A team of researchers from Harvard University, Dana-Farber Cancer Institute, and other institutes have discovered some genomic changes in testicular cancer, the most common cancer in men 20 to 35 years old. The findings, which have been reported in the journal Nature, would extend the understanding of this highly treatable cancer. Approximately 95 percent of testicular cancers begin in germ cells. This type of cancer is highly treatable, even when cancer has spread to other places. The majority of patients respond quite well to chemotherapy drugs, and the cure rate of testicular cancer is very high. But patients cured of it have a risk of developing the cancer within the 15 years after initial diagnosis. Moreover, there are still some patients who are resistant to the drugs. It is estimated that 350 to 400 people in United States die of testicular cancer each year. Earlier research on testicular cancer have identified some mutations and chromosome damage. For example, a gain of extra DNA copies on chromosome arm 12p is present in many testicular cancers. But mechanisms of drug resistance or sensibility remain unclear. Christopher Sweeney and Eliezer M Van Allen from Dana-Farber Cancer Institute conducted this study to determine the genomic and molecular features of testicular cancer. Using clinical whole-exome and transcriptome sequencing, the team fully examined 59 tumor samples from 49 patients. Results showed that there were many chromosome changes with multiple parts of the genome having gain of one parental allele while simultaneously losing a copy of the other parental allele. The gain and loss of DNA copies represent a hallmark of testicular cancer, according to Van Allen. Furthermore, the team found that germ cell tumors that were sensitive to chemotherapy had intact copies of p53 -- a well known tumor suppressor gene that produces a protective protein. This gene is frequently mutated in human tumors. In addition, the researchers found testicular tumor cells tend to self-destruct through apoptosis. This feature of testicular cancer may help explain why it is highly sensitive to chemotherapy. They evaluated apoptotic signalling of tumors and found that testicular tumor cells contain high mitochondrial priming that facilitates chemotherapy-induced apoptosis. Flarebio is a manufacturer of bio-molecules including p53 protein and mouse polyclonal antibody. Compared to other types of cancers, testicular cancer is relatively rare (0.7% of all cancers). But over the past years, its incidence has increased about 1.2 percent per year.
