Cancer & Cell Biology Graduate Program

It is well known that neurofibromin (NF1), a tumor suppressor produced by the NF1 gene, keeps cancer growth in check by repressing the activity of a cancer driver gene called Ras. It then follows that when NF1 is lost, Ras can drive cancer growth by promoting treatment resistance and metastasis. NF1, however, can do more than regulate Ras. BCM researchers and their colleagues have discovered new insights into the function of neurofibromin that improve our understanding of breast cancer resistance and suggest novel therapeutic approaches to overcome it.

A protein naturally produced in the body has been found to suppress breast cancer metastasis in animal models of human tumors. In this study, the same team at BCM that published a pioneering study that brought alternative splicing to the field of cancer research, investigated how alternative splicing contributes to cancer metastasis by looking for proteins that regulate alternative splicing events linked to metastasis.

BCM researchers and colleagues uncovered evidence about how glioma manipulates its environment in ways that favor its own growth. This research, published in Nature, suggests new strategies to treat patients with this condition, one of the most aggressive malignant primary brain tumors.

Which therapy will benefit this particular patient the most? BCM researchers and colleagues offer insights that might help physicians better answer this question for endometrial cancer, commonly known as uterine cancer.

Analysis of proteogenomics data enables scientists to get up close and personal with cancer and more likely to be able to identify tumor weaknesses that may make it susceptible to specific therapies. Researchers have not been able to apply proteogenonics analysis to cancer diagnosis in the clinic simply because the size of the tissue sample required for this type of analysis is larger than the biopsy sample usually obtained for diagnosis. This study describes methods developed that enable detailed analyses of high-quality DNA, RNA and proteins from a single core needle biopsy.

When experimental findings are not compatible with the textbook view, scientists know they have quite a challenge in their hands. BCM researchers and their colleagues faced this situation when they were investigating how cells modulate their responses to estrogen at single-cell and -gene level. In the current study, researchers worked with human breast cancer cell lines grown in the lab.  Using both molecular and imaging analyses, they determined, at single-cell and -allele levels, the expression of two well-characterized genes whose activity is regulated by estrogen.

To get a detailed picture of the cellular processes that differentiate normal versus cancer cells, researchers resort to conduct several independent screening assays at the expense of time and additional cost. In this study, the goal of the BCM researchers was to measure multiple cellular pathways at once in a single biological sample, which would also minimize experimental errors resulting from conducting multiple separate assays using different samples.

About 75 percent of breast cancers have estrogen receptors, hence they are called estrogen receptor positive (ER+). Original ER+ breast cancer cells depend on estrogen to grow, and therapies that make estrogen unavailable to cells, called hormone therapies, can result in long-term remission in some patients. However, most patients with metastatic disease, including those whose tumors responded initially to hormone therapy, eventually relapse and die due to the tumors’ acquired resistance to hormone therapy. BCM researchers and colleagues unveiled a novel mechanism that helps explain how endocrine-resistant breast cancer acquires metastatic behavior, opening the possibility of new therapeutic strategies.

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