Cancer Pathobiology Research
Researchers at the Center for Childhood Cancer Research are investigating the molecular mechanisms behind the loss of the CD19 epitope after CART19 therapy.
A link between dysregulation of DNA damage and repair systems has been implicated in tumorigenesis and etiology of many cancers.
Researchers are examining how the enzyme APOBEC3 contributes to the malignant transformation of cells.
Researchers at the Center for Childhood Cancer Research are using a transgenic mouse model to demonstrate that somatic inactivation of Tp53 predisposed mice to thymic lymphomas with translocations.
Studies are underway to develop molecular tests that can help to preselect patients who are likely to respond to specific cancer therapeutics based on epistatic profiling of their tumor types.
A link between viral infection, disruption of DNA damage response (DDR) pathways and cellular transformation/tumorigenesis has been established for a variety of oncogenic human DNA viruses.
Identifying and understanding the dynamic rewiring of gene network is critical for understanding cancer pathogenesis and development of therapeutic interventions.
Elucidating the roles that E2F transcription factors play in cancer biology will help identify potential targets for therapeutic intervention.
Researchers at the Center for Childhood Cancer Research, led by Kai Tan, PhD, are developing a general computational framework for identifying noncoding genetic mutations that confer cancer risk.
Studies are underway using a Lnk-/- mouse model system to decipher the underlying molecular mechanisms of pediatric Ph-like ALL and to explore new therapeutic strategies to treat the disease.
Studies are currently underway to more clearly define the relationship between Myc-induced deregulation of miR-17-92 and BCR signaling.
Researchers at the Center for Childhood Cancer Research have developed an ATM-/- deficient-transgenic mouse model to study the effect of germline TCR gene translocations on the development of T-ALL.
Researchers at the Center for Childhood Cancer Research, led by Kai Tan, PhD, are developing cutting-edge genomic and computational tools to profile and model the gene regulatory circuitry during HSC development.
Researchers demonstrated that in solid tumors, such as pediatric neuroblastoma and colon adenocarcinoma, deregulation of miR-17-92 leads to profound suppression of TGFβ signaling and diminished production of many anti-angiogenic TGFβ-inducible factors such as thrombospondin-1, CTGF, and clusterin.
A panel of microscopic tissue samples contributes to the arsenal of tools used to analyze solid tumors for specific surface proteins that can be targeted for tumor treatment.