The Laboratories of Anna Lasorella and Antonio Iavarone are seeking two postdoctoral scientists/postdoctoral associates to join our research program in Neuro-Oncology. Our studies focus on the molecular genetics and biology of brain tumors with an emphasis on the characterization and therapeutic targeting of driver mutations involved in the pathogenesis and progression of malignant brain tumors. We use a diverse combination of experimental approaches, including next-generation DNA/RNA sequencing, single cell RNA and ATAC sequencing and special transcriptomic. We model malignant glioma using glioma patient derived organoids and xenografts, and engineered mouse brain tumor models to understand tumor biology and design rational therapeutic strategies for patients with brain tumors. The labs are also a dynamic environment in which bench work and computational/systems biology intersect to facilitate biological research and identify new avenues through which to understand the complexity of brain cancer.
The ideal candidate will have research experience in cellular and molecular biology and mouse models of disease. Candidates should have a proven track record of peer-reviewed publications in respected journals. Previous experience in cancer biology, pharmacology, bioinformatics, and cancer genomics would be a positive consideration. We also encourage candidates who are trained in other research fields, such as developmental biology, immunology, and neuroscience, to apply these positions if they feel their skill sets are translatable to the goals described above. Strong mentoring support is available from Dr. Lasorella and Dr. Iavarone to write and win competitive postdoctoral grants.
Medical degree or Doctoral degree and life science research experience.
Technical aptitude for learning and executing complex experimental techniques for molecular biology, cell-based assays, single cell assays, and rodent procedures.
Impeccable experimental documentation and organized record-keeping skills.
Ability to effectively work independently and in a team environment in a fast-paced lab.
Independently perform bench work involving DNA/RNA sequencing, single cell RNA and ATAC sequencing and special transcriptomic and mammalian cell culture/cell-based assays of tumor cell growth and response to therapeutic agents.
Conduct mouse surgeries and subsequent animal health monitoring for intracranial tumors models.
Evaluate and interpret collected data and prepare reports and analyses setting forth progress, adverse trends, and appropriate recommendations or conclusions.
Review scientific literature to follow new developments and to obtain information regarding previous experiments to aid in the design and development of original procedures and techniques.
Independently write and submit (with appropriate mentorship) postdoctoral fellowship grants.
Communicate scientific results to colleagues, mentors, and the broader scientific community.
Work from the labs includes:
Garofano L et al. Pathway-based classification of glioblastoma uncovers a mitochondrial subtype with therapeutic vulnerabilities. Nature Cancer Feb;2(2):141-156; doi: 10.1038/s43018-020-00159-4, 2021. [see also Hubert, C.G. and Lathia J.D. Seeing the GBM diversity spectrum. Nature Cancer, Feb;2(2):135, 2021].
Lee SB et al. Proline Hydroxylation Primes protein kinases for autophosphorylation and activation. Mol. Cell 79:376-389, 2020.
D’Angelo F. et al. The molecular landscape of glioma in patients with Neurofibromatosis 1. Nature Medicine, 25:176-187, 2019
Frattini Vet al. A metabolic function of FGFR3-TACC3 gene fusions in cancer. Nature, 553: 222–227, 2018. Nature, 553: 222–227, 2018; [see also RESEARCH WATCH “FGFR3–TACC3 Activates Mitochondrial Respiration via PIN4 Phosphorylation” Cancer Discovery Published Online First January 12, 2018 doi: 10.1158/2159-8290.CD-RW2018-008; RESEARCH HIGHLIGHTS “Fusion Power” Nature Reviews Cancer Published online January 25, 2018 doi:10.1038/nrc.2018.2; NATURE.COM/PATHOLOGY “Gene fusions in cancer metabolism” Laboratory Investigation 98:271, 2018].
Lee SB et al. An ID2-dependent-mechanism for VHL inactivation in cancer. Nature (Article), 529:172-177, 2016; [see also RESEARCH WATCH “Hypoxia promotes cancer stem cells via ID2-dependent VHL inactivation” Cancer Discovery (6: 120, 2016). RESEARCH HIGHLIGHTS “Pathway to stemness” Nature Reviews Cancer (16: 70, 2016)]