Recent highlights in cancer research

Two recent developments in cancer research have caught my eye this past week. The first involves the mapping of cancer genomes (looking at the DNA sequences of mutated genes), while the second looks at the karyotypes (the arrangement of chromosomes) of cancer cells.

Hopkins Medicine has announced two back-to-back papers published (currently online) in Science Magazine, involving researchers from a number of institutions, which examines head and neck cancers and identified new gene mutations. They found that mutations in NOTCH 1 and FBXW7 have a role in head and neck cancer based on their large-scale genome analysis. For those who have some understanding or level of comfort with cell biology details, NOTCH 1 is a receptor in the Notch signalling pathway responsible for cell differentiation, while FBXW7 is a component of the ubiquitin ligase enzyme SCF and aids in the targeting and degradation of cell cycle regulators.

One interesting note from this study is that the mutation in NOTCH 1 has one effect in head and neck cancer that differs from tumors in blood and bone marrow cancers. When mutations shutoff NOTCH 1 in head and neck cancers, differentiation stops and cells become cancerous and grow in an out-of-control manner. In essence, an active NOTCH 1 acts as a tumor suppressor for head and neck cancer. Conversely, mutations that activate NOTCH 1 in blood and bone marrow will accelerate the growth of relevant cancer cells, making it an oncogene in these cases. Nishant Agrawal, lead author of one of the papers and a head and neck surgical oncologist at Hopkins, notes that understanding the role of specific genetic mutations and identifying them in patients can help predict a patient’s prognosis and specify cancer treatments.

The other development regarding cancer karyotypes comes from U.C. Berkeley. In this paper, published in Cell Cycle, lead author Peter Duesberg and his colleagues find that cancer cells have a radically different arrangement of chromosomes than do normal cells. Such changes can be fatal for a cell or keep it from reproducing; if neither applies as in the case of cancer cells, then Duesberg asserts that cancer cells may very constitute a new species that is parasitic to its human hosts. This view would constitute a major upheaval in the way researchers approach cancer if his work gains the necessary ground to have a significant impact.

As a recap for those whose genetics knowledge is somewhat lacking, all of the DNA (and the genes encoded) in human cells (as well as other eukaryotes) are organized and compacted into chromosomes, and humans have 23 pairs of chromosomes that are homologous for the most part. They carry the same genes although the copies may not be exactly the same, and the major exception to this is the sex chromosomes that determine your gender. Generally speaking, a human whose karyotype deviates from this will either die if the alteration is fatal or simply fail to reproduce.

I mention Duesberg specifically as I had recalled reading a profile about him in Newsweek almost two years ago. While his early career in cancer research had been very promising and his cancer cell karyotype theory had been under development for many years, his professional reputation has never quite recovered from the blow that his rejection of the HIV-AIDS connection had sustained the past two decades. It is interesting to see whether the scientific community will further embrace his work in cancer, especially with the attention that Berkeley has given him with their press release, or continue to hold him accountable for his actions in the AIDS crisis.

—Ian Yu, Science & Technology Editor


Leave a Comment

Fill in your details below or click an icon to log in: Logo

You are commenting using your account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s