Lamassu Biotech Inc. has announced that its IND for SA53-OS has been cleared by the FDA in the U.S. The planned phase I/IIa trials will investigate the genetically targeted therapy that blocks the MDM2 protein, a key regulator of the tumor suppressor p53 gene.
Replay Holdings LLC has entered into an exclusive, worldwide license agreement with the National Institutes of Health (NIH) for intellectual property related to a library of T-cell receptors (TCRs) directed against multiple cancer neoantigens.
Why cancer? The mechanisms that drive and maintain tumorigenesis are still a mystery. This is a play with different actors who have different roles in several contexts. One of these scenarios is represented by genetic and epigenetic conditions that determine the early trajectories of cancer cells. In addition, different mechanisms will control phenotypes and states that can take one or another direction toward cancer.
Some cancers with a poor prognosis have had no new treatments in decades. Advances in the genetic characterization of these tumors now offer a range of possibilities for the development of new therapies that could completely change the quality of life and survival of these patients.
Some cancers with a poor prognosis have had no new treatments in decades. Advances in the genetic characterization of these tumors now offer a range of possibilities for the development of new therapies that could completely change the quality of life and survival of these patients.
Astex Pharmaceuticals Inc. is getting $35 million up front and up to $500 million per program as it extends its drug discovery collaboration with Merck & Co. Inc. to include small-molecule activators of the p53 tumor suppressor protein. The number of programs was not disclosed, but they will target forms of p53 that have lost their function as a result of cancer-induced mutations in the TP53 gene. The aim will be to override the mutation and restore the ability of the wild-type protein to bind DNA and perform its functions as a transcription factor.
Alterations in chromosome number can play a role in cancer progression. An analysis of recurrent aneuploidies, such as the duplication of the long arm of chromosome 1, revealed that it was required for the proliferation of cancer cells carrying this alteration, an effect that was similar to so-called oncogene addiction. These findings have therapeutic implications that could benefit cancer patients depending on the genetic singularity of their tumor cells.
The development of cancer after p53 inactivation is determined by a series of genomic changes that occur in four steps. The loss of heterozygosity of TP53 (the gene encoding p53 in humans, named Trp53 in mice) is followed by an accumulation of deletions, genome doubling, and the emergence of gains and amplifications. In a study published in the August 17, 2022, issue of Nature, researchers have further observed that these four phases of genomic evolution are associated with specific histological stages before and after the malignant condition developed.
While Aprea Therapeutics Inc.’s data disclosed July 21 from the phase II trial with eprenetapopt – also known as APR-246, a reactivator of mutant tumor suppressor protein p53 – plus azacitidine (AZA) whetted interest in taking aim at the “guardian of the genome,” the company’s fortune took an unexpected turn when the FDA smacked a partial clinical hold on work with the duo.