Tumor

Antigen-loss relapse after successful CAR-T therapy; What do we do now?

Acute lymphoblastic leukemia disease bioinformatics

By Jacqueline Carrico, BS, MD

Developmental regulator Daam2 promotes glial cell tumors by degrading Von Hippel-Lindau protein

Autophagy Inhibition in Cancer: Clinical Trials Update

Adenosine Inhibits T cell Tumor Infiltration: KCa3.1, a New Anticancer Target

Novel Approaches to Improve Efficacy and Safety of CAR-T Therapy

CAR-T Therapy

By Jacqueline Carrico, BS, MD Candidate

Targeting Success in CAR-T Therapy for Solid Tumors

CAR-T poster

By Jacqueline Carrico, BS, MD Candidate

Mitochondrial ATPase inhibitory factor 1 (IF1) provides an explanation of cancer growth in anoxia or pseudo-anoxia

Dual applications of a c-Myc antibody in mitochondrial research

c-Myc, a proto-oncogene, has documented involvement in cellular differentiation, cell growth, cell death and tumor formation.  Target genes of the Myc family include those that participate in cell survival, translation, transcription, metabolism and more.  On a more specific level, c-Myc is a transcription factor that can both activate and repress its target protein by way of DNA modifications.  This allows for the use of a c-Myc antibody in two manners; it can be used to monitor the actual c-Myc protein expression levels, or, it

FSH R - a hormone receptor critical for both female and male reproductive systems

FSH R, or follicle-stimulating hormone receptor, is a transmembrane G-protein coupled receptor that is expressed in the ovaries, uterus, and testes. The ligand for this receptor, considered to be the central hormone of mammalian reproduction, is called follicle stimulating hormone (FSH) [1]. In females, FSH R is essential for proper ovarian development and follicle maturation. In males, it is required for normal spermatogenesis.

AHR - A transcription factor regulating immunity and tumorigenesis

The aryl hydrocarbon receptor (AHR) is a ligand activated transcription factor that controls the expression of a diverse set of genes. In the absence of ligand, AHR is retained in the cytoplasm. Upon ligand binding AHR translocates to the nucleus where it forms a heterodimer with aryl hydrocarbon receptor nuclear translocator (ARNT) (1). This receptor complex then recognizes AHR-response elements in target genes to regulate their transcription.

Pages