Claudia earned her PhD (Dr. rer.nat) at the Institute for Molecular Pathology (IMP) in Vienna, where she trained in cancer signaling, and conducted postdoctoral studies on neural stem cells and asymmetric cell division in the Lab of Dr. Yuh Nung Jan at the Howard Hughes Medical Institute and University of San Francisco, California. After two years as an instructor and head of a research team in Munich, Germany, Dr. Petritsch returned to UCSF to conduct research in oligodendrocyte progenitor cells, angiogenesis and immune regulation in glioma. Dr. Petritsch is an expert in brain stem and progenitor cells and glioma biology, in vitro and in vivo model development and tumor-immune interactions. Her research identified conserved mechanisms of cell fate determination in mammalian brain progenitors and led to a paradigm shift in understanding how brain progenitor cells self-renew and differentiate. She guided the generation and distribution of several immune competent mouse models for studies of the glioma immune microenvironment.
Brain and Learning Sciences
Current Research and Scholarly Interests
The Petritsch lab broadly investigates underlying causes for the intra-tumoral heterogeneity and immune suppression in brain tumors from a developmental neuro-developmental perspective. Proper cell fate decisions by neuroglia stem cells are critical for growing the cell lineages that form the brain during development and to maintain adult brain homeostasis. The mechanisms for cell fate decisions in the human brain are largely unknown. By using patient-derived cells from brain surgeries, we investigate cell fate decision mechanisms in the normal brain and in brain malignancies. We think that defective cell fate decisions fuel the intra-humoral heterogeneity and plasticity that makes treatment of human brain tumors so challenging. We therefore work to gain an understanding of how brain cells control the fate of their progeny, whereby we unravel novel points of vulnerabilities in brain tumor cells, that could be exploited therapeutically.
Excessive proliferation, apoptotic evasion, and migratory spread are all hallmarks of tumorigenesis. However, these defects fail to explain the incredible heterogeneity and immune suppression observed in malignant brain tumors, two major hurdles to their treatment, which remains mostly palliative.
In the healthy brain, neuroglia stem cells generate progenitors, which in turn give rise to differentiating cells that will eventually acquire their final functional state. Cell fate decisions within these hierarchical brain cell lineages are tightly controlled and irreversible: e.g. cells in the state of differentiation will not turn into progenitor cells or stem cells. It is known that brain tumor cells, on the other hand, defy many general principles of neurobiology. This is especially true for malignant glioma cells, which simultaneously express markers of different lineages and states exhibiting incomplete differentiation. Tumor cell hierarchies are poorly understood, providing no explanation for why tumor cells with stem-like, progenitor-like, and differentiated features co-exist and interact with normal brain cells and immune-infiltrating cells within a single tumor entity, and how this heterogeneity relates to the lack of active immune infiltration.
Defects in cell fate control could explain many key defects present in brain tumors Of special emphasis, we study the establishment of cell fates within normal hierarchical brain lineages for comparison to the dysregulated cell-fate hierarchies seen in brain tumors. Our lab was the first to demonstrate that normal adult oligodendrocyte progenitor cells (OPCs) undergo asymmetric divisions to make cell fate decisions, i.e. to generate OPCs as well as differentiating cells each time they divide. Drawing from these data, we investigate whether brain tumors divide along hierarchical lineages and how oncogenic mutations might affect cell fate decisions within these hierarchies. A major line of investigation in our lab focuses on whether defects in asymmetric division lead to aberrant cell fate decisions that cause the paradigm mixed lineage phenotypes and the intra-tumoral heterogeneity present across tumors. We complement our work with human cells with orthotopic and genetically engineered mouse models of gliomagenesis to conduct molecular, cellular and bioinformatic analyses
Lgl1 controls NG2 endocytic pathway to regulate oligodendrocyte differentiation and asymmetric cell division and gliomagenesis
2018; 9: 2862
Oligodendrocyte progenitor cells (OPC) undergo asymmetric cell division (ACD) to generate one OPC and one differentiating oligodendrocyte (OL) progeny. Loss of pro-mitotic proteoglycan and OPC marker NG2 in the OL progeny is the earliest immunophenotypic change of unknown mechanism that indicates differentiation commitment. Here, we report that expression of the mouse homolog of Drosophila tumor suppressor Lethal giant larvae 1 (Lgl1) is induced during OL differentiation. Lgl1 conditional knockout OPC progeny retain NG2 and show reduced OL differentiation, while undergoing more symmetric self-renewing divisions at the expense of asymmetric divisions. Moreover, Lgl1 and hemizygous Ink4a/Arf knockouts in OPC synergistically induce gliomagenesis. Time lapse and total internal reflection microscopy reveals a critical role for Lgl1 in NG2 endocytic routing and links aberrant NG2 recycling to failed differentiation. These data establish Lgl1 as a suppressor of gliomagenesis and positive regulator of asymmetric division and differentiation in the healthy and demyelinated murine brain.
View details for PubMedID 30131568
Pan-cancer analysis of the extent and consequences of intratumor heterogeneity
2016; 22 (1): 105-?
Intratumor heterogeneity (ITH) drives neoplastic progression and therapeutic resistance. We used the bioinformatics tools 'expanding ploidy and allele frequency on nested subpopulations' (EXPANDS) and PyClone to detect clones that are present at a ≥10% frequency in 1,165 exome sequences from tumors in The Cancer Genome Atlas. 86% of tumors across 12 cancer types had at least two clones. ITH in the morphology of nuclei was associated with genetic ITH (Spearman's correlation coefficient, ρ = 0.24-0.41; P < 0.001). Mutation of a driver gene that typically appears in smaller clones was a survival risk factor (hazard ratio (HR) = 2.15, 95% confidence interval (CI): 1.71-2.69). The risk of mortality also increased when >2 clones coexisted in the same tumor sample (HR = 1.49, 95% CI: 1.20-1.87). In two independent data sets, copy-number alterations affecting either <25% or >75% of a tumor's genome predicted reduced risk (HR = 0.15, 95% CI: 0.08-0.29). Mortality risk also declined when >4 clones coexisted in the sample, suggesting a trade-off between the costs and benefits of genomic instability. ITH and genomic instability thus have the potential to be useful measures that can universally be applied to all cancers.
View details for DOI 10.1038/nm.3984
View details for Web of Science ID 000367590700022
Targeting a Plk1-Controlled Polarity Checkpoint in Therapy-Resistant Glioblastoma-Propagating Cells
2015; 75 (24): 5355–66
The treatment of glioblastoma (GBM) remains challenging in part due to the presence of stem-like tumor-propagating cells that are resistant to standard therapies consisting of radiation and temozolomide. Among the novel and targeted agents under evaluation for the treatment of GBM are BRAF/MAPK inhibitors, but their effects on tumor-propagating cells are unclear. Here, we characterized the behaviors of CD133(+) tumor-propagating cells isolated from primary GBM cell lines. We show that CD133(+) cells exhibited decreased sensitivity to the antiproliferative effects of BRAF/MAPK inhibition compared to CD133(-) cells. Furthermore, CD133(+) cells exhibited an extended G2-M phase and increased polarized asymmetric cell divisions. At the molecular level, we observed that polo-like kinase (PLK) 1 activity was elevated in CD133(+) cells, prompting our investigation of BRAF/PLK1 combination treatment effects in an orthotopic GBM xenograft model. Combined inhibition of BRAF and PLK1 resulted in significantly greater antiproliferative and proapoptotic effects beyond those achieved by monotherapy (P < 0.05). We propose that PLK1 activity controls a polarity checkpoint and compensates for BRAF/MAPK inhibition in CD133(+) cells, suggesting the need for concurrent PLK1 inhibition to improve antitumor activity against a therapy-resistant cell compartment.
View details for DOI 10.1158/0008-5472.CAN-14-3689
View details for Web of Science ID 000367552000020
View details for PubMedID 26573800
View details for PubMedCentralID PMC4698003
Heterogeneously Expressed fezf2 Patterns Gradient Notch Activity in Balancing the Quiescence, Proliferation, and Differentiation of Adult Neural Stem Cells
JOURNAL OF NEUROSCIENCE
2014; 34 (42): 13911–23
Balancing quiescence, self-renewal, and differentiation in adult stem cells is critical for tissue homeostasis. The underlying mechanisms, however, remain incompletely understood. Here we identify Fezf2 as a novel regulator of fate balance in adult zebrafish dorsal telencephalic neural stem cells (NSCs). Transgenic reporters show intermingled fezf2-GFP(hi) quiescent and fezf2-GFP(lo) proliferative NSCs. Constitutive or conditional impairment of fezf2 activity demonstrates its requirement for maintaining quiescence. Analyses of genetic chimeras reveal a dose-dependent role of fezf2 in NSC activation, suggesting that the difference in fezf2 levels directionally biases fate. Single NSC profiling coupled with genetic analysis further uncovers a fezf2-dependent gradient Notch activity that is high in quiescent and low in proliferative NSCs. Finally, fezf2-GFP(hi) quiescent and fezf2-GFP(lo) proliferative NSCs are observed in postnatal mouse hippocampus, suggesting possible evolutionary conservation. Our results support a model in which fezf2 heterogeneity patterns gradient Notch activity among neighbors that is critical to balance NSC fate.
View details for DOI 10.1523/JNEUROSCI.1976-14.2014
View details for Web of Science ID 000343142800007
View details for PubMedID 25319688
View details for PubMedCentralID PMC4198537
ASYMMETRIC CELL DIVISION: IMPLICATIONS FOR GLIOMA DEVELOPMENT AND TREATMENT
2013; 4 (4): 484–503
Glioma is a heterogeneous disease process with differential histology and treatment response. It was previously thought that the histological features of glial tumors indicated their cell of origin. However, the discovery of continuous neuro-gliogenesis in the normal adult brain and the identification of brain tumor stem cells within glioma have led to the hypothesis that these brain tumors originate from multipotent neural stem or progenitor cells, which primarily divide asymmetrically during the postnatal period. Asymmetric cell division allows these cell types to concurrently self-renew whilst also producing cells for the differentiation pathway. It has recently been shown that increased symmetrical cell division, favoring the self-renewal pathway, leads to oligodendroglioma formation from oligodendrocyte progenitor cells. In contrast, there is some evidence that asymmetric cell division maintenance in tumor stem-like cells within astrocytoma may lead to acquisition of treatment resistance. Therefore cell division mode in normal brain stem and progenitor cells may play a role in setting tumorigenic potential and the type of tumor formed. Moreover, heterogeneous tumor cell populations and their respective cell division mode may confer differential sensitivity to therapy. This review aims to shed light on the controllers of cell division mode which may be therapeutically targeted to prevent glioma formation and improve treatment response.
View details for DOI 10.2478/s13380-013-0148-8
View details for Web of Science ID 000328844200010
View details for PubMedID 25530875
View details for PubMedCentralID PMC4269374
Proteoglycans and their roles in brain cancer
2013; 280 (10): 2399–2417
Glioblastoma, a malignant brain cancer, is characterized by abnormal activation of receptor tyrosine kinase signalling pathways and a poor prognosis. Extracellular proteoglycans, including heparan sulfate and chondroitin sulfate, play critical roles in the regulation of cell signalling and migration via interactions with extracellular ligands, growth factor receptors and extracellular matrix components, as well as intracellular enzymes and structural proteins. In cancer, proteoglycans help drive multiple oncogenic pathways in tumour cells and promote critical tumour-microenvironment interactions. In the present review, we summarize the evidence for proteoglycan function in gliomagenesis and examine the expression of proteoglycans and their modifying enzymes in human glioblastoma using data obtained from The Cancer Genome Atlas (http://cancergenome.nih.gov/). Furthermore, we demonstrate an association between specific proteoglycan alterations and changes in receptor tyrosine kinases. Based on these data, we propose a model in which proteoglycans and their modifying enzymes promote receptor tyrosine kinase signalling and progression in glioblastoma, and we suggest that cancer-associated proteoglycans are promising biomarkers for disease and therapeutic targets.
View details for DOI 10.1111/febs.12109
View details for Web of Science ID 000318701700023
View details for PubMedID 23281850
View details for PubMedCentralID PMC3644380
Asymmetry-Defective Oligodendrocyte Progenitors Are Glioma Precursors
2011; 20 (3): 328-340
Postnatal oligodendrocyte progenitor cells (OPC) self-renew, generate mature oligodendrocytes, and are a cellular origin of oligodendrogliomas. We show that the proteoglycan NG2 segregates asymmetrically during mitosis to generate OPC cells of distinct fate. NG2 is required for asymmetric segregation of EGFR to the NG2(+) progeny, which consequently activates EGFR and undergoes EGF-dependent proliferation and self-renewal. In contrast, the NG2(-) progeny differentiates. In a mouse model, decreased NG2 asymmetry coincides with premalignant, abnormal self-renewal rather than differentiation and with tumor-initiating potential. Asymmetric division of human NG2(+) cells is prevalent in non-neoplastic tissue but is decreased in oligodendrogliomas. Regulators of asymmetric cell division are misexpressed in low-grade oligodendrogliomas. Our results identify loss of asymmetric division associated with the neoplastic transformation of OPC.
View details for DOI 10.1016/j.ccr.2011.08.011
View details for Web of Science ID 000295205700009
View details for PubMedID 21907924
View details for PubMedCentralID PMC3297490
Dronc caspase exerts a non-apoptotic function to restrain phospho-Numb-induced ectopic neuroblast formation in Drosophila
2011; 138 (11): 2185-2196
Drosophila neuroblasts have served as a model to understand how the balance of stem cell self-renewal versus differentiation is achieved. Drosophila Numb protein regulates this process through its preferential segregation into the differentiating daughter cell. How Numb restricts the proliferation and self-renewal potentials of the recipient cell remains enigmatic. Here, we show that phosphorylation at conserved sites regulates the tumor suppressor activity of Numb. Enforced expression of a phospho-mimetic form of Numb (Numb-TS4D) or genetic manipulation that boosts phospho-Numb levels, attenuates endogenous Numb activity and causes ectopic neuroblast formation (ENF). This effect on neuroblast homeostasis occurs only in the type II neuroblast lineage. We identify Dronc caspase as a novel binding partner of Numb, and demonstrate that overexpression of Dronc suppresses the effects of Numb-TS4D in a non-apoptotic and possibly non-catalytic manner. Reduction of Dronc activity facilitates ENF induced by phospho-Numb. Our findings uncover a molecular mechanism that regulates Numb activity and suggest a novel role for Dronc caspase in regulating neural stem cell homeostasis.
View details for DOI 10.1242/dev.058347
View details for Web of Science ID 000290430100004
View details for PubMedID 21558368
View details for PubMedCentralID PMC3091490
Non-stem cell origin for oligodendroglioma.
2010; 18 (6): 669–82
Malignant astrocytic brain tumors are among the most lethal cancers. Quiescent and therapy-resistant neural stem cell (NSC)-like cells in astrocytomas are likely to contribute to poor outcome. Malignant oligodendroglial brain tumors, in contrast, are therapy sensitive. Using magnetic resonance imaging (MRI) and detailed developmental analyses, we demonstrated that murine oligodendroglioma cells show characteristics of oligodendrocyte progenitor cells (OPCs) and are therapy sensitive, and that OPC rather than NSC markers enriched for tumor formation. MRI of human oligodendroglioma also suggested a white matter (WM) origin, with markers for OPCs rather than NSCs similarly enriching for tumor formation. Our results suggest that oligodendroglioma cells show hallmarks of OPCs, and that a progenitor rather than a NSC origin underlies improved prognosis in patients with this tumor.
View details for DOI 10.1016/j.ccr.2010.10.033
View details for PubMedID 21156288
View details for PubMedCentralID PMC3031116
miR-124 and miR-137 inhibit proliferation of glioblastoma multiforme cells and induce differentiation of brain tumor stem cells
2008; 6: 14
Glioblastoma multiforme (GBM) is an invariably fatal central nervous system tumor despite treatment with surgery, radiation, and chemotherapy. Further insights into the molecular and cellular mechanisms that drive GBM formation are required to improve patient outcome. MicroRNAs are emerging as important regulators of cellular differentiation and proliferation, and have been implicated in the etiology of a variety of cancers, yet the role of microRNAs in GBM remains poorly understood. In this study, we investigated the role of microRNAs in regulating the differentiation and proliferation of neural stem cells and glioblastoma-multiforme tumor cells.We used quantitative RT-PCR to assess microRNA expression in high-grade astrocytomas and adult mouse neural stem cells. To assess the function of candidate microRNAs in high-grade astrocytomas, we transfected miR mimics to cultured-mouse neural stem cells, -mouse oligodendroglioma-derived stem cells, -human glioblastoma multiforme-derived stem cells and -glioblastoma multiforme cell lines. Cellular differentiation was assessed by immunostaining, and cellular proliferation was determined using fluorescence-activated cell sorting.Our studies revealed that expression levels of microRNA-124 and microRNA-137 were significantly decreased in anaplastic astrocytomas (World Health Organization grade III) and glioblastoma multiforme (World Health Organization grade IV) relative to non-neoplastic brain tissue (P < 0.01), and were increased 8- to 20-fold during differentiation of cultured mouse neural stem cells following growth factor withdrawal. Expression of microRNA-137 was increased 3- to 12-fold in glioblastoma multiforme cell lines U87 and U251 following inhibition of DNA methylation with 5-aza-2'-deoxycytidine (5-aza-dC). Transfection of microRNA-124 or microRNA-137 induced morphological changes and marker expressions consistent with neuronal differentiation in mouse neural stem cells, mouse oligodendroglioma-derived stem cells derived from S100 beta-v-erbB tumors and cluster of differentiation 133+ human glioblastoma multiforme-derived stem cells (SF6969). Transfection of microRNA-124 or microRNA-137 also induced G1 cell cycle arrest in U251 and SF6969 glioblastoma multiforme cells, which was associated with decreased expression of cyclin-dependent kinase 6 and phosphorylated retinoblastoma (pSer 807/811) proteins.microRNA-124 and microRNA-137 induce differentiation of adult mouse neural stem cells, mouse oligodendroglioma-derived stem cells and human glioblastoma multiforme-derived stem cells and induce glioblastoma multiforme cell cycle arrest. These results suggest that targeted delivery of microRNA-124 and/or microRNA-137 to glioblastoma multiforme tumor cells may be therapeutically efficacious for the treatment of this disease.
View details for DOI 10.1186/1741-7015-6-14
View details for Web of Science ID 000257414200001
View details for PubMedID 18577219
View details for PubMedCentralID PMC2443372
HIF1 alpha induces the recruitment of bone marrow-derived vascular modulatory cells to regulate tumor angiogenesis and invasion
2008; 13 (3): 206–20
Development of hypoxic regions is an indicator of poor prognosis in many tumors. Here, we demonstrate that HIF1alpha, the direct effector of hypoxia, partly through increases in SDF1alpha, induces recruitment of bone marrow-derived CD45+ myeloid cells containing Tie2+, VEGFR1+, CD11b+, and F4/80+ subpopulations, as well as endothelial and pericyte progenitor cells to promote neovascularization in glioblastoma. MMP-9 activity of bone marrow-derived CD45+ cells is essential and sufficient to initiate angiogenesis by increasing VEGF bioavailability. In the absence of HIF1alpha, SDF1alpha levels decrease, and fewer BM-derived cells are recruited to the tumors, decreasing MMP-9 and mobilization of VEGF. VEGF also directly regulates tumor cell invasiveness. When VEGF activity is impaired, tumor cells invade deep into the brain in the perivascular compartment.
View details for DOI 10.1016/j.ccr.2008.01.034
View details for Web of Science ID 000253932300006
View details for PubMedID 18328425
View details for PubMedCentralID PMC2643426
TGF beta inhibits p70 S6 kinase via protein phosphatase 2A to induce G1 arrest
AMER SOC CELL BIOLOGY. 2000: 289A
View details for Web of Science ID 000165525901509
- GENERATION OF NOVEL MOUSE MODELS FOR BRAF V600E MUTANT GLIOMAGENESIS TO GAIN MECHANISTIC INSIGHTS INTO TUMOR FORMATION AND PROGRESSION OXFORD UNIV PRESS INC. 2021: 32
THE IMMUNE MICROENVIRONMENT IN LOWER GRADE GLIOMAS
OXFORD UNIV PRESS INC. 2020: 214
View details for Web of Science ID 000590061300897
A NOVEL BRAF V600E LOW-GRADE GLIOMA MOUSE MODEL HIGHLIGHTS EXOMIC AND TUMOR IMMUNE ALTERATIONS AND DIFFERING THERAPEUTIC RESPONSES IN LOW- AND HIGH-GRADE GLIOMAS
OXFORD UNIV PRESS INC. 2020: 232–33
View details for Web of Science ID 000590061300973
DETERMINING THE NEUROANAFOMICAL AND CELLULAR ORIGIN OF BRAEV600E MUTANT CDKN2A DELETED GLIOMAS AND MECHANISMS OF TRANSFORMATION BY BRAEV600E EXPRESSION IN "FRANSGENIC MICE
OXFORD UNIV PRESS INC. 2019: 122
View details for Web of Science ID 000473243700244
GAINING A MECHANISTIC UNDERSTANDING OF THERAPY EVASION FROM DUAL MAPK PATHWAY INHIBITION IN A SYNGENEIC BRAFV600E MUTANT CDKN2A DELETED MOUSE MODEL'TO PREEMPT RESISTANCE IN PATIENTS WITH BRAFV600E MUTANT E PEDIATRIC ClIOMA
OXFORD UNIV PRESS INC. 2019: 121–22
View details for Web of Science ID 000473243700243
Impaired neural stem cell expansion and hypersensitivity to epileptic seizures in mice lacking the EGFR in the brain
2018; 285 (17): 3175–96
Mice lacking the epidermal growth factor receptor (EGFR) develop an early postnatal degeneration of the frontal cortex and olfactory bulbs and show increased cortical astrocyte apoptosis. The poor health and early lethality of EGFR-/- mice prevented the analysis of mechanisms responsible for the neurodegeneration and function of the EGFR in the adult brain. Here, we show that postnatal EGFR-deficient neural stem cells are impaired in their self-renewal potential and lack clonal expansion capacity in vitro. Mice lacking the EGFR in the brain (EGFRΔbrain ) show low penetrance of cortical degeneration compared to EGFR-/- mice despite genetic recombination of the conditional allele. Adult EGFRΔ mice establish a proper blood-brain barrier and perform reactive astrogliosis in response to mechanical and infectious brain injury, but are more sensitive to Kainic acid-induced epileptic seizures. EGFR-deficient cortical astrocytes, but not midbrain astrocytes, have reduced expression of glutamate transporters Glt1 and Glast, and show reduced glutamate uptake in vitro, illustrating an excitotoxic mechanism to explain the hypersensitivity to Kainic acid and region-specific neurodegeneration observed in EGFR-deficient brains.
View details for DOI 10.1111/febs.14603
View details for Web of Science ID 000443814200004
View details for PubMedID 30028091
View details for PubMedCentralID PMC6174950
- Tumor suppression by regulator of asymmetric cell division in glioma AMER ASSOC CANCER RESEARCH. 2018
- MAPK pathway blockade effects on glioma stem cells and immunotherapy in BRAF(V600E) mutant gliomas AMER ASSOC CANCER RESEARCH. 2018
Regulation of Asymmetric Cell Division in Mammalian Neural Stem and Cancer Precursor Cells
ASYMMETRIC CELL DIVISION IN DEVELOPMENT, DIFFERENTIATION AND CANCER
2017; 61: 375–99
Stem and progenitor cells are characterized by their abilities to self-renew and produce differentiated progeny. The balance between self-renewal and differentiation is achieved through control of cell division mode, which can be either asymmetric or symmetric. Failure to properly control cell division mode may result in premature depletion of the stem/progenitor cell pool or abnormal growth and impaired differentiation. In many tissues, including the brain, stem cells and progenitor cells undergo asymmetric cell division through the establishment of cell polarity. Cell polarity proteins are therefore potentially critical regulators of asymmetric cell division. Decrease or loss of asymmetric cell division can be associated with reduced differentiation common during aging or impaired remyelination as seen in demyelinating diseases. Progenitor-like glioma precursor cells show decreased asymmetric cell division rates and increased symmetric divisions, which suggests that asymmetric cell division suppresses brain tumor formation. Cancer stem cells, on the other hand, still undergo low rates of asymmetric cell division, which may provide them with a survival advantage during therapy. These findings led to the hypotheses that asymmetric cell divisions are not always tumor suppressive but can also be utilized to maintain a cancer stem cell population. Proper control of cell division mode is therefore not only deemed necessary to generate cellular diversity during development and to maintain adult tissue homeostasis but may also prevent disease and determine disease progression. Since brain cancer is most common in the adult and aging population, we review here the current knowledge on molecular mechanisms that regulate asymmetric cell divisions in the neural and oligodendroglial lineage during development and in the adult brain.
View details for DOI 10.1007/978-3-319-53150-2_17
View details for Web of Science ID 000417903300017
View details for PubMedID 28409314
MAPK PATHWAY BLOCKADE PRIMES BRAFV600E MUTANT GLIOMA FOR IMMUNOTHERAPY
OXFORD UNIV PRESS INC. 2016: 90
View details for Web of Science ID 000398604102102
- Pan-cancer analysis of the etiology and consequences of intra-tumor heterogeneity AMER ASSOC CANCER RESEARCH. 2015
- Pan-cancer analysis of the causes and consequences of Intra-tumor heterogeneity AMER ASSOC CANCER RESEARCH. 2015
- Divergent effects of BRAF activation in neural stem and progenitor-like glioblastoma cells AMER ASSOC CANCER RESEARCH. 2014
TREATMENT EFFECTS ON STEM AND PROGENITOR SUBPOPULATIONS IN A MODEL OF GLIOBLASTOMA
OXFORD UNIV PRESS INC. 2013: 209
View details for Web of Science ID 000327456200820
CLONAL EXPANSIONS AND EVOLVING SUBPOPULATIONS IN GLIOBLASTOMA MULTIFORME
OXFORD UNIV PRESS INC. 2013: 136–37
View details for Web of Science ID 000327456200548
- Deletion of the asymmetry regulator Lgl1 contributes to tumor sternness and invasiveness. AMER ASSOC CANCER RESEARCH. 2013
ANALYSIS OF CELLULAR AND MOLECULAR CHANGES ACCOMPANYING BRaf(V600E) - TARGETED TREATMENT IN A MODEL OF PEDIATRIC ASTROCYTOMA
OXFORD UNIV PRESS INC. 2013: 14–15
View details for Web of Science ID 000318570500054
GENE EXPRESSION AND METHYLATION ANALYSES OF ATYPICAL TERATOID/RHABDOID TUMORS AND MEDULLOBLASTOMAS
OXFORD UNIV PRESS INC. 2012: 119
View details for Web of Science ID 000310971300471
- Deregulation of asymmetry genes in oligodendrogliomas and glioblastomas AMER ASSOC CANCER RESEARCH. 2012
ASYMMETRY-DEFECTIVE OLIGODENDROCYTE PROGENITORS ARE GLIOMA PRECURSORS
OXFORD UNIV PRESS INC. 2011: 25
View details for Web of Science ID 000297026600107
The divergent caspase DRONC processes Notch and regulates neurogenesis.
AMER SOC CELL BIOLOGY. 2000: 290A
View details for Web of Science ID 000165525901516