Brian Elenbaas
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View article: p70S6K/Akt dual inhibitor DIACC3010 is efficacious in preclinical models of gastric cancer alone and in combination with trastuzumab
p70S6K/Akt dual inhibitor DIACC3010 is efficacious in preclinical models of gastric cancer alone and in combination with trastuzumab Open
The PI3K-Akt-mTOR (PAM) pathway is implicated in tumor progression in many tumor types, including metastatic gastric cancer (GC). The initial promise of PAM inhibitors has been unrealized in the clinic, presumably due, in part, to the up-r…
View article: Supplementary Table S2 from Identification of <i>SFRP1</i> as a Candidate Mediator of Stromal-to-Epithelial Signaling in Prostate Cancer
Supplementary Table S2 from Identification of <i>SFRP1</i> as a Candidate Mediator of Stromal-to-Epithelial Signaling in Prostate Cancer Open
Supplementary Table S2 from Identification of SFRP1 as a Candidate Mediator of Stromal-to-Epithelial Signaling in Prostate Cancer
View article: Supplementary Table S1 from Identification of <i>SFRP1</i> as a Candidate Mediator of Stromal-to-Epithelial Signaling in Prostate Cancer
Supplementary Table S1 from Identification of <i>SFRP1</i> as a Candidate Mediator of Stromal-to-Epithelial Signaling in Prostate Cancer Open
Supplementary Table S1 from Identification of SFRP1 as a Candidate Mediator of Stromal-to-Epithelial Signaling in Prostate Cancer
View article: Data from Identification of <i>SFRP1</i> as a Candidate Mediator of Stromal-to-Epithelial Signaling in Prostate Cancer
Data from Identification of <i>SFRP1</i> as a Candidate Mediator of Stromal-to-Epithelial Signaling in Prostate Cancer Open
Genetic changes in epithelial cells initiate the development of prostatic adenocarcinomas. As nascent tumors grow and undergo progression, epithelial tumor cells are intimately associated with stromal cells. Stromal cells within the tumor …
View article: Supplementary Table S1 from Identification of <i>SFRP1</i> as a Candidate Mediator of Stromal-to-Epithelial Signaling in Prostate Cancer
Supplementary Table S1 from Identification of <i>SFRP1</i> as a Candidate Mediator of Stromal-to-Epithelial Signaling in Prostate Cancer Open
Supplementary Table S1 from Identification of SFRP1 as a Candidate Mediator of Stromal-to-Epithelial Signaling in Prostate Cancer
View article: Data from Identification of <i>SFRP1</i> as a Candidate Mediator of Stromal-to-Epithelial Signaling in Prostate Cancer
Data from Identification of <i>SFRP1</i> as a Candidate Mediator of Stromal-to-Epithelial Signaling in Prostate Cancer Open
Genetic changes in epithelial cells initiate the development of prostatic adenocarcinomas. As nascent tumors grow and undergo progression, epithelial tumor cells are intimately associated with stromal cells. Stromal cells within the tumor …
View article: Supplementary Table S2 from Identification of <i>SFRP1</i> as a Candidate Mediator of Stromal-to-Epithelial Signaling in Prostate Cancer
Supplementary Table S2 from Identification of <i>SFRP1</i> as a Candidate Mediator of Stromal-to-Epithelial Signaling in Prostate Cancer Open
Supplementary Table S2 from Identification of SFRP1 as a Candidate Mediator of Stromal-to-Epithelial Signaling in Prostate Cancer
View article: ATR inhibition augments the efficacy of lurbinectedin in small cell lung cancer
ATR inhibition augments the efficacy of lurbinectedin in small cell lung cancer Open
/Summary Small cell lung cancer (SCLC) is the most lethal type of lung cancer. Specifically, MYC-driven non-neuroendocrine SCLC are particularly resistant to standard therapies. Lurbinectedin was recently approved for the treatment of rela…
View article: ATR Inhibition Augments the Efficacy of Lurbinectedin in Small Cell Lung Cancer
ATR Inhibition Augments the Efficacy of Lurbinectedin in Small Cell Lung Cancer Open
View article: Therapeutic targeting of ATR yields durable regressions in small cell lung cancers with high replication stress
Therapeutic targeting of ATR yields durable regressions in small cell lung cancers with high replication stress Open
View article: MEK inhibition leads to BRCA2 downregulation and sensitization to DNA damaging agents in pancreas and ovarian cancer models
MEK inhibition leads to BRCA2 downregulation and sensitization to DNA damaging agents in pancreas and ovarian cancer models Open
Targeting the DNA damage response (DDR) in tumors with defective DNA repair is a clinically successful strategy. The RAS/RAF/MEK/ERK signalling pathway is frequently deregulated in human cancers. In this study, we explored the effects of M…