Hsu, P., & Shaw, A. (2017). Lung Cancer: A Wily Genetic Opponent. Cell, 169(5), 777-779. doi: https://doi.org/10.1016/j.cell.2017.05.001It is safe to say that most people know of someone who has been affected by lung cancer. As the leading cause of cancer deaths in both men and women, thousands are diagnosed with the disease every year. While most people blame lung cancer on smoking, it is in fact common for non- smokers to contract lung cancer. The most common type of lung cancer for non- smokers to get is non- small cell lung cancer (NSCLC). Unfortunately, despite many medical advances, this type of lung cancer remains incurable. Even with chemotherapy and other methods of treatment, recurrence rates are still very high. Using DNA bonds, researchers are trying to determine clinical impacts of intratumor heterogeneity (ITH) and cancer genome evolution in early stage cases of NSCLC.
In the study, researchers selected NSCLC specimens from 100 different patients and sampled multiple regions per lung tumor. They found that there were substantial ITH that had 30% of somatic mutations and 48% of somatic copy number alterations identified as subclonal. It was interesting to me to learn that tumors that had a high burden of subclonal copy- number alterations that were independent of tumor stage and were associated with an increased likelihood of recurrence or even death. They determined that ITH has the possibility to represent a poor prognostic factor in NSCLC.
After reading more into the study, I found it interesting to learn that when NSCLC is in its early stages, the surgical resection samples are more sufficient to study ITH. Still, in metastatic disease cases in which tumors have spread to distant sites, multiple biopsies would be needed to assess for ITH, which as you can imagine, would not be safe for the patient. During the study, researchers looked into how to possibly counter cancer genome in the clinic and ITH. The assumption that they went along with was that clinical outcomes would be improved if the tumors are not as complex and less substrate for evolution is present. The problem with capturing tumors prior to subclonal diversification requires earlier detection and screening, which most people don’t get. The current standard screening method, imaging with low- dose chest CT’s, could possibly be augmented in the future with ctDNA, serum protein biomarker, or exhaled volatile organic compound testing. A final, but more difficult, mode of attack would be to actively shape the cancer genome evolution actively.
Ultimately, as time goes on, science will find a way to handle this disease that thousands of people die from. Additionally, sciences understanding of the chemistry of cancer will become more advanced and the ways they assess tumor response will evolve. While this study had the potential to do a lot of good in tracking the genetics of cancer, its difficult on the patients in more ways than one. For one study, it cost $1,750 per patient for sequencing of just a single tumor region. After reading through this study, I do think that it shows some promise. As time goes I do think that there will be more efficient ways to track the evolution of lung cancer and hopefully save lives. Finally, there is the hope that maybe therapeutic interventions can possibly limit tumor heterogeneity and reshape tumor evolution and could hold the key to improving cancer outcomes for all.
Hsu, P., & Shaw, A. (2017). Lung Cancer: A Wily Genetic Opponent. Cell, 169(5), 777-779. doi:https://doi.org/10.1016/j.cell.2017.05.001