Stiff Breast Tissue Could Indicate Aggressive Cancer

by Chiara Salemi

Breast Cancer

Millions of dollars are spent each year on cancer research, but despite that, cancer remains the second highest cause of death in the United States.  Cancer is so deadly because the DNA itself changes and our own cells become our body’s enemy, making it more difficult to treat.  Researchers are now trying to find out why certain cells become cancerous and why some people’s cancer grows faster and is harder to treat.

DNAScientists at the Center for Bioengineering and Tissue Regeneration have discovered that breast cancer patients who have stiff breast tissue are more likely to have an aggressive form of the disease.  In these patients, pressure from surrounding tissue causes cells to stop production of tumor suppressor chemicals.  The cell stops this production because it stops reading the genes in its DNA that code for the suppressors.  Although all of a person’s cells have the same DNA, many factors go into determining which parts of the DNA are used by each cell.  That is why our brain cells and skin cells, for example, function differently.  Even the same types of cells can function in varying ways.  One factor that tells cells what functions to do at certain times is their surrounding environment.  When a cell is under more pressure, such as when it is surrounded by stiff tissue, it acts differently than when it is under less pressure.  For example, cells do not divide as rapidly when they are under pressure from surrounding cells because there is not room for more cells.  With breast tissue, however, pressure can mutate a cell’s DNA, making the sequence that codes for tumor suppressors unreadable.  This in turn leads the cell to divide rapidly to form the tumor, the opposite of healthy functioning!

The mechanism behind this influence of outside factors on cell function is not well understood, but researchers have recently been investigating the topic because of its importance in cell cycle and cancer research.  Cancer is characterized by problems in the cell cycle, which is the progression of a cell’s lifetime from its formation to its division into new cells.  One of the stages of this cycle is its normal function, called interphase.  Here, cells produce proteins and other chemicals, but factors such as pressure can influence which chemicals are made and the quantity produced. In the case of breast tissue, being under pressure turns off cells’ production of tumor suppressors, making cancer in the region more aggressive and therefore more likely to spread.  The opposite is also true–men and women with softer tissue structure have fewer tumors and the tumors they do have are more easily treatable.

Another study, by Georgetown University Medical Center’s Department of Oncology, showed that survival rates for patients with mutations related to the production of tumor suppressors is only about 20%, compared to 80% for those without mutations.  Clearly survival rates such as these indicate an area of future treatment research.  The finding by the Center for Bioengineering and Tissue Regeneration, “may eventually lead to new treatments based on mechanical properties of surrounding tissue instead of only molecular targets within malignant cells,” said Valerie Weaver, the lead scientist in the discovery.  In addition, more aggressive treatment options can be taken for those at high risk due to stiff tissue.

For further reading:
An illustrated guide on mutations and cancer from the National Cancer Institute
The genetics of tumor suppressors

Source articles:
Tissue mechanics modulate microRNA-dependent PTEN expression to regulate malignant progression (
Mouw, Janna K., et al. “Tissue mechanics modulate microRNA-dependent PTEN expression to regulate malignant progression.” Nature medicine (2014).
DOI: 10.1038/nm.3497

SYK Allelic Loss and the Role of Syk-Regulated Genes in Breast Cancer Survival (
Blancato, Jan, et al. “SYK Allelic Loss and the Role of Syk-Regulated Genes in Breast Cancer Survival.” PloS one 9.2 (2014): e87610.
DOI: 10.1371/journal.pone.0087610