Study finds genetic mutation responsible for making humans more prone to cancer

A team of US researchers has identified a genetic mutation that increased the risk of humans getting cancer paving the way for new treatments for the deadly diseaseResearchers from the University of California Davis US explain why certain immune cells in humans are less effective at fighting solid tumours compared to nonhuman primatesThe study published in the journal Nature Communications revealed a tiny genetic difference in an immune protein called Fas Ligand FasL between humans and nonhuman primatesThis genetic mutation makes the FasL protein vulnerable to being disabled by plasmin a tumourassociated enzyme This vulnerability seems unique to humans and is not found in nonhuman primates such as chimpanzeesThe evolutionary mutation in FasL may have contributed to the larger brain size in humansrdquo said Jogender TushirSingh Associate Professor in the Department of Medical Microbiology and ImmunologyldquoBut in the context of cancer it was an unfavorable tradeoff because the mutation gives certain tumours a way to disarm parts of our immune systemrdquo TushirSingh addedFasL is an immune cell membrane protein that triggers a programmed cell death called apoptosis Activated immune cells including CART cells made from a patientrsquos immune system use apoptosis to kill cancer cellsThe UC Davis team discovered that in human genes a single evolutionary amino acid change serine instead of proline at position 153 makes FasL more susceptible to being cut and inactivated by plasminPlasmin is a protease enzyme that is often elevated in aggressive solid tumors like triplenegative breast cancer colon cancer and ovarian cancerThis means that even when human immune cells are activated and ready to attack the tumor cells one of their key death weapons FasL can be neutralised by the tumour environment reducing the effectiveness of immunotherapiesThe findings may help explain why CART and Tcellbased therapies can be effective in blood cancers but often fall short in solid tumours Blood cancers often do not rely on plasmin to metastasize whereas tumors like ovarian cancer rely heavily on plasmin to spread the cancerSignificantly the study also showed that blocking plasmin or shielding FasL from cleavage can restore its cancerkilling power That finding may open new doors for improving cancer immunotherapyBy combining current treatments with plasmin inhibitors or specially designed antibodies that protect FasL scientists may be able to boost immune responses in patients with solid tumoursldquoHumans have a significantly higher rate of cancer than chimpanzees and other primates There is a lot that we do not know and can still learn from primates and apply to improve human cancer immunotherapiesrdquo said TushirSinghldquoRegardless this is a major step toward personalising and enhancing immunotherapy for the plasminpositive cancers that have been difficult to treatrdquo he addedThis story has been sourced from a third party syndicated feed agencies Midday accepts no responsibility or liability for its dependability trustworthiness reliability and data of the text Midday managementmiddaycom reserves the sole right to alter delete or remove without notice the content in its absolute discretion for any reason whatsoever