CTD²: Cancer Target Discovery and Development

The Cancer Target Discovery and Development (CTD²) Network, a functional genomics initiative, bridges the gap between cancer genomics and biology. The Network aims to understand how tumor heterogeneity leads to drug resistance in order to develop optimal combinations of chemotherapy or small molecules in combination with immunotherapy.

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Last updated: January 03, 2019

News & Publications

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Heterogeneous mechanisms of tumor response to α-PD-1 and α-TGFβ therapy.

CTD²

March 04, 2019

α-PD-1 therapy elevates Treg/Th balance and increases tumor cell pSmad3 that are both targeted by α-TGFβ antibody to promote durable rejection and immunity in squamous cell carcinomas.

Background: Checkpoint blockade immunotherapy has improved metastatic cancer patient survival, but response rates remain low. There is an unmet need to identify mechanisms and tools to circumvent resistance. In human patients, responses to checkpoint blockade therapy correlate...

Graphical abstract from Krug et al., 2019.

CTD²

March 01, 2019

A Curated Resource for Phosphosite-specific Signature Analysis

Signaling pathways are orchestrated by post-translational modifications (PTMs) such as phosphorylation. However, pathway analysis of PTM data sets generated by mass spectrometry (MS)-based proteomics is typically performed at a gene-centric level because of the lack of appropriately curated PTM...

CTD²

February 18, 2019

MCL1 and DEDD promote urothelial carcinoma progression.

Focal amplification of chromosome 1q23.3 in patients with advanced primary or relapsed urothelial carcinomas (UC) is associated with poor survival. We interrogated chromosome 1q23.3 and the nearby focal amplicon 1q21.3, as both are associated with increased lymph node disease in UC patients....

Graphical abstract from Harris, et al (2019).

CTD²

February 13, 2019

Deubiquitinases Maintain Protein Homeostasis and Survival of Cancer Cells upon Glutathione Depletion.

Cells are subjected to oxidative stress during the initiation and progression of tumors, and this imposes selective pressure for cancer cells to adapt mechanisms to tolerate these conditions. Here, we examined the dependency of cancer cells on glutathione (GSH), the most abundant cellular...

Proposed working model: p85α in the PI3K heterodimeric complex stabilizes but inhibits p110, whereas p110-free 85α molecules form homodimers to stabilize PTEN.

CTD²

February 12, 2019

Deregulated Gab2 phosphorylation mediates aberrant AKT and STAT3 signaling upon PIK3R1 loss in ovarian cancer.

Copy number loss of PIK3R1 (p85α) most commonly occurs in ovarian cancer among all cancer types. Here we report that ovarian cancer cells manifest a spectrum of tumorigenic phenotypes upon knockdown of PIK3R1. PIK3R1 loss activates AKT and p110-independent JAK2/STAT3 signaling through inducing...