This is the Zhao lab.

The work of our laboratory integrates molecular biology, tissue engineering and novel mouse models of human cancer to study oncogenic alterations in kinases that are involved in tumor formation and metastasis.

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Dr. Jean Zhao's lab is interested in how kinases in general, and phosphatidylinositol 3-kinases (PI3K) in particular, control malignant transformation. The work of our laboratory integrates molecular biology, tissue engineering and novel mouse models of human cancer to study oncogenic alterations in kinases that are involved in tumor formation and metastasis. In addition to our unique genetically engineered mouse models, we have developed a number of additional experimental systems, including, synthetic human tumors, and kinome-wide libraries of activated kinases to elucidate the mechanisms by which kinases function in cancer.

Lab News

July 17, 2015

The Zhao lab took two of the three top honors in the Poster Contest of this year’s Cancer Biology Retreat held at UMass Boston on Friday, July 17th. Dr. Jing Ni’s poster entitled “Orthotopic PDX models of HER2+ breast cancer brain metastases facilitates discovery of a selective targeted therapy yielding durable remissions” won the category “Most Promising Preliminary Result”.

Dr. Yubao Wang’s poster entitled “CDK7-Dependent Transcriptional Addiction in Triple-Negative Breast Cancer” took the prize for the “Best Mature Project”. Dr. Wang’s work has also resulted in a paper recently accepted for publication in Cell.

Congratulations to Dr. Wang and Dr. Ni!

September 23, 2011
Study Finds Key to Drug Resistance

Sophisticated "targeted" drug therapies are improving cancer care by selectively shutting down abnormal growth switches in tumor cells while avoiding toxicity to normal tissues. In some cases, though, tumors that are initially sensitive to these drugs first regress but then activate different, “backup” genetic signals that enable them to circumvent the therapy.

A new discovery by Jean Zhao, PhD, and colleagues may help physicians predict which tumors are likely to become resistant to a given drug, and identify the secondary pathways they are activating to escape the original therapy... read the full story here

Recent Publications

Yuzugullu et al. A PI3K p110beta-Rac signaling loop mediates Pten-loss-induced perturbation of hematopoiesis and leukemogenesis. Nature Communication.
2015, In Press

Wang et al., CDK7-Dependent Transcriptional Addiction in Triple-Negative Breast Cancer. Cell.
2015, In Press

Vantler et al., Class IA Phosphatidylinositol 3-Kinase Isoform p110α Mediates Vascular Remodeling. Arterioscler Thromb Vasc Biol.
June 2015

Tan et al., Light-triggered, self-immolative nucleic Acid-drug nanostructures. J Am Chem Soc.
May 2015

Usman et al., Chemopreventive effects of aspirin at a glance. Biochim Biophys Acta.
April 2015

Matheny et al., Role of phosphoinositide 3-OH kinase p110β in skeletal myogenesis. Mol Cell Biol.
January 2015

Costa et al., Measurement of PIP3 levels reveals an unexpected role for p110β in early adaptive responses to p110α-specific inhibitors in luminal breast cancer. Cancer Cell.
January 2015

Thorpe et al., PI3K in cancer: divergent roles of isoforms, modes of activation, and therapeutic targeting. Nature Rev Cancer.
December 2014

Li et al., Cyclin C is a haploinsufficient tumour suppressor. Nat Cell Biol.
November 2014

Wang et al., MELK is an oncogenic kinase essential for mitotic progression in basal-like breast cancer cells. Elife.
May 2014

Schmit et al., PI3K isoform dependence of PTEN-deficient tumors can be altered by the genetic context. Proc Natl Acad Sci USA.
April 2014

Gritsman et al., Hematopoiesis and RAS-driven myeloid leukemia differentially require PI3K isoform p110α. J Clin Invest.
April 2014

Cheng et al., A genetic mouse model of invasive endometrial cancer driven by concurrent loss of Pten and Lkb1 is highly responsive to mTOR inhibition. Cancer Res.
January 2014