Gene Dog Blog

Cancer biology, in brief, is the study of the life and development of cancer cells.  As the field has expanded, some aspects of the life of cancer cells have been targeted as key points of research — namely which mutation exactly is most directly responsible for the spread of cancer.

Recently, scientists at Massachusetts’ premiere research institution, Massachusetts Institute of Technology (MIT), have discovered evidence that points to a specific gene they believe controls the spread of the mutated cells in an aggressive kind of cancer called small cell lung cancer.

To uncover this evidence, the researchers used a newly developed method called whole-genome profiling.  The process of whole-genome profiling is like taking a genetic fingerprint of multiple subjects, and then comparing the results to highlight similarities, differences, and aberrations.

In the lab, scientists were able to follow the progression of the cancer from start to finish in mice.  Humans diagnosed with small cell lung cancer typically die within five years of being diagnosed.  The cancer spreads so quickly, in fact, that researchers are unable to study it, because people are very frequently diagnosed late in the disease’s progression.

With the mice, however, who were developed without two important tumor-suppressing genes, they could track the cancer’s metastasis and from there — using whole-genome profiling — isolate chromosomes that had been deleted or duplicated.  In the case of small cell lung cancer, a few short strands of genetic code had been replicated in the mice, specifically a piece of chromosome 4, including a gene known as Nuclear Factor I/B, or NFIB.

While MIT scientists are uncertain of NFIB’s precise role, they do know that it does play a part in the generation of lung cells.  Furthermore, when their findings were compared with some from another important cancer research facility, the Dana-Farber Cancer Institute, they discovered that NFIB is also duplicated in human small cell lung tumors.

Current knowledge of NFIB suggests that it codes for a transcription factor — it controls the expression of other genes — so MIT scientists now are beginning to search for the other genes associated with NFIB.

Developments like this are pivotal as scientists seek the elusive cure for cancer.  This new information about overexpressed NFIB in small cell lung cancer, for example, will probably drive new pharmaceutical campaigns that will attempt to target and slow or stop the mutation in humans, thus at least halting the progression of one very aggressive kind of cancer.

Byline:

This is a guest post by Jane Smith from background check. She is a Houston based freelance writer and blogger. Questions and comments can be sent to: janesmth161 @ gmail.com