Pathways in Human Cancer

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Robert Weinberg, Ph.D.

Robert Weinberg, Ph.D., Whitehead Institute and Koch Institute at MIT Signals Triggering the EMT and Cancer Stem Cell Formation

Dr. Weinberg reviews evidence that cancer stem cells (CSCs) arise from tumor cell/stromal interactions that promote activation of transcriptional programs similar to those activated during early embryogenesis. These transcriptional programs push tumor cells through a multi-phased epithelial to mesenchymal transition (EMT) eventually making them stem-like and metastatic. Such findings may provide investigators with the tools needed to identify CSCs and target them therapeutically.

Stephen Baylin, M.D.

Stephen Baylin, M.D., John Hopkins University School of Medicine Cell signaling and clues to the origin of the cancer epigenome

Dr. Baylin explores the hypothesis that the changes in promoter methylation state associated with normal transient stress may become permanent during chronic stress or inflammation. These epigenetic changes may form the backdrop for epigenomic abnormalities that promote cellular progression from risk state to malignancy.

Giulio Draetta, M.D., Ph.D.

Giulio Draetta, M.D., Ph.D., The University of Texas MD Anderson Cancer Center Understanding Context-Dependent Relevance of Potential Cancer Drug Targets

How some cancer cells survive to re-initiate tumor formation after successful treatment with a signal transduction inhibitor still remains an open question. Dr. Draetta discusses evidence that residual cells may survive the initial treatment regimen by up-regulating mitochondrial activity, which suggests a mechanism whereby the mitochondrial activity of surviving cells could be targeted using OXPHOS inhibitors to reduce tumor re-initiation and improve therapeutic outcomes.

Steven Gygi, Ph.D.

Steven Gygi, Ph.D., Harvard Medical School Measuring cellular signaling using MS-based proteomics

Dr. Gygi describes newly emerging multiplex labeling techniques for use in mass spectrometry (MS)-based proteomics. Multiplex labeling allows investigators to design comprehensive MS-based experiments, which include multiple treatment groups, triplicates and time-resolved samples. Such experiments can be employed to identify changes in signaling networks between normal and cancerous cells.

Sir Philip Cohen, Ph.D.

Sir Philip Cohen, Ph.D., University of Dundee Will drugs that target components of the MyD88-dependent signaling network be useful for the treatment of Diffuse Large B cell Lymphoma?

Diffuse large B-cell lymphoma is often associated with activating mutations of MyD88, an adapter protein that activates the innate immune response in an ubiquitin-mediated manner. Dr. Cohen presents evidence that compounds targeting the ubiquitin system (specifically E2 ubiquitin-conjugating enzymes) may block the downstream effects of MyD88 hyper-activation, opening up therapeutic possibilities for the treatment of this complex disease.

Yossi Shiloh, Ph.D.

Yossi Shiloh, Ph.D., Tel Aviv University Sackler School of Medicine ATM: regulating the cellular response to genotoxic stress, and more

Ataxia Telangiectasia Mutated (ATM) is a protein kinase that was primarily thought to be responsible for activating the cellular response to double-stranded DNA breaks. Dr. Shiloh describes recent phospho-proteomic screens that were used to identify about 1,100 ATM substrates. These data suggest that ATM is actually a versatile, homeostatic protein kinase that plays an integral role in the cellular response to genotoxic stress more generally.

John Blenis, Ph.D.

John Blenis, Ph.D., Harvard Medical School Tumor Cell Signaling and Metabolism

Malignancies resulting from gain-of-function mTORC1 mutations must increase nutrient uptake and energy production to support the anabolic processes that in turn support cell growth, survival, and proliferation. Dr. Blenis discusses how mTORC1 mutant cells regulate their increased nutritive and metabolic needs, and suggests that the special requirements of cancer cells may prove to be a vulnerability that can be exploited to develop novel therapies.

William Sellers, M.D.

William Sellers, M.D., Novartis Institutes for BioMedical Research Towards robust and systematic translational systems for cancer therepeutic development

Research models that reflect the complexities of cancer are critical for predicting the success of therapeutic compounds in a clinical setting. Dr. Sellers describes initiatives at Novartis to develop encyclopedias of cell line and patient-based xenograft model systems that integrate proteomic, genomic, metabolomic, and drug sensitivity data, to serve as robust platforms for therapeutic compound development.

Neal Rosen, M.D., Ph.D.

Neal Rosen, M.D., Ph.D., Memorial Sloan-Kettering Cancer Center Oncoprotein-activated Feedback–Biologic and Therapeutic Implications

Oncoproteins may exert their oncogenic effect through the constitutive activation of signaling pathways. Theoretically, constitutive activation of a pathway is balanced by feedback inhibition, but by necessity cancer cells become insensitive to such inhibition. Dr. Rosen uses the ERK-signaling pathway to illustrate possible mechanisms that may allow cancer cells to escape inhibition of the relevant signaling cascade and how this may shape our thinking about potential therapeutics.