Douglas Hanahan

Biography

Douglas Hanahan, born in Seattle, Washington, USA, received a bachelors degree in Physics from MIT (1976), and a Ph.D. in Biophysics from Harvard (1983). He worked at Cold Spring Harbor Laboratory in New York (1978-88) initially as a graduate student and then as a group leader. From 1988-2010 he was on the faculty of the Department of Biochemistry & Biophysics at UCSF in San Francisco. He has been elected to the American Academy of Arts & Sciences (2007), the Institute of Medicine (USA) (2008), the US National Academy of Science (2009), and EMBO (2010). In 2011, Hanahan received an honorary degree from the University of Dundee (UK).

Official source

https://people.epfl.ch/douglas.hanahan

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The mechanisms underlying the multistep process of tumorigenesis can be distilled into a logical framework involving the acquisition of functional capabilities, the so-called hallmarks of cancer, which are collectively envisaged to be necessary for malignancy. These capabilities, embodied both in transformed cancer cells as well as in the heterotypic accessory cells that together constitute the tumor microenvironment (TME), are conveyed by certain abnormal characteristics of the cancerous phenotype. This perspective discusses the link between the nervous system and the induction of hallmark capabilities, revealing neurons and neuronal projections (axons) as hallmark-inducing constituents of the TME. We also discuss the autocrine and paracrine neuronal regulatory circuits aberrantly activated in cancer cells that may constitute a distinctive "enabling"characteristic contributing to the manifestation of hallmark functions and consequent cancer pathogenesis.

CELL PRESS2023

A pan-cancer classification based on fmrp pathway activity that informs differential prognosis and therapeutic responses

Douglas Hanahan

The present invention relates to methods and compositions which provide a companion diagnostic for cancer therapy. A method for identifying and stratifying a patient or group of patients with cancer as (i) being high or low for FMRP activity, (ii) having a high or low risk prognosis, and/or (iii) being a responder or non-responder to cancer therapy, and/or (iv) having high or low immune cell infiltrated tumor.

2022

Cancer cell autophagy, reprogrammed macrophages, and remodeled vasculature in glioblastoma triggers tumor immunity

Agnieszka Alicja Chryplewicz, Douglas Hanahan, Krisztian Homicsko, Julie Laetitia Scotton, Ksenya Shchors, Mélanie Louise Tichet

Glioblastoma (GBM) is poorly responsive to therapy and invariably lethal. One conceivable strategy to circumvent this intractability is to co-target distinctive mechanistic components of the disease, aiming to concomitantly disrupt multiple capabilities required for tumor progression and therapeutic resistance. We assessed this concept by combining vascular endothelial growth factor (VEGF) pathway inhibitors that remodel the tumor vasculature with the tricyclic antidepressant imipramine, which enhances autophagy in GBM cancer cells and unexpectedly reprograms immunosuppressive tumor-associated macrophages via in-hibition of histamine receptor signaling to become immunostimulatory. While neither drug is efficacious as monotherapy, the combination of imipramine with VEGF pathway inhibitors orchestrates the infiltration and activation of CD8 and CD4 T cells, producing significant therapeutic benefit in several GBM mouse models. Inclusion up front of immune-checkpoint blockade with anti-programmed death-ligand 1 (PD-L1) in eventually relapsing tumors markedly extends survival benefit. The results illustrate the potential of mech-anism-guided therapeutic co-targeting of disparate biological vulnerabilities in the tumor microenvironment.

2022