Patients with four types of cancer have new treatment options available after approval of three new drugs by the United States Food and Drug Administration in recent weeks.

The highly targeted drugs focus their firepower on specific types of cancer cells to treat groups of patients with non-small cell lung cancer, metastatic melanoma, Hodgkin lymphoma and anaplastic large cell lymphoma (ALCL). They offer new options for late-stage patients after frontline treatments have failed.

All three drugs were available at MD Anderson via clinical trials before FDA approval.

"This is an ideal example of personalized therapy," says Faye Johnson, M.D., Ph.D., associate professor in Thoracic /Head and Neck Medical Oncology. "The drug is given only to a small group of patients with the target genetic variation in their tumors. It worked great and the toxicities are trivial, especially compared to chemotherapy."

While Johnson is talking about the drug crizotinib (known commercially as Xalkori®), approved for advanced-stage non-small cell lung cancer patients whose tumors have the ALK gene fusion, the same can be said for the other two drugs.

An intravenously delivered genetic bomb primed to go off only in breast cancer cells kills tenacious breast cancer-initiating cells, MD Anderson researchers report in this week's edition of Cancer Cell.

In cell line and mouse studies, expression of a mutant version of Bik, a gene known to promote cell suicide, reduced these treatment-resistant breast cancer stem cells by blocking three proteins that prevent cellular self-destruction.

"There are no effective methods to target breast cancer-initiating cells, and they're urgently needed, especially for relapsed breast cancer patients," said senior author Mien-Chie Hung, Ph.D., vice president for basic research, professor and chair of MD Anderson's Department of Molecular and Cellular Oncology. "This research suggests a potential therapeutic approach to breast cancer stem cells that will minimize recurrence and drug resistance."

The BikDD therapy reduced tumor volume and extended survival in mice with resistant breast cancer while sparing normal cells because the gene therapy package is tuned to stay silent in non-cancerous cells. It also increased the impact of the chemotherapy drug lapatinib, known commercially as Tykerb®.

The gene therapy system has been successfully applied in pancreatic, lung, liver and ovarian cancer preclinical models. MD Anderson clinical researchers are preparing a phase I clinical trial for pancreatic cancer that is planned for early 2012.

Day 2 of the  Proton Therapy Center National Education Conference picks up where day 1 left off with insights into lung cancer, physics, dosimetry and more. The conference is designed to educate healthcare professionals on the recent advances, current treatment modalities, and clinical trials in radiation oncology using proton therapy.

The Proton Therapy Center National Education Conference is designed to educate healthcare professionals on the recent advances, current treatment modalities, and clinical trials in radiation oncology using proton therapy.

   

This post features key insights from most of the Day 1 speakers including information on proton therapy for multiple disease sites, and recent advances in the field.

Phyiscs of Proton Therapy (Radhe Mohan, PhD)

• Proton therapy has an inherent advantage because proton radiation dose patterns can be shaped to conform to the shape of a tumor.
• Physicists ensure equipment is performing correctly, that treatment plans are optimal for each patient and that the complex ways in which the particles travel within the body are deeply understood so they can be distributed effectively.
• To make protons useful for radiation therapy thin beams entering the treatment "nozzle" must be spread laterally and longitudinally, and shaped appropriately.

A blend of histone proteins and DNA that packs genes into chromosomes, chromatin influences gene expression, DNA repair and chromosome recombination.  

Scientists at The University of Texas MD Anderson Cancer Center, writing this week in the journal Cell, have identified another function - signaling molecule.  Chromatin is on the receiving end of signaling pathways that turn genes off and on, but research by Sharon Dent, Ph.D., and colleagues found that chromatin talks back.

"It's a basic change in our way of thinking about cell signaling - that all signals go into the nucleus and dead-end at DNA, that they point to chromatin and stop," says Dent, professor and chair of MD Anderson's Department of Molecular Carcinogenesis and director of its Center for Cancer Epigenetics.

 "Our data show that's not the case. We have a new fundamental aspect of cellular regulation that we need to now explore," Dent says.