Junjie Chen, Ph.D. (Chairman)
- Molecular mechanisms of DNA damage response and repair pathways in genome maintenance and tumor suppression
- Proteomic analysis of oncogenic and tumor suppressive pathways
- Investigation of gene-gene and gene-drug interactions involved in cancer development and therapy
Our lab studies the roles of nutrient sensing and energy metabolism in cancer. Our current efforts aim to study
• The role of energy sensor AMPK and FoxO as well as their
associated long non-coding RNAs (IncRNAs) in energy sensing and tumor
• The crosstalk between cancer metabolism and epigenetics
• The role of glutamate/cystine antiporter SLC7A11 in the regulation of nutrient dependency and ferroptosis, a metabolic stress-induced non-apoptotic cell death
Our work aims to translate our understanding of cancer metabolism into novel effective cancer therapeutics.
- The role of cyclin E in breast and salivary tumorigenesis
- Generating transgenic mice to determine the requirement of LMW cyclin E for tumor maintenance and recurrence
- Identifying potential LMW-E/CDK2 substrates on a proteome-wide scale that could serve as targets for treatment of triple negative breast cancer
- Identifying the salivary gland-specific cyclin E-associated kinase that drives cyclin E-induced salivary gland cancer
- Molecular mechanisms of DNA damage repair and cell cycle checkpoint mechanisms
- How DNA damage is sensed and transduced into checkpoint signals
- Interaction of chromatin remodeling mechanisms with DNA repair and damage checkpoint pathways
- Repair of DNA interstrand cross-links, as many chemotherapy agents are bifunctional DNA cross-linkers
- Molecular mechanisms of Fanconi anemia
The overarching goal of my laboratory is to understand the molecular mechnisms of breast tumor progression and metastasis. Our major interest include regulatory RNAs and deubiquitinating enzymes. We have played a major role in establishing the current models of non-coding RNA regulation of epithelial-mesenchymal transition, metastasis, and therapy resistance. Moreover, we discovered the deubiquitinases for key cancer proteins; some of these deubiquitinases are promising therapeutic targets.
- Pancreatic and Lung Cancer - the leading causes of cancer death
- Adoptive immunotherapy - CAR-T cell-based therapy development
- Biochemistry - novel and "orphan" enzymes substrates discovery
- Genetics - CRISPR/Cas9 animal models for cancer pharmacogenomics
Our aim is to define upfront polytherapy approaches based upon deep systematic interrogation of the aberrant molecular pathways operating in lung and pancreatic cancer to combat or eliminate targeted and immunotherapy resistance and transform the two most deadly human cancers from lethal disease into a curable condition.
Our approach is to (1) develop novel promising immunotherapy approaches using T lymphocytes engineered with Chimeric Antigen Receptors (CAR-T cells) to act as a "living drug" to kill cancer cells, (2) utilize our recently published method for in vivo CRIPSR-mediated somatic-engineering to generate a pharmacogenomic map that will guide patient treatment and (3) identify novel and “orphan” enzymes substrates important in driving cancer progression and drug resistance.
Our vision is to build a comprehensive disease modeling platform to study novel signaling networks and generate innovative therapeutics using animal models that frightfully represent human disease and to decipher mechanisms of cancer progression and drug resistance. --> Join Our Team
- The effects of radiation and chemotherapy on male germ cells
- Studying Wnt pathways in cancer cells, embryonic stem cells, frog embryogenesis, mouse intestine and skin
- Regulation of telomerase in regeneration and disease
The goal of our research program is to understand how tissue stem cells and self-renewing tumor cells contribute to tissue regeneration and tumorigenesis. Our comprehensive research approaches include genetically engineered mouse models, organoids, cell biology and molecular biology.
- Identifying and targeting drivers of breast cancer metastasis
- Identifying and targeting vulnerabilities in treatment-refractory primary TNBC
- Defining features that enable indolent breast cancer to advance to aggressive disease
- Generating annotated collections of patient-derived xenograft (PDX) models of breast cancer for discovery science
The Piwnica-Worms Laboratory identifies alterations with functional significance to the development and progression of invasive triple negative breast cancer (TNBC); and translating results from basic, omic and preclinical studies into improved clinical interventions for breast cancer patients.
- Normal tissue complications of cancer treatments
- The genetic basis of radiation induced pulmonary fibrosis
- Mechanisms of radiation-induced alveolitis
- Protection and mitigation of radiation injury in normal tissues