FACULTY

The Alberti lab is working to better understand the genetic and molecular basis of splicing factor gene mutations in the initiation, development, and progression of clonal hematopoiesis and myeloid malignancies, such as myelodysplastic syndromes (MDS).

Our lab is interested in studying metabolic properties of myelodysplastic syndrome cells in order to develop novel therapeutic strategies.

Dr. Bitler is committed to the fight against cancer through his work to elucidate the impact of cancer-related signaling and epigenetic regulation.

The Bonetto Lab investigates the molecular mechanisms responsible for abnormal muscle, bone and liver crosstalks in cachexia due to cancer and/or anticancer treatments. In order to achieve our goals, we leverage different in vitro and in vivo models, paired with a set of comprehensive molecular, metabolic, and pharmacologic tools to dissect the causes of musculoskeletal abnormalities associated with cancer.

The Bouchard lab investigates metabolic reprogramming within the irradiated tumor microenvironment through a spatial biology approach. We utilize a variety of models including 3D patient-derived assembloids and tissues to investigate cellular rearrangements following treatment with the primary goal of uncovering spatial features linked to metabolic resistance, ultimately aiming to enhance the effectiveness of radiotherapy in cancer patients.

Our group aims to understand how mitochondria reprogramming in tumors impact cellular behaviors that drive progressive and lethal cancer. We use a broad repertoire of biochemistry, cell biology, live cell imaging and animal models to study the impact of mitochondria shape, number and subcellular distribution in metastatic dissemination.

Deciphering the mechanisms underlying increased risk of brain metastases in young women with triple negative breast cancer. These include ovarian estrogen effects on reactive astrocytes that results in paracrine activation of EGFR and TRKB signaling in brain metastatic cells.

Within the broad scope of systems biology, my lab focuses on 3 research areas: 1) Network inference for identifying drug targets, 2) Predicting drug sensitivity from -omics datasets, and 3) Modeling temporal effects of drug combinations.

Prostate Cancer Tumor Suppressors, Stem Cells, Tumor Initiating cells, Signal Transduction, Receptor Signaling.

Our long-term goals are to develop novel approaches for treating immunorefractory cancers and to develop predictive models and diagnostics to identify compounds that sensitize tumors to T cell-based therapies.

Exploring the conditions that foster somatic evolution and discovering cancer vulnerabilities.

Our group focuses on epigenetic mechanisms regulating normal hematopoiesis and leukemia focusing on MLL-family histone methyltransferases.

Our main research goal is to understand how gene networks control cell behavior in homeostasis and human disease. Our two main focus areas are cancer biology and Down syndrome.

Dr. Ferrer Torres' lab focuses on understanding the molecular mechanisms driving human esophageal development, injury, and repair, with an emphasis on epithelial-mesenchymal interactions and differences in gastroesophageal reflux disease (GERD) among various populations. The lab investigates protective factors in esophageal tissues and uses patient-derived human organoids as a model system to study these processes. Additionally, the lab is interested in understanding esophageal cancer progression, aiming to elucidate injury responses specific to different ancestries and identify protective compounds through drug screening.

My research interests are to understand what causes neuroendocrine tumors to form (pheochromocytomas, paragangliomas, gastrointestinal and pancreatic neuroendocrine tumors). I am particularly interested in studying the inherited and tumor specific genetic changes that lead to tumor formation. The long terms goals of my research are to identify markers to predict aggressive or metastatic disease which can ultimately be used to develop therapies for prevention and/or treatment of these tumors.

Our laboratory focuses on a specific family of homeoproteins, the Six family, and their transcriptional cofactors, Eya and Dach. The Six1 homeobox gene is overexpressed in 50% of primary breast cancers and 90% of metastatic lesions, and its overexpression.

My lab has investigated biological roles and molecular regulations of 1) IL-1, inflammasomes and autoinflammation in human melanoma and skin diseases; 2) IL-37 and immune tolerance; 3) Tumor heterogeneity and plasticity in melanoma and its therapeutic resistance; and 4) ALDH2 and melanocyte activation and melanoma.

Dr Haugen is a physician-scientist who sees patients with thyroid cancer and does basic/translational and clinical research on thyroid cancer therapeutics. More recently, his research group and collaborators have been using multi-omic approaches and single cell RNA sequencing to better understand advanced thyroid cancer in humans and animal models.

My lab investigates signaling networks involving RTKs, GPCRs, and chemokine/cytokine receptors that function as oncogene drivers and acquired/intrinsic resistance pathways to targeted therapeutics in lung cancer, head and neck cancer and mesothelioma. Our approach blends in vitro and in vivo functional genomics approaches with human and murine cancer cell line models to define both cancer cell autonomous signals as well as tumor microenvironment-derived signals that contribute to the overall sensitivity of these cancers to targeted drugs and immune therapies.

Research conducted in the Henry laboratory focuses on understanding how cancer-associated comorbidities promote cancer with the goal of improving the efficacy of chemo- and immune-based therapies in patients falling within high-risk demographics.

To distinguish the role of HIF-1a and HIF-2a in cancer progression, Molecular Mechanisms of Hypoxic Transcriptional Response.

Mechanism and targeting of aggressive properties of pediatric sarcomas.

Dr. Jimeno’s laboratory and clinical research efforts aim at discovering new therapies and improving the outcomes of patients with head and neck cancer (HNC). He has developed PDX and humanized models to study cancer, and their application in new drug testing. He serves as the Director of the Colorado HNC SPORE, Director of the HNC Program, and co-Director of the Phase One Developmental Therapeutics.

Dr. Jordan serves as the Chief of the Hematology Division and directs a research program focused on the development of novel therapies for the treatment of leukemia.

Dr. Kabos’ interest is in translating preclinical findings into novel treatments for patients with breast cancer. The Kabos lab focuses on the role of breast cancer stem cells and tumor microenvironment in treatment resistance.

Dr. Keith's main research interest is lung cancer chemoprevention and early detection. He was Principal Investigator (PI) of the NCI-sponsored Lung Cancer Biomarkers and Chemoprevention Consortium (LCBCC) Iloprost Chemoprevention Trial and is the PI of an ongoing VA lung cancer chemoprevention trial evaluating pioglitazone in high risk current and former smokers. He is also the co-PI on a recently initiated chemoprevention trial examining inhaled iloprost.

My research interest is in endocrine neoplasia with focus on adrenocortical carcinoma. Our labs has generated first human adrenocortical carcinoma cell lines and patient derived xenografts in over three decades and are interested in new therapeutic targets. We have been exploring the targeting and mechanisms of several mitotic kinases, as well targeting immune checkpoints in our newly derived humanize mouse models of adrenal cancer.

Our laboratory is investigating the potential of the small molecule drug AMPI-109 as a novel therapeutic agent for triple-negative breast cancer.

The Lanning lab uses optical frequency domain imaging (OFDI) to elucidate in vivo longitudinal and microscopic changes in the tumor microenvironment (TME).

Role of PI3K/PTEN/AKT pathway in HNSCC progression.

Dr. Lyons laboratory focuses on mechanisms of lymphatic mediated metastasis of breast cancer. Specifically, utilizing mouse models to investigate developmentally regulated programs of inflammation and lymphangiogenesis that are utilized in the adult mammary gland and may be hijacked by breast tumor cells. The results of these translational studies have the potential to instruct therapy aimed at prevention of breast cancer metastasis.

The Mitra Lab investigates the role of myeloid cells in brain tumors, aiming to identify new therapeutic modalities for macrophage-based immunotherapies.

Molecular regulation of the microtubule network in cell division and disease.

My lab is interested in studying the molecular connections between aging and cancer. The focus is on understanding how the shortening of telomeres during cellular aging triggers autophagy and innate immune signaling pathways to suppress the early stages of tumor development. Our overarching goal is to deepen our understanding of cancer biology and develop innovative strategies to combat this disease.

My laboratory is focused on examining molecular pathways that regulate the progression and metastasis of lung cancer.

The study of lipid accumulation in non-adipocytes and how that process is regulated in multiple tissues, and in normal and pathologic situations.

Centrosome and cilia biology in cell division, motility, and disease.

Interplay between inflammation and metabolism as a driver of leukemia development; targeting of pre-malignant and malignant blood-forming stem cells.

The Pitts (GI Translational Research) Lab is focused on developing new novel therapies for colorectal and pancreatic cancers. The lab is interested in finding rational combination partners for molecularly-targeted anticancer and immunotherapy agents. The Pitts lab has a special interest in predictive biomarker and resistance mechanisms using correlative biological assays for early phase clinical trials.

We use informatics to solve clinically relevant problems in thyroid cancer, such as risk assessment based on the analysis of thyroid ultrasound images and genetics, personalized thyroid hormone replacement therapy, and understanding thyroid cancer development and response to treatment at the level of a single cell. We employ methods of clinical informatics, artificial intelligence/machine learning and population genetics to address problems encountered while taking care of patients with thyroid cancer.

Regulation of cell division, cell polarity and cell migration.

Regulation of Cell Death by the Protein Kinase C Family: Implications for Tissue Damage and Tumorigenesis.

The focus of my research is on the role of sex steroid receptors in breast and gynecological cancers, mechanisms of resistance to hormone therapy, and the differences between hormone dependent and independent breast cancers.

The major areas of our research currently are: 1. Understanding how metabolism contributes to cancer chemoresistance and developing approaches to overcome chemoresistance; 2) Investigating MCJ as a target to enhance CD8 T cell mitochondrial metabolism and efficacy of CAR-T immunotherapy.

The Sartorius laboratory studies the role of sex steroid hormones and their cognate receptors (i.e. estrogen receptor (ER) and progesterone receptor (PR)) in breast cancer.

The focus of my lab is to identify novel molecular targets relevant to papillary and anaplastic thyroid cancer (PTC and ATC) with the ultimate goal of advancing these studies to clinical trials for thyroid cancer patients who do not respond to standard treatment. Trainings Completed: Certificate in Multicultural Mentoring, Implicit Bias Training, Bystander/Upstander Training, Active Listening Training to Support Student Mental Health

My research focuses on melanocyte (pigment-producing cells) and melanocyte-related diseases, including melanoma and pigmentation disorders, with the aim of developing treatments and moving our research from bench to bedside. For melanoma research, we aim to improve patient survival by better understanding tumorigenesis and progression of melanoma, and host factors of antitumor immunity, and by developing melanoma treatments. For studies of melanocyte biology, we focus on SASH1, a novel pigmentation protein we identified, by studying a Hispanic family with an inherited pigmentation disorder.

Our lab specializes in translational research on multiple myeloma, a debilitating and incurable blood cancer. We are focused on developing new therapies, including both large-molecule immunotherapies and small-molecule pathway inhibitors. We are also developing approaches to personalize treatment through real-time monitoring of drug resistance development using ex vivo drug sensitivity testing.

The overall goal of the Sikora Laboratory is to understand mechanisms of response and resistance to steroid hormones and anti-estrogen therapies in breast cancer, with a special emphasis on invasive lobular carcinoma of the breast.

Using an animal model for colon cancer, we are determining what substitutions in tumor antigen peptides improve antitumor immunity.

The Tennis lab is primarily focused on translational lung cancer prevention research, including chemoprevention and interception of premalignant lesion progression. We have published work on markers for targeted application of lung cancer chemoprevention, signaling pathways in lung cancer, and premalignant lung lesion biology. We are interested in developing preclinical models for premalignant lesions, investigating the biology of premalignant lung lesions and progression to tumors, and conducting correlative studies related to chemoprevention trials. We also have a strong interest in education and outreach, including running CU Science Discovery Anschutz programs, and are committed to supporting the development of diverse scientists-in-training through cancer research experiences in our lab.

As part of the Developmental Therapeutics/GI Laboratory at UCD, my research is focused on pre-clinical studies of novel, rationally-based drugs for the treatment of advanced colorectal cancer, utilizing both cell culture and in vivo mouse model systems. These studies serve as a basis for therapeutic treatment options/choices for patients with advanced GI cancers in the UC Phase I Clinical Trials Program.

My lab is focused on deciphering the role of the tumor suppressor and transcription factor p53 in developmental malformations, pigmentary disorders and in tumorigenesis. For this we are using unique and extant mouse models of the p53 pathway and 3D primary cell cultures.

The overall goal of the Theiss Lab is to elucidate the role and mechanism whereby mitochondrial signaling pathways in intestinal epithelial cells contribute to gastrointestinal diseases, specifically inflammatory bowel diseases (IBD) and colorectal cancer.

My research focuses on genetic mechanisms by which normal brain cells become cancerous and how these genetic differences can be used to better diagnose and treat children with brain tumors,

I am interested in Reproductive Endocrinology, Neuroendocrinology, Pituitary Disease, Disorders of Adolescence and Menopause and Hypogonadism in Men and Women.

We are dedicated to collaborative research investigating B-cell acute lymphoblastic leukemia (B-ALL) - the most common cancer in children. Many B-ALL patients will succumb to disease resistant to existing chemotherapy and immunotherapies, such as CD19-directed chimeric antigen receptor (CAR) T cell therapy. We aim to uncover how the immune system is remodeled by leukemic cells to foster their survival throughout therapy. Ultimately, we will endeavor to develop novel treatment approaches that modulate components of the leukemic immune microenvironment in order to improve B-ALL treatment outcomes.

My lab studies the mechanism of pre-mRNA splicing and the role of the Six1/Eya transcriptional complex in cancer. We are also developing small molecule or RNA-based approaches to target splicing or the Six1/Eya complex as potential cancer therapeutics

My research interest in cancer immunotherapy focuses on 1) identifying novel immune checkpoints, 2) characterizing pathways that limit intratumoral T cell infiltration.