Proposals for Next Classification Schema of Myeloid Neoplasms
We are looking for postdoc candidates with experience in cancer biology, mouse models and genome-engineering. Please email CV and 3 letters of recommendation to Wen.Xue@umassmed.edu.
Our lab uses CRISPR tools to speed up cancer gene discovery and disease gene repair. Rotation projects are available to explore experimental techniques such as molecular cloning of CRISPR plasmids, measuring genome-editing efficiency, dissecting mice, and processing of mouse tumor/tissue for histology.
Endowed Chair in Biochemistry and Molecular Biotechnology I
Endowed Chair in Biochemistry and Molecular Biotechnology II
For more information about the Postdoctoral position in Dr. Rando’s lab please use the link provided. Post doc position
Rotation projects are available to study chromatin structure and function. Project 1. Measure histone dynamics in yeast. Histone dynamics play major roles in chromatin metabolism and in the inheritance of chromatin states. To measure histone replacement rates in yeast, we have created yeast strains carrying inducible epitope-tagged histones H3 and H2A. Using microarrays, we will measure histone replacement rates in a variety of mutant yeast to ascertain the role of various chromatin remodeling factors in histone exchange reactions. Project 2. Characterize mechanisms for epigenetic inheritance in yeast. We have identified a variety of genes whose expression state in yeast is epigenetically heritable. We will screen the yeast genome for genes that affect the inheritance of these expression patterns. Project 3. Measure histone dynamics in embryonic stem cells. Embryonic stem cells are pluripotent cells that can give rise to every type of cell in the adult animal. The role of chromatin structure in maintaining this pluripotent state is poorly understood, but it appears that stem cell chromatin is exceptionally labile relative to that in differentiated cells. We will create stem cell lines with inducible tagged histones to measure histone replacement rates across the mouse genome.
Our Danny Cancer Fund Chair in Biomedical Research I
A postdoctoral position is available to study in this laboratory. Contact Dr. Kelliher for additional details.
Please visit the Kelliher Lab website at: http://labs.umassmed.edu/kelliherlab/ to learn more about our current research areas. 1. Identify genes/pathways that mediate leukemia-initiating cell survival 2. Understand the molecular basis of glucocorticoid resistance in leukemia 3. Examine contribution of RIPK1 kinase in inflammatory and autoimmune disease mouse models. 4. Reveal tissue-specific roles for RIPK1 in cell death and inflammation. Use conditional Ripk1 allele to investigate effects of Ripk1 deletion in liver, pancreas and antigen presenting cells.
Rotations <p >Project 1: Genetic screens for proteins that modify or regulate the activity of microRNAs in C. elegans.
Penelope Booth Rockwell Chair in Biomedical Research
Focus: Adeno-associated virus vector mediated gene transfer for gene therapy, gene therapy of inherited neurodegenerative Canavan Disease
Postdoctoral positions are available for this lab. Please contact Junhao Mao directly, 508-856-4149 or via email, Junhao.Mao@umassmed.edu
Governor Paul Cellucci Chair in Neuroscience Research
Project 1: Dervelop RNA-based therapies for frontotemporal dementia (FTD) and related disroders. Project 2: Study pathogenic mechanisms of FTD and related disorders in mouse models.
Our lab uses a combination of molecular, cellular, genetic, and behavioral approaches to further dissect the pathogenic mechanisms of Frontotemporal Dementia and Amyotrophic Lateral Sclerosis with a focus on mutant CHMP2B, progranulin and C9ORF72. We will identify common underlying pathways as potential targets for therapeutic interventions.
A postdoctoral position is available to study in this laboratory. Please contact Dr. Fazzio for details.
Rotation Projects <p >Rotation projects are available on any of the main topics being studied in the lab. Our recent RNAi screen identifying chromatin regulators necessary for ES cell self-renewal has opened up several new potential projects aimed at identification of the important functions of these regulators in ES cells. Alternatively, projects focusing on the mechanisms of action and regulation of Tip60-p400 complex, or examining the functions of chromatin regulators in cancer stem cells are also possible, depending on the student’s interests. Rotation projects will usually involve some combination of mammalian cell culture, cell and molecular biology, biochemistry, and genomic approaches.
Worcester Foundation for Biomedical Research Chair III
Please email Kate.Fitzgerald@umassmed.edu if you are interested in rotations.
Isadore and Fannie Foxman Chair in Medical Research
A postdoctoral position is available to study in this laboratory. Contact Dr. Czech for additional details.
Mentoring……………………………………………………………………………………………………… The Czech laboratory is active in mentoring graduate students and postdoctoral fellows. Many former student and postdoctoral trainees of the Czech laboratory are now internationally recognized professors at major universities and medical schools. These former lab members include: Paul Pilch, Professor of Biochemistry, Boston University School of Medicine Jeffrey Pessin, Professor and Director of the Diabetes Center, Einstein College of Medicine Joan Massague, Director, Sloan Kettering Institute Roger Davis, HHMI investigator and Professor of Molecular Medicine, UMASS Medical School Silvia Corvera, Professor of Molecular Medicine, Co-Director of the MD/PhD Program, UMASS Medical School Carla Greenbaum, Vice Chair and Director of Clinical Research, Benaroya Research Institute Jes Klarlund, Professor of Ophthalmology, University of Pittsburgh Medical Center Rob Lewis, Professor of Biochemistry and Molecular Biology, Eppley Cancer Institute, University of Nebraska Medical Center Richard MacDonald, Professor of Biochemistry and Molecular Biology, Eppley Cancer Institute, University of Nebraska Medical Center Assia Shisheva, Professor of Physiology, Wayne State School of Medicine. Mark Sleeman, Professor of Physiology, Monash University, Australia John Harris, Associate Professor of Medicine, UMASS Medical School Zhen Jiang, Associate Professor of Pharmacology and Medicine, Boston University Vishu Puri, Professor of Biomedical Sciences, Ohio University Olga Gupta, Assistant Professor of Pediatrics and Medicine, University of Texas Southwestern Medical Center Tim Fitzgibbons, Assistant Professor of Medicine, UMASS Medical School Myriam Aouadi, Assistant Professor, Integrated Cardio Metabolic Centre, Karolinska Institute Adilson Guilherme, Associate Professor, University of Massachusetts Medical School Our laboratory currently offers graduate student Rotation Projects (examples below and others available) and Thesis Research Projects for students following a rotation: Developing CRISPR technology for gene editing in adipocytes: Adipocytes function as master regulators of whole body metabolism and deletions of specific adipocyte genes in knockout mice promote dramatic improvements in glucose tolerance and insulin sensitivity in diabetic models. Thus the ability to direct gene editing in adipocytes in vivo has great potential in developing therapeutic strategies for obesity, type 2 diabetes and cardiovascular complications. Alternatively, an ex vivo approach is also feasible since adipose cells can be genetically altered in vitro prior to implantation into mice with beneficial effects. Such projects are designed to be performed in collaboration with other Czech lab members with the goal of specifically deleting or editing genes in adipose depots that drive increases in fatty acid oxidation, energy expenditure and systemic metabolic activity. Exciting preliminary data at the “proof of principle” stage has been achieved and this project is designed to focus on specific genes of high interest for therapeutics. Signaling by the lipogenesis pathway through Acetyl CoA: A major function of adipocytes is to store calories as triglyceride, in part through the process of fatty acid synthesis (lipogenesis). This metabolic pathway involves a number of metabolites including Acetyl CoA, which is also a substrate for acetylation reactions that modify proteins such as histones. Thus metabolic flux through adipocyte lipogenesis may also function as a signaling pathway to the nucleus to modulate transcription via levels of Acetyl CoA that accumulate during this process. This rotation project is designed to test this idea at the molecular level by monitoring histone acetylations and resultant transcriptional events during changes in Acetyl CoA levels caused by altering physiological conditions such as exercise, obesity and diabetes. If this concept is correct, the project could lead to developing therapeutic strategies for metabolic disease based on targeting lipogenic enzymes.
A postdoctoral position is available
H. Arthur Smith Chair in Cancer Research
Rotation Projects Laboratory rotations are available to study signal mammalian transduction mechanisms. Several projects are available, including studies of protein kinase cascades, gene expression, the cell cycle, and apoptosis. Targeted gene disruption approaches in mice combined with biochemical and molecular biology studies will be examined.
Potential Rotation Projects 1) Coordination of replication and recombination by the S-phase DNA damage checkpoint The replication checkpoint coordinates replication and recombinational repair to allow for the replication of damaged templates, however the mechanism by which the checkpoint regulates recombination is unknown. We have identified a number of potential checkpoint-kinase targets by phosphoproteomics. One possible rotation project would be to create site-directed mutations that would prevent kinase regulation of one or more of the targets. These mutations could be used to validate the role of the target in the checkpoint and to test the importance of checkpoint regulation in S-phase DNA repair. 2) Regulation of replication timing Heterochromatin regulates the timing of replication origin firing, however the mechanism by which it affects origin function is unknown. We have developed a model of how origin timing is regulated in non-heterochromatic chromatin; now we want to test how heterochromatin affects this mechanism. In particular, we want to manipulate the heterochromatic context at specific loci, measure the changes in origin timing and investigate the molecular mechanisms responsible for the change. One possible rotation project would be to establish heterochromatin at a well-characterized origin, measure origin timing, which we presume will be delayed, and then test at which step origin firing is delayed. <p >
A postdoctoral fellow position is available for a highly motivated candidate to join us in the Program in Molecular Medicine at the University of Massachusetts Medical School. Our research interests are focused on understanding how aneuploidy affects cellular physiology and metabolism, and how aneuploidy influences cell evolution leading to further gross genomic alterations.<?xml:namespace prefix = o ns = "urn:schemas-microsoft-com:office:office" /><o:p></o:p> <o:p> </o:p> The Candidates should have a recent Ph.D or M.D/Ph.D degree in Cancer Biology, Genetics, Biochemistry, Cell Biology or related field. The candidates must also have a proven track record of productivity and research experience. They should be highly motivated, have a strong desire to learn and excellent communication skills.<o:p></o:p> <o:p> </o:p> <o:p></o:p>Applicats should send their CV, summary of previous research and the name of three references that may be contacted to Dr. Eduardo Torres, e-mail: Eduardo.torres@umassmed.edu (address: 364 Plantation Street, LRB -523, Worcester, MA 01605-4321
Rotations are available in this laboratory. Please contact Dr. Torres for details.
Immediate opening! Two postdoctoral positions are available immediately to study cellular andmolecular mechanisms resulting in immunosuppression after alcohol use. Thefocus of this research is the role of monocytes and dendritic cells indecreased antigen-specific T cell activation after alcohol use.Intracellular signalling mechanisms resulting in decreased NF-kBactivation and inflammatory cytokine induction after acute alcoholconsumption are being investigated. Please contact Dr. Szabo for details.
Postdoctoral positions are available to study the relationship(s) between the Rb/E2F proliferation pathway and p53-dependent apoptosis. Areas of investigation include understanding why E2F1 is unique among the E2F family in its strong apoptosis signaling ability and determining the pathways that lead from E2F1 activation to cell death. Fellows will be associated with a highly motivated and interactive group of researchers studying aspects of cell cycle, apoptosis signaling and cancer using cell culture, virology and animal models. If interested, please contact: Timothy Kowalik Department of Molecular Genetics and Microbiology University of Massachusetts Medical School 55 Lake Avenue North Worcester, MA 01655 The University of Massachusetts Medical School is an Affirmative Action / Equal Opportunity Employer.
Rotation Projects Identify the region on E2F1 responsible for p53-mediated apoptosis. We know that a transcriptionally functional E2F1 is required for apoptosis signaling. We also know that E2F2 does not induce apoptosis in our system. Therefore, domains on E2F1 and E2F2 will be swapped to determine which E2F1 domain is responsible for apoptosis signaling. Role of nuclear kinases in E2F1 mediated apoptosis. Our recent efforts have revealed that E2F1 expression leads to the phosphorylation of p53 and this modification correlates with apoptosis. There are several candidate kinases that need to be analyzed for their contribution to p53 phosphorylation. A dominant negative approach will be used in this project to identify which kinase(s) contribute to the E2F1 signal to p53. Role of CMV IE proteins in proliferation. We have found that both IE1 and IE2 target different Rb family members. IE2 binds to Rb and IE1 interacts with p107. We now know that IE2 is a strong inducer of S phase but IE1 can only significantly modulate proliferation in cells lacking p53. We are interested in knowing why p53 can prevent IE1 from inducing S phase. Mechanism of p53 accumulation by CMV. It has recently been shown that CMV infection results in an accumulation of p53. We have recently found that IE1 expression also leads to p53 accumulation. We wish to determine the steps leading to p53 accumulation and the consequences of this event.
Focus: Cellular and organismal studies of viral infections
The Castilla laboratory is accepting applications for postdoctoral positions. The candidates should be close to or have recently graduated with a Ph.D. or M.D./Ph.D. degree (within 1 year) in the fields of Cancer Biology, Genetics, Biochemistry, Cell Biology or related field. The candidates must also have a proven track record of productivity and research experience. Previous experience using immunocompromised and transgenic mice, in vitro and in vivo assays with small molecules or nanoparticles, or hematopoietic stem cells is preferred. We are looking for highly motivated candidates with excellent communication skills, and able to work independently and in cooperation with other members of the laboratory. Applicants should send their CV, a cover letter summarizing background and research interests, and three letters of references by electronic mail to: Dr. Lucio H. Castilla, Associate Professor University of Massachusetts Medical School Lucio.Castilla@umassmed.edu
Potential Rotation Projects<?xml:namespace prefix = u5 /><u5:p></u5:p><?xml:namespace prefix = o ns = "urn:schemas-microsoft-com:office:office" /><o:p></o:p> <u5:p> </u5:p><o:p></o:p> 1. Role of core binding factors on hematopoietic stem cell function and survival. We use molecular pharmacologic and functional approaches to study the role of the RUNX factors in self renewal and proliferation of hematopoietic stem and progenitor cells, using genetically modified mice and human progenitor cells. <u5:p></u5:p><o:p></o:p> <u5:p> </u5:p><o:p></o:p> 2. Study the molecular mechanism of leukemia initiation and maintenance. Transcription factors and components of cytokine signaling are frequently mutated in human cancer, including leukemia. These mutations deregulate the proliferation, differentiation and survival of hematopoietic stem cells. We study the role of members of RUNX and RAS protein families in the function of hematopoietic stem cell function, pre-leukemic progenitors, and leukemia-initiating cells. <u5:p></u5:p><o:p></o:p> <u5:p> </u5:p><o:p></o:p> 3. Translational research: Recent evidence suggests that inhibition of pathways activated by gene mutations can be used to eliminate leukemia cells, and not affecting normal cells. We use small molecule inhibitors of leukemia oncogenes to test whether repression of activated pathways hinder survival of leukemia initiating cells, and eliminate leukemia. We use a combination of mouse models and human leukemia cells to test the efficacy, specificity and toxicity of candidate inhibitors, as single agents or in combination with first line leukemia drugs.<u5:p></u5:p><o:p></o:p>
Please contact Dr. Imbalzano to discuss the possibility of a postdoctoral training.See lab research interests and publications for recent topics of research. http://www.umassmed.edu/imbalzanolab/ http://www.umassmed.edu/imbalzanolab/publications/
Please contact Dr. Imbalzano to discuss the possibility of a rotation project. Rotation projects are generally based on current work and tailored to the interests of the student. See lab research interests and publications for recent topics. http://www.umassmed.edu/imbalzanolab/ http://www.umassmed.edu/imbalzanolab/publications/
A postdoctoral position is available to study in this laboratory. Contact Dr. McCollum for additional details.
Rotation Projects Analog sensitive LATS kinase: The goal of this project is to use CRISPR based genome modification to make mutations in the endogenous LATS kinase that cause it to be inhibited by a synthetic ATP analog. This will allow LATS kinase activity to be turned on and off using the ATP analog. The analog sensitive cell line will be a valuable tool for studying Hippo pathway responses to various stimuli and will be used to test whether dephosphorylation of LATS substrates is an important regulatory mechanism. This project will also set the stage for future experiments to create mice that have analog sensitive versions of LATS. These mice will be used to test whether LATS inhibition is a viable treatment for regenerative therapies for the heart, gut, pancreas and other organs. TRIP6 and Angiomotin interacting proteins: We know that cells monitor their mechanical environment by sensing F-actin levels and by measuring tension at cell-cell junctions. We have identified angiomotins as sensors for F-actin and the TRIP6 protein as part of a tension sensor at cell-cell junctions. However, to understand how these sensors work, we need know the network of proteins that they each interact with, and how those networks change in response to mechanical perturbations. To do this we will fuse each sensor to the promiscuous biotin ligase protein BirA, and express the fusion proteins in cells under various conditions. The biotin ligase will label proteins in close proximity with biotin. Labeled proteins will be purified and analyzed by mass spectrometry, and the spectrum of interacting partners under different conditions will be compared.
A postdoctoral position is available to study in this laboratory. Contact Dr. Ip for additional details.
Rotation Projects Project #1: Mechanistic study of isolated mutants that show abnormal intestinal stem cell division phenotypes. Project #2:Perform transgenic RNAi-based genetic screen for genes required for intestinal stem cell response to tissue damage.
Herman G. Berkman Chair in Diabetes Care Innovation
UMass Memorial Kaur Chair in Anesthesia and Perioperative Medicine
Joseph J. Byrne Chair in Biomedical Research
? Rotation Projects Multiple rotation projects are available in several areas related to long-range gene regulation and higher order chromosome organization. Projects include thorough analyses of the biochemical mechanisms of long-range gene regulation of specific disease-related genes, as well as large-scale analyses of chromosome organization using high-throughput genomics technologies (5C and Hi-C). The lab employs a wide range of experimental approaches, including cell culture, protein biochemistry, microscopy, genomics as well computational approaches such as bioinformatics and modeling. Specific rotation projects are determined dependent on the interest of the student.
A post-doctoral position is available immediately to study the role of genes found in a genome-wide RNAi screen to regulate the cellular response to the chemotherapy agent, cisplatin. The goal is to determine whether these genes function as tumor suppressor and/or regulate the mechanism of DNA repair processing. The laboratory is interested in understanding the role of hereditary cancer genes of the BRCA-Fanconi anemia pathway in DNA damage repair and tumor suppression. We seek motivated candidates with a PhD and background in cancer cell biology. Experience in mouse cancer models is desirable. The exceptional training environment within the Department of Cancer Biology at UMASS Medical School offers a rigorous and interactive research environment covering several aspects of tumor biology. Applicants should have excellent communication skills, and ability to conduct research independently and as a team. To apply, please send your CV with bibliography, a brief description of research experience and contact information for at least two references via email.
The laboratory is interested in a range of DNA replication/repair-related topics including (i) Defining biomarkers of “BRCAness” that signifies deficiency in the hereditary breast/ovarian cancer genes, BRCA1 or BRCA2, (ii) Targeting BRCAness as a replication gap vulnerability, (iii) Defining why replication proficiency requires the FANCJ helicase disengage mismatch repair proteins, (iv) Determining if suppressing gaps improves the health of Fanconi anemia patient cells, (v) Hunting down the cancer vulnerability that defines curability, (vi) performing functional genomic screens to uncover mechanisms regulating chemotherapy resistance.
Please visit the Socolovsky lab website at: http://labs.umassmed.edu/socolovskylab/ to learn about our current research areas. Rotation and graduate student projects are available in all areas, including: 1. Regulation of the transition from self-renewal to differentiation in erythroid progenitors. Mouse models deleted for one or more of the relevant regulators will be analyzed. 2. understanding the mechanism of global DNA demethylation in erythroid progenitors. Specifically, what is the role of the Tet family of proteins and 5-hydroxymethylcytosine in this process? 3. the regulation of the erythropoietic stress response in vivo.
<p >Rotation Projects <p >Rotation projects are designed to expose students to the molecular cell biology of solid tumors and to provide them with an appreciation for translational cancer research. Specific rotation projects, which are focused on the major themes of the lab, include: <p >Function and Regulation of Integrins (Cell Adhesion Receptors) in Cancer Epigenetic mechanisms that regulate integrin gene expression in human cancers Regulation of integrin expression and function during the EMT Role of specfic microRNAs (miRs) in regulating integrin function and signaling Contribution of integrins to carcinoma progression using mouse models of breast carcinoma <p >Vascular Endothelial Growth Factor (VEGF) Signaling, EMT and Carcinoma Progression Function and expression of VEGF receptors in carcinoma cells Regulation of VEGF transcription in response to EMT stimuli Role of miRs in regulating VEGF receptors and signaling Contribution of VEGF signaling to the behavior of aggressive, de-differentiated carcinomas <p >Nuclear Hormone Receptors and EMT Role of estrogen receptors in regulating the EMT Regulation of VEGF transcription by estrogen receptors
A postdoctoral position is available to study in this laboratory. Contact Dr.Guertin for additional details.
Anesthesiology and Perioperative Medicine
Population and Quantitative Health Sciences
Biochemistry and Molecular Biotechnology
Preventing Osteoarthritis After an ACL Injury
Preventing Osteoarthritis After an ACL Injury Playing the Long Game: Consensus for Preventing OA
Preventing Osteoarthritis After an ACL Injury Playing the Long Game: Consensus for Preventing OA Characteristics of Accelerated Hand Osteoarthritis
Joseph D. Early Chair in Biomedical Research
Eleanor Eustis Farrington Chair in Cancer Research
Prevention Strategies for Second Primary Malignancies After CAR-T Therapy
The Darkest Side of AML: The TP53 Mutation
Clonal Hematopoiesis in Clinical Practice: Real-World Insights
Unpacking CHIP: Recent Updates, Remaining Questions
Dr Patel on the Impact of Donor-Engrafted Clonal Hematopoiesis on Outcomes With Auto-/Allo-HSCT
Effects of donor-engrafted clonal hematopoiesis in stem cell transplantation
High-Risk Myelodysplastic Syndrome Findings in the SELECT-MDS-1 Study
Stem Cell Transplantation: How Clonal Hematopoiesis Shapes Patient Outcomes
Olutasidenib as a Breakthrough for R/R mIDH1 AML Patients
The Impact of Mutations in Clonal Hematopoiesis
TP53 in MDS & AML Prognostication & Treatment Strategies
Exploring the Biological Basis of TP53-Aberrant MDS & AML
Improving Outcomes in Blast Phase Chronic Myeloid Leukemia
ASH Clinical News - Practical Solutions Amid Cuts to Federally Funded Research
OncLive with Dr. Patel and Dr. Gerber: p53 Immunohistochemistry
Early Identification of TP53-Mutant MDS and AML Using p53 Immunostaining
Point-of-Care p53 IHC Unveils TP53-Mutant MDS/AML
IHC Enables Rapid Identification of TP53-Mutant MDS/AML
ASH Clinical News: p53 Immunohistochemistry for TP53-Mutant MDS/AML
p53 Immunostain in TP53-Mutant MDS and AML