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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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

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...

Lung Cancer, Non-Small Cell, Stage IIIB
CTD²
February 01, 2019

Chromosomal rearrangements involving receptor tyrosine kinases (RTK) are a clinically relevant oncogenic mechanism in human cancers. These chimeric oncoproteins often contain the C-terminal kinase domain of the RTK joined in cis to various N-terminal, nonkinase fusion partners. The functional...

Bone Chordoma
CTD²
January 21, 2019

Chordoma is a primary bone cancer with no approved therapy1. The identification of therapeutic targets in this disease has been challenging due to the infrequent occurrence of clinically actionable somatic mutations in chordoma tumors2,3. Here we describe the discovery of...

Pancreatic Cancer Stage 3
CTD²
January 18, 2019

Objective: Pancreatic ductal adenocarcinoma (PDA) has among the highest stromal fractions of any cancer and this has complicatedattempts at expression-based molecular classification. The goal of this work is to profile purified samples of human PDA epithelium and stroma and...

Unique Crenolanib DNA variants
CTD²
January 16, 2019

FLT3 mutations are prevalent in AML patients and confer poor prognosis. Crenolanib, a potent type I pan-FLT3 inhibitor, is effective against both internal tandem duplications and resistance-conferring tyrosine kinase domain mutations. While crenolanib monotherapy has demonstrated clinical...

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