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Jumping Genes Can Help Fight Against Blood Cancer:

  • Uncategorized
  • Jun 09, 2021

A new study was originated that informs regarding the jumping genes which are considered as a source of a genetic mutation and are certainly responsible for several human diseases. Human disease can have uncertain, long-lasting effects. The role of this jumping gene is surprising, where scientists made this unexpected discovery that these DNA sequences, also named, transposons help protect against blood cancers. Many people are suffering from blood cancer and they are not even aware of its treatment because the treatment has a very low success rate. This study happened in the children’s medical center research institute at UT southwestern. The finding was actively published in the online journal and it is also published in Nature Genetics that assisted scientists to discover and identify a new biomarker that helps place a prediction that how will patients respond to cancer therapies. Also, they will be able to find new therapeutic targets for acute myeloid leukemia (AML). 

Many cancer types are deadly and are found in children and adults. Transposons are considered DNA sequences that can move or do a regular shift and can jump from one desired location in the genome to another when they are highly activated. Though there are lots of different classes of transposons that exist in nature. Scientists present in the XU laboratory focused on a type known as long interspersed element 1 retrotransposons. L1 can manage work by a process of replica in which they copied and then pasted themselves into a different location of the genome.

This process leads to a mutation that can cause diseases such as cancer and it has serious consequences. The process often leads to mutations that can cause diseases such as cancer. Nearly half of all cancers contain mutations caused by L1 insertion into other genres, particularly lung, colorectal, and head-and-neck cancers. The incidence of L1 mutations in blood cancers such as AML is extremely low, but the reasons are poorly understood. When researchers screened human AML cells to identify genes essential for cancer cell survival, they found MPP8, a known regulator of L1, to be selectively required by AML cells. Curious to understand the underlying basis of this connection, scientists in the Xu lab studied how L1 sequences were regulated in human and mouse leukemia cells.