The year 2022 marked another major step in the quest to towards making cancer history. Below are several highlights among many that caught my attention and admiration. These advances rest squarely on the foundation of sustained investment in cancer research from the public and private sectors. These advances continue to save more and more lives. […]
2022 Cancer Highlights Read More »
Pat Gulhati1and Ronald DePinho2 1Department of Medical Oncology, Rutgers Cancer Institute of New Jersey, New Brunswick, New Jersey, USA. 1Department of Cancer Biology, MD Anderson Cancer Center, Houston, Texas, USA. Pat Gulhati1and Ronald DePinho2 Pancreatic cancer (PDAC) is one of the most lethal human cancers1. The mainstay of treatment for metastatic PDAC is chemotherapy, which
Even in this market meltdown, seasoned biotech innovators with decades of experience know that strong novel science in the hands of experienced teams will eventually succeed. We’re in a painful, protracted biotech market correction. The XBI index is down 39% YTD and 60% over the past 14 months. But I contend that this is not
Opportunity in the Biomedical Roller Coaster Read More »
Twentieth-century health activist Mary Lasker, who devoted her life to securing greater research funding for cancer, is quoted as saying: “If you think research is expensive, try disease.” That battle for adequate cancer research funding is never-ending. Indeed, it’s not just cancer that needs greater funding. Despite advances through the tireless efforts of numerous organizations,
The Battle for Foundational Research Funding Read More »
Inactivation of the adenomatous polyposis coli (APC) is common across many cancer types and serves as a critical initiating event in most sporadic colorectal cancers (CRC). APC-deficiency activates WNT signaling which remains an elusive target for cancer therapy, prompting us to apply the synthetic essentiality framework to identify druggable vulnerabilities for APC-deficient cancers. Tryptophan 2,3-dioxygenase
Synthetic Essentiality of Tryptophan 2,3-dioxygenase 2 in APC-Mutated Colorectal Cancer Read More »
Inactivation of the adenomatous polyposis coli (APC) is common across many cancer types and serves as a critical initiating event in most sporadic colorectal cancers (CRC). APC-deficiency activates WNT signaling which remains an elusive target for cancer therapy, prompting us to apply the synthetic essentiality framework to identify druggable vulnerabilities for APC-deficient cancers. Tryptophan 2,3-dioxygenase
Synthetic Essentiality of Tryptophan 2,3-dioxygenase 2 in APC-Mutated Colorectal Cancer Read More »
Paradigmatic work from PJ Dey’s Lab reveals the co-conspiratory roles of oncogenic KRAS and intratumoral fungi in promoting immune modulating cytokine IL33 in pancreas cancer. This study, published February 3, 2022 in Cancer Cell, expands the therapeutic points of attack for this dreaded disease. Summary: TH2 cells and innate lymphoid cells 2 (ILC2) can stimulate
Fungal Mycobiome Drives IL-33 Secretion and Type 2 Immunity in Pancreatic Cancer Read More »
TH2 cells and innate lymphoid cells 2 (ILC2) can stimulate tumor growth by secreting pro-tumorigenic cytokines such as interleukin-4 (IL-4), IL-5, and IL-13. However, the mechanisms by which type 2 immune cells traffic to the tumor microenvironment are unknown. Here, we show that oncogenic KrasG12D increases IL-33 expression in pancreatic ductal adenocarcinoma (PDAC) cells, which
Fungal Mycobiome Drives IL-33 Secretion and Type 2 Immunity in Pancreatic Cancer Read More »
2021 marked the 20th anniversary of the first human genome draft sequence, which led to such revolutionary landmarks as The Cancer Genome Atlas (TCGA) Program and the birth of Spatial single-cell multi-omics. We also witnessed victories against hard-to-treat drug targets, FDA approval of Amgen’s sotorasib to treat non-small-cell lung cancer, novel therapeutic strategies such as
2021 Cancer Highlights Read More »
Amyloid-induced neurodegeneration plays a central role in Alzheimer’s disease (AD) pathogenesis. Here, we show that telomerase reverse transcriptase (TERT) haploinsufficiency decreases brain-derived neurotrophic factor and increases amyloid-β precursor in the murine brain. Moreover, before disease onset, the TERT locus sustains accumulation of repressive epigenetic marks in murine and human AD neurons, implicating TERT repression in
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