Research led by the Wellcome Trust Sanger Institute has revealed the long - mystic molecular underpinnings of an important anti - cancer cistron site on the X chromosome and suggests that a complementary gene on the Y chromosome , known as the UTY gene , can protect against an fast-growing profligate cancer calledacute myeloid leukemia ( AML ) . woman have two X chromosomes while men have an ex and a Y , so the UTY gene is only present in gentleman .
The study , published inNature Genetics , initially sought to determine the character of the UTX gene , which is found on the go chromosome , in AML development following preceding research that suggest mutated UTX sequences are present in many types of tumor and that reintroducing a functional transcript into cancerous cells quells their life-threatening activity .
Unlike many other gene on the 10 - chromosome , UTX does not undergoX deactivation , an early embryonic unconscious process where one transcript of the go chromosome is basically silenced , preventing gene expression . UTX ’s ability to avoid deactivation explains why blood cancers such as AML occurmore oftentimes in males than females – females have two copies of UTX , so if only one edition is mutated , the other can tread in to do the tumor - suppressing oeuvre . male person whose sole written matter is mutated appeared to be out of circumstances .
The probe involved a series of experiment in mice who had undergone genome editing to inactivate one or both copies of the UTX cistron in their flushed origin cell lines .
First , the mouse results illuminated how UTX acts as a sort of anti - cancer supervisory program by order other tumor - suppressing genes . It appear to help intermediate tidy cellphone processes by acting as a “ scaffold ” that represses yield of certain proteins involve inpossibly genus Cancer - get pathwaysand promotes product of proteins thatcircumvent cancerous demeanour .
Yet amazingly , none of the male mouse with a nonadaptive UTX factor developed any eccentric of blood cancer , and molecular analyses confirm that the rescuing agent was the UTY gene . Until now , it was thought that UTY could not do like UTX , despite similarities , because it has no catalytic action .
To explicate why males still develop AML and other cancers despite the newly discovered properties of UTY , the team analyzed a variety of UTX - mediated human malignant neoplastic disease cell credit line . This component part of the study showed that in many instances , chromosomal mutation in the UTX gene are accompanied bydeletions in the UTY gene .
“ antecedently it had been suggested that the only subprogram of the Y chromosome is in produce male intimate characteristic , but our upshot betoken that the Y chromosome could also protect against AML and other genus Cancer , " said first author Dr Malgorzata Gozdecka in astatement .
" Treatments for AML have not commute in 10 and there is a expectant unmet need for new therapies , ” add joint project drawing card Dr George Vassiliou . “ This study helps us understand the exploitation of AML and gives us clues for developing Modern drug targets to interrupt leukemia - causing appendage . "
