CLEVELAND -- Dr. Marianne Alciati, the head of research science for Susan G. Komen for the Cure, visited Cleveland last week to see what local researchers are doing to fight breast cancer. 

Komen has a long history of sustained commitment to funding breast cancer research.

Dr. Joseph Baar, of University Hospitals, is investigating a vaccine that could help breast cancer patients with triple negative cancer to boost their immune system and avoid recurrance.

To learn more click on the video.

Breast cancer mortality rates have been declining since 1990, by more than 2 percent per year. These reductions have been credited for saving 50,000 lives from breast cancer.

Researchers now understand that breast cancer is not one disease; there are distinct subtypes that are characterized by their biology.

And we now have treatments that target those biologic differences.

Seventy to 75 percent of all breast cancers are a subtype called estrogen receptor positive. That's because these tumor cells have estrogen receptors on the surface and inside the cell and when estrogen attaches to the receptor, much like a key inserted into a lock, the key/lock complex sends growth signals into the cell.

Hormone-based therapies, like Tamoxifen, block the receptor and can be very effective, not only in treatment but now in shrinking tumors before surgery and providing information about treatment response. 

Fifteen to 20 percent of cancers are HER2 positive and we now have a drug called Herceptin (Trastuzumab, 1998) that inhibits the growth-signaling of HER 2 receptors on the surface of cancer cells.

New advances will not only add therapeutic options but will allow doctors to better select which patients are most likely to benefit. ­      

An enzyme called CYP2D6 (cytochrome P450 2D6) is critical in tamoxifen metabolism and individuals with little or no CYP2D6 function do not metabolize tamoxifen to endoxifen.

Endoxifen binds to estrogen receptors more effectively than tamoxifen itself and, therefore, is a critical part of tamoxifens effectiveness.

CYP2D6 function is an inherited trait and analysis of CYP2D6 geneotype is an early example of a tool that might be used for optimizing breast cancer therapy. ­      

A new class of treatments that is very exciting is called PARP inhibitors - PARP stands for Poly (ADP-Ribose) polymerase - an enzyme involved in DNA repair.

Resistance to chemotherapy can occur when tumor cells become very efficient at repairing the therapy induced DNA damage, which results in death of the cancer cell.

This drug inhibits or blocks the ability of tumor cells to repair chemotherapy induced damage and the therapy can continue to kill cancer cells. 

This drug also has a role in cancers associated with BRCA 1 and 2 mutations.

When BRCA 1/2 genes are missing, 'normal' DNA damage is not repaired and the resulting genetic instability causes cancer.

PARP acts to repair enough of the DNA damage in these resulting cancer cells to allow them to keep growing and PARP inhibitors can take away this back-up system allowing the cancer cells to self-destruct under the weight of increasing DNA damage and die.