Similarities among three pediatric brain tumors that arise in different structures of the CNS – pineoblastoma, retinoblastoma and Group 3 medulloblastoma – have been linked to their shared origin during pineal gland development. Scientists at St. Jude Children’s Research Hospital have identified the molecular signatures that drive these tumors from pinealocyte progenitor cells that conserve a common differentiation program, providing a shared therapeutic target for these three cancer types.
The exact genetic and epigenetic cause of the sporadic form of amyotrophic lateral sclerosis (ALS), which affects approximately 90% of patients, are largely unknown. Previous work found that mitochondrial dysfunction and metabolic dysregulation are crucial to ALS pathophysiology.
Similarities among three pediatric brain tumors that arise in different structures of the CNS – pineoblastoma, retinoblastoma and Group 3 medulloblastoma – have been linked to their shared origin during pineal gland development. Scientists at St. Jude Children’s Research Hospital have identified the molecular signatures that drive these tumors from pinealocyte progenitor cells that conserve a common differentiation program, providing a shared therapeutic target for these three cancer types.
A recent study published in Cancer Research by scientists at The University of Texas MD Anderson Cancer Center (USA) and collaborators aimed to identify and characterize a target that elicits an anticancer response through both disrupting cancer cell redox homeostasis and increasing the immunogenicity of pancreatic ductal adenocarcinoma (PDAC).
Approximately 10%-15% of breast cancer cases are classified within the invasive lobular carcinoma (ILC) type, and a great majority of them are estrogen receptor-positive (ER+). Despite the significant clinical differences between ILCs and invasive carcinoma of no special type (or ductal), ICL treatment still follows ductal paradigms, relying on endocrine therapy plus surgery and radiotherapy.
HIV-1 persistence in latent reservoirs of T lymphoid and myeloid origin is a major barrier for the cure of the disease, with complex and multifactorial mechanisms behind HIV-1 latency; thus, investigating these mechanisms is key for future targeted HIV therapies.
Neuroblastoma cells harbor a pattern of chromosomal aberrations that include chromosomes 1p and 11q deletions and 2p and 17q gains, as well as MYCN gene amplification with MYC overexpression. Recent research has identified RuvB-like 1 (RUVBL1) and RUVBL2 to be key mediators of the therapeutic response to a promising strategy such as serine/threonine-protein kinase ATR inhibition.
In a recent study published in Molecular Therapy: Oncology, researchers from the City of Hope National Medical Center and Beckman Research Institute (USA) and collaborators aimed to identify differentially expressed genetic pathways in glioblastoma multiforme (GBM) tumor cells after 48 hours of hypoxia treatment by performing RNA sequencing.
Hepatic ischemia-reperfusion injury (HIRI) is a severe pathologic condition associated with poor outcomes when individuals suffer from hemorrhagic shock, liver resection or transplantation surgery, leading to severe liver impairment and sometimes dysfunction in other organs. Chinese researchers have explored the potential of prolyl 3-hydroxylase OGFOD1 as a target for HIRI management, since it has been reported as a crucial regulator of gene expression, especially for translation.
