Genotyping of African Americans suggest that with regard to somatic driver mutations in non-small-cell lung cancer (NSCLC), black patients do not significantly differ from white patients, according to a new study.
Genotyping of African Americans suggest that with regard to somatic driver mutations in non–small-cell lung cancer (NSCLC), black patients do not significantly differ from white patients, according to a new study.
“The molecular profile of NSCLC in African Americans has been poorly explored thus far,” wrote study authors led by David P. Carbone, MD, PhD, of the Ohio State University Medical Center in Columbus. “This ethnic group comprises approximately 13% of the US population and presents higher lung cancer incidence and mortality rates.” The reason for that difference, they added, is still up for debate.
In the new study, researchers used targeted massively parallel sequencing to assess somatic mutations and copy alterations in NSCLC samples from African Americans. In total, 99 NSCLC samples were used, representing 31 squamous and 68 nonsquamous tumors. Results of the study were published online ahead of print on April 27 in the Journal of Clinical Oncology.
The investigators detected 227 nonsilent varients in 81 selected genes. Of those 81 genes, 51 were mutated in at least one patient. The most frequently mutated genes included the following: TP53 in 33 patient cases, LRP1B in 19 cases, and KRAS in 16 patient cases. EGFR was mutated in 6 patient cases, and the authors noted these tended to occur in nonsquamous tumors.
Next, researchers compared these results with analysis of 283 NSCLC samples from white patients in the Cancer Genome Atlas database. They found no significant differences between black and white patients in any driver mutation. This included KRAS (18% in whites vs 16% African Americans; P = .760), EGFR (6% vs 5%; P = 1.00), or any driver mutation (32% vs 24%; P = .163).
Because African American race was self-reported in these patients, the researchers also evaluated their genetic ancestry: the mean proportions of African, European, and Amerindian genetic background were 0.65, 0.25, and 0.10, respectively. There were no links found between the presence of KRAS or EGFR mutations and the proportions of the various ancestries, which the authors wrote corroborated the lack of connection between race and oncogenic driver mutations.
“In summary, we demonstrated a relatively low frequency of classic driver mutations in NSCLC among African Americans,” the authors wrote. “However, these results are comparable with the data reported for whites and suggest that African American ethnicity may not be a surrogate marker for the presence of specific driver mutations.”