National Cancer Research — Right Here in NM

May is National Cancer Research Month. Join us in celebrating recent research breakthroughs and findings in our search for the causes and cures of cancer.

Help us to make cancer research a top national priority. Federal funding for medical research continues to decline, threatening the future health of Americans. Learn more on the American Association for Cancer Research site.

Jim Liu, PhD


Targeting Tumors with Toxins

Arsenic is a naturally occurring toxin found in groundwater that is absorbed into what we eat and drink – including foods such as rice and apple juice – and New Mexico has some of the highest concentrations of the metallic mineral in the U.S.

“Everything you do leads to something more interesting.”

— Jim Liu, PhD

It’s considered a co-carcinogen, because it promotes the activity of other cancer-causing agents. Despite this, UNM researcher Jim Liu, PhD, thinks arsenic has potential as an anti-cancer treatment.

Read the full article from UNM Health Sciences Center.


FROM THE LAB TO CANCER TREATMENT

Clinical research at the UNM Cancer Center impacts how we help people in the future and may even help the people enrolled in clinical trials today. Our clinical trials include studies to prevent, screen, diagnose and treat cancer. And the New Mexico Cancer Care Alliance offers access to clinical trials to all New Mexicans, in their own communities.

CLINICAL TRIALS MAY OFFER NEW TREATMENTS THAT ARE NOT YET AVAILABLE TO ALL PATIENTS


New Clinical Trial Combines Two Methods to Defeat Ovarian Cancer

Fewer than half of women diagnosed with ovarian cancer live for five years or more. Sarah Adams, MD, hopes her new clinical trial will change this outcome. Adams recently opened a clinical trial at The University of New Mexico Comprehensive Cancer Center to test a new approach to defeat ovarian cancer. The clinical trial treats women whose ovarian cancer results from mutated BRCA genes. It uses one drug that kills the ovarian cancer cells and another that boosts the immune system in response to the dying cancer cells.

Ovarian cancer has unclear symptoms and no screening tests that catch it in its early stages. Often, ovarian cancer spreads to other organs before a woman even knows she has it. Surgery and chemotherapy can help women at the beginning of their treatment, and this gave Adams the idea for her new approach.

Sarah Adams, MD

“If you knock out BRCA,” says Adams, “the cell can still live. If you knock out PARP, the cell can still live. But if you knock out both, the cell dies.”

— Sarah Adams, MD

Adams’ therapy combines the PARP inhibitor with a specific antibody. An antibody is a protein that attaches to a target cell. The antibody in Adams’ therapy helps one type of immune cell, called a T-cell, to find and devour ovarian tumor cells. Untreated ovarian tumors often produce chemical signals that keep T-cells away. But, the PAPR inhibitor combined with the antibody alert the entire immune system to the ovarian cancer cells.

The clinical trial is currently open to women with BRCA1 or BRCA2 mutations. Watch the news interviews for full details.


BIG DATA TO FIGHT CANCER

UNM Cancer Center is a founding member of the Oncology Research Information Exchange Network. ORIEN is an innovative partnership between top cancer centers to share information that will help search for cures and bring personalized care to New Mexicans.

A NATIONAL DATABANK TO SUPPORT PERSONALIZED MEDICINE


Forcing Cancer Cell Death

UNM Cancer Center scientists use already-approved drugs Cancer cells don’t die when they’re supposed to. Animal and human bodies follow an orderly process of birthing new cells and killing old ones. But cancer cells escape programmed cell death, called apoptosis, and multiply uncontrollably.

“There are mechanisms that eliminate mutated cells, normally,” says Alexandre Chigaev, PhD. “But one of the ways that cancer cells survive [is] that those mechanisms break.” Chigaev and his team described their discovery of the apoptosis-evading process that leukemia cells use in a paper published in Oncotarget.

All cells produce a molecule called cyclic adenosine monophosphate, or cyclic AMP, through normal cellular processes. If it builds up, cyclic AMP can harm the cell, so the cell converts it to a nontoxic form. Most normal cells can maintain low levels of cyclic AMP because their conversion system can keep up. If too much cyclic AMP piles up, though, the apoptosis process starts and the cell dies.

“Cyclic AMP reduces cell adhesion and maybe that’s one of the mechanisms by which [leukemic] cells leave bone marrow niches.”

– Alexandre Chigaev, PhD

Chigaev and his team discovered that leukemia cells could pump cyclic AMP out. But when they loaded cyclic AMP into normal blood cells, the cyclic AMP remained inside. The team confirmed their model by testing several different drugs that block leukemia cells’ ability to pump cyclic AMP out.

The drugs, all approved by the Food and Drug Administration, are used to fight malaria and fungal infections. They disable the cellular machinery that leukemia cells have to pump out cyclic AMP. When that machinery is disabled, the leukemia cells died. Because normal cells don’t have such machinery, the drugs had no effect on them. Chigaev and his team hope to begin leukemia clinical trials soon.

Read the full press release.


LATEST IN DRUG, GENOME AND PREVENTION SCIENCE

Our team of scientists develop new approaches to treat cancer by studying: genome sequencing, cell signaling, behaviors and habits in different populations, and new drug compounds. They work within four NCI research  programs.


Fighting Rare Immune Cancers

Tracy George, MD

New drug holds promise for treating advanced mastocytosis

Most people have never heard of mastocytosis. It’s a rare, sometimes deadly, immune disorder. New research may help those with advanced mastocytosis and possibly many more people, too.

“This is the first drug that’s shown to be effective in this very rare disease.”

— Tracy George, MD

George was part of the international team that recently published the results of its study on mastocytosis in the New England Journal of Medicine.

“Mast cells are normal cells in the body that mediate the body’s allergic and inflammatory responses,” says George. “But people with mast cell disease have too many mast cells and they’re abnormal.” Too many abnormal mast cells can cause allergic reactions and inflammation.

Different subtypes of the disease differ in the how serious these responses are. People with indolent mastocytosis may have mild symptoms and lead normal lives but those with advanced mastocytosis — the most deadly subtype is called mast cell leukemia — live less than six months after their diagnosis.

The Food and Drug Administration has approved only one drug, called imatinib, to treat advanced mastocytosis. Imatinib blocks the action of a cellular protein called a tyrosine kinase receptor. But people with a mutation in a gene that codes for a tryrosine kinase receptor do not respond to imatinib. And, George says, most people with advanced mastocytosis have the mutation.

George, who is the American expert in mastocytosis pathology, served as the pathologist for the international clinical trial. Sixteen people in the clinical trial had mast cell leukemia. “For those patients who did respond,” says George, “their median survival has not been reached. So that means [some are] still living, which is unbelievable.”

Watch the news interviews.


Smoking Gun

Study shows how smoking causes the changes that lead to lung cancer

Smoking tobacco causes added mutations in the DNA of lung cells and in the DNA of other cells in the body. Ludmil Alexandrov, PhD, Sir Michael Stratton, PhD, FMedSci, FRS, and their international team published their research in a paper in Science. This was the first study to show the process by which smoking causes these cancers.

Mutations are changes in DNA, deoxyribonucleic acid. DNA is the genetic code that governs how a cell carries out its tasks. Cancer results when DNA mutations disturb how certain genes function.

This study looked at the DNA changes in the cancers of more than 5,000 patients. The researchers compared tumor cells from people who smoked with tumor cells from people who never smoked. They found that smokers’ tumor cells had more mutations than nonsmokers’ tumor cells for almost every type of cell they tested. The researchers were able to estimate the number of mutations caused by smoking a pack of cigarettes per day for a year: every smokers’ lung cell amassed, on average, 150 additional mutations.

Previous studies have shown a strong link between smoking and lung cancer and a link between smoking and other types of cancers. But until now, these studies did not show how smoking caused the cellular changes that led to cancer. Watch the news interview.