Tracking Down the Cellular Culprit that Helps Breast Cancer Spread

Hani Goodarzi in front of white board (Assistant Professor Department of Biochemistry and Biophysics Department of Urology, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco)
(Photo: Marco Sanchez, UCSF DM. Photography; The copyright is owned by the UC Regents.)

Researchers in San Francisco are taking a new approach to uncovering the regulatory pathways in cells that cause breast cancer to spread. Breast cancer that has spread to other organs is called metastatic cancer, it tends to be harder to treat and to have poorer outcomes

Scientists aren’t putting enough effort into creating drugs that specifically target metastatic breast cancer, says Hani Goodarzi, PhD, head of the research lab at the University of California, San Francisco (UCSF) that is studying the problem. “While metastatic disease is the ultimate cause of death in many breast cancer patients, anti-metastatic drugs are not commonly pursued,” says Goodarzi. He thinks that figuring out the pathways cancer uses to spread could lead to treatments that specifically target metastasis.

To track down these pathways, Goodarzi’s research group developed cutting-edge techniques that allow them to pinpoint certain key differences between normal cells and cancerous ones. “Cancer cells, for the most part, share the same genetic code with the normal cells. What gives cells cancerous and metastatic capacity is how this genetic code is interpreted,” Goodarzi says.

He is trying to figure out why and how this interpretation process goes wrong in cancer cells. Goodarzi explains that it is our cellular messengers that seem to be at the center of the problem. Inside of each cell, molecules read and then copy messages from specific points (genes) in the massive genomic scroll that is your DNA. These copies of DNA messages are called messenger RNA – aptly named, because like carrier pigeons, RNA carries these messages to other parts of the cell. Then, other molecules read the messages and carry out the task of making the requested proteins, which are key to how the cell functions.

Cells rely on regulatory pathways to keep this process moving smoothly. “Cancer cells hijack these pathways to express genes that shouldn’t be expressed or silence those that should be expressed,” says Goodarzi. This means that in cancer cells, protein production can get out of whack. Some cancer cells produce too much of a particular type of protein, while others produce too little – or none.

Goodarzi is using his advanced computing techniques to measure how fast cells produce new proteins. This protein production analysis lets Goodarzi know how the cancer cells differ from the normal ones.  He can then work backwards to find out what is going wrong in the cancer cells – and ultimately uncover the underlying corrupt regulatory pathway that is setting off the cancerous chain of events.

Goodarzi’s unique technique already led him to discover a pathway that appears to play a role in helping breast cancer cells metastasize. His findings were published last year in the journal Cell. Goodarzi is now working to learn more about this pathway with the help of a grant from the American Cancer Society. Goodarzi will also be using his computer modeling to discover other pathways involved in the spread of breast cancer.

Goodarzi is optimistic that the strides he is making in understanding the basic biology of cancer metastasis are going to lead to outcomes for patients in the future: “I want patients to know that we are taking a significant stride towards understanding what makes cancer cells tick. We need this knowledge to then be able to stop it from ticking.”

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