Established the principle of “collateral lethality” and identified ENO2 as a target for therapeutic intervention by demonstrating that ENO2-depleation selectively inhibited growth, survival and the tumorigenic potential of ENO1-deleted GBM cells. Read the Abstract Download the PDF
Passenger Deletions Generate Therapeutic Vulnerabilities in Cancer Read More »
Progressive DNA damage and mitochondrial decline are both considered to be prime instigators of natural ageing. Traditionally, these two pathways have been viewed largely in isolation. However, recent studies have revealed a molecular circuit that directly links DNA damage to compromised mitochondrial biogenesis and function via p53. This axis of ageing may account for both
Axis of Ageing: Telomeres, p53 and Mitochondria Read More »
Glioblastoma is both the most common and lethal primary malignant brain tumor. Extensive multiplatform genomic characterization has provided a higher-resolution picture of the molecular alterations underlying this disease. These studies provide the emerging view that “glioblastoma” represents several histologically similar yet molecularly heterogeneous diseases, which influences taxonomic classification systems, prognosis, and therapeutic decisions. Read the
Emerging Insights into the Molecular and Cellular Basis of Glioblastoma Read More »
Genetic modeling of telomerase extinction reveals vulnerabilities that motivate coincidental inhibition of mitochondrial maintenance and oxidative defense mechanisms to enhance antitelomerase cancer therapy. Read the Abstract Download the PDF
Antitelomerase Therapy provokes ALT and Mitochondrial Adaptive Mechanisms in Cancer Read More »
A few minutes before Ronald DePinho was to give a speech to his graduating class at Fordham College in the Bronx, he sat with his father in a student lounge. It was May 1977. His father had been in the United States for nearly 40 years. The son was on his way to a career
Leader in the Cancer Fight, and Son of an Illegal Immigrant Read More »
Here, we determined that entrenched multi-system degeneration in adult mice with severe telomere dysfunction can be halted and/or reversed by reactivation of endogenous telomerase activity. Read the Abstract Download the PDF
Telomerase Reactivation reverses Tissue Degeneration in Aged Telomerase-deficient Mice Read More »
This study demonstrated that telomere dysfunction activates p53, which in turn binds and represses PGC-1α and PGC-1β promoters, thereby establishing a direct link between telomere and mitochondrial biology. Read the Abstract Download the PDF
Telomere Dysfunction induces Metabolic and Mitochondrial Compromise Read More »
This model-informed progression analysis, together with genetic, functional and translational studies, established SMAD4 as a key regulator of PCA progression in mice and humans. This work led to the development of a clinical test enabling stratification of men with prostate cancer into benign and aggressive groups. Read the Abstract Download the PDF
SMAD4-Dependent Barrier Constrains Prostate Cancer Growth and Metastatic Progression Read More »
Ronald DePinho wants to reverse the aging process and increase years of healthy living so that older people can continue to work. Watch the Video
Myriad genetic and epigenetic alterations are required to drive normal cells toward malignant transformation. These somatic events commandeer many signaling pathways that cooperate to endow aspiring cancer cells with a full range of biological capabilities needed to grow, disseminate and ultimately kill its host. Cancer genomes are highly rearranged and are characterized by complex translocations
Telomeres and Telomerase in Cancer Read More »
Sign up for the latest news and updates from Ron DePinho, MD
