagnosed with head and neck already have disease that has spread, or metastasized, to the lymph nodes, explained Jennifer Grandis, M.D., distinguished professor and vice chair of research, Department of Otolaryngology, Pitt School of Medicine, and director of the Head and Neck Program at UPCI, partner with UPMC CancerCenter. About 20 to 30 percent of patients thought to be cured of the disease go on to develop recurrent cancer, which typically doesn't respond to standard treatments.

"We decided to compare the genetic signatures of tumor cells from primary tumors with those from disease that had spread and cancers that were thought cured but then came back in the hopes of getting some clues about how best to guide therapy in these different settings," Dr. Grandis said. "We found that recurrent cancers might have an Achilles' heel we can exploit to kill them."

The team conducted the first whole-exome genetic sequencing study on what Dr. Grandis called its "treasure trove" of frozen patient samples and found similar both in primary tumors and in the lymph nodes to which their cancers had already spread. But there were different mutations in tumors that had recurred after a period of remission that were not found in their original cancers.

"The recurrent tumors carried mutations in a gene area that encodes for DDR2 cell receptors," Dr. Grandis said. "Other studies have shown that DDR2 mutations can confer sensitivity to the drug dasatinib, which could mean that drug has promise in the treatment of recurrent head and neck cancers."

The researchers suggest that further investigation of dasatinib treatment is warranted.

Explore further: No 'brakes': Study finds mechanism for increased activity of oncogene in certain cancers

Related Stories

No 'brakes': Study finds mechanism for increased activity of oncogene in certain cancers

January 6, 2014
The increased activation of a key oncogene in head and neck cancers could be the result of mutation and dysfunction of regulatory proteins that are supposed to keep the gene, which has the potential to cause cancer, in check, ...

Recurrent mouth and throat cancers less deadly when caused by virus, study shows

February 20, 2014
People with late-stage cancer at the back of the mouth or throat that recurs after chemotherapy and radiation treatment are twice as likely to be alive two years later if their cancer is caused by the human papillomavirus ...

Recurrent but rare mutations might underlie cancer growth

February 26, 2014
A potential new gene mutation that might drive lung cancer development and growth has been identified by researchers at The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard ...

Genomic testing links 'exceptional' drug response to rare mutations in bladder cancer

March 13, 2014
A patient with advanced bladder cancer in a phase I trial had a complete response for 14 months to a combination of the targeted drugs everolimus and pazopanib, report scientists led by a Dana-Farber Cancer Institute researcher, ...

Number of cancer stem cells might not predict outcome in HPV-related oral cancers

January 22, 2014
(Medical Xpress)—New research from The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC – James) suggests that it may be the quality ...

Recommended for you

Researchers release first draft of a genome-wide cancer 'dependency map'

July 27, 2017
In one of the largest efforts to build a comprehensive catalog of genetic vulnerabilities in cancer, researchers from the Broad Institute of MIT and Harvard and Dana-Farber Cancer Institute have identified more than 760 genes ...

Cancer-death button gets jammed by gut bacterium

July 27, 2017
Researchers at Michigan Medicine and in China showed that a type of bacterium is associated with the recurrence of colorectal cancer and poor outcomes. They found that Fusobacterium nucleatum in the gut can stop chemotherapy ...

Long-sought mechanism of metastasis is discovered in pancreatic cancer

July 27, 2017
Cells, just like people, have memories. They retain molecular markers that at the beginning of their existence helped guide their development. Cells that become cancerous may be making use of these early memories to power ...

Manmade peptides reduce breast cancer's spread

July 27, 2017
Manmade peptides that directly disrupt the inner workings of a gene known to support cancer's spread significantly reduce metastasis in a mouse model of breast cancer, scientists say.

Blocking the back-door that cancer cells use to escape death by radiotherapy

July 27, 2017
A natural healing mechanism of the body may be reducing the efficiency of radiotherapy in breast cancer patients, according to a new study.

Glowing tumor technology helps surgeons remove hidden cancer cells

July 27, 2017
Surgeons were able to identify and remove a greater number of cancerous nodules from lung cancer patients when combining intraoperative molecular imaging (IMI) - through the use of a contrast agent that makes tumor cells ...

0 comments

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.