A5022556102- Cancer-related Molecular Pathways
- PARP inhibition in cancer therapy
- Lung Cancer Research Studies
- Epigenetics and DNA Methylation
- Peptidase Inhibition and Analysis
- Pancreatic and Hepatic Oncology Research
- Cancer Treatment and Pharmacology
- HER2/EGFR in Cancer Research
- Glioma Diagnosis and Treatment
- DNA Repair Mechanisms
- Lung Cancer Treatments and Mutations
- Histone Deacetylase Inhibitors Research
- interferon and immune responses
- BRCA gene mutations in cancer
- Ubiquitin and proteasome pathways
- Neuroblastoma Research and Treatments
- Cancer, Hypoxia, and Metabolism
- NF-κB Signaling Pathways
- Colorectal Cancer Treatments and Studies
- Cancer Genomics and Diagnostics
- Protein Degradation and Inhibitors
- Protein Tyrosine Phosphatases
- T-cell and B-cell Immunology
- Cytokine Signaling Pathways and Interactions
- Viral-associated cancers and disorders
University of Turku
2012-2023
Åbo Akademi University
2014-2023
Turku Centre for Computer Science
2020-2023
Turku Centre for Biotechnology
2016
Regional Centre for Biotechnology
2014
Monash University
2011-2013
Ludwig Cancer Research
2009-2011
Monash Institute of Medical Research
2011
Austin Hospital
2009
Abstract Activating epidermal growth factor receptor (EGFR) mutations are common in many cancers including glioblastoma. However, clinical responses to EGFR inhibitors infrequent and short-lived. We show that the Src family kinases (SFK) Fyn effectors of oncogenic signaling, enhancing invasion tumor cell survival vivo. Expression a constitutively active mutant, EGFRvIII, resulted activating phosphorylation physical association with Fyn, promoting motility. Gene silencing limited EGFR-...
Abstract Basal-like breast cancers (BLBC) are characterized by defects in homologous recombination (HR), deficient mitotic checkpoint, and high-proliferation activity. Here, we discover CIP2A as a candidate driver of BLBC. was essential for DNA damage–induced initiation mouse BLBC-like mammary tumors survival HR–defective BLBC cells. dispensable normal gland development unperturbed mitosis, but selectively progression damaged A direct interaction between repair scaffold protein TopBP1...
The epidermal growth factor receptor (EGFR) is overexpressed or mutated in glioma. Recently, a series of missense mutations the extracellular domain (ECD) EGFR were reported glioma patients. Some these clustered within cysteine-rich region targeted by therapeutic antibody mAb806. This only exposed when activates and appears to locally misfold during activation. We expressed two (R324L E330K) NR6 mouse fibroblasts, as they do not express any EGFR-related receptors. Both mutants...
A common mutation of the epidermal growth factor receptor in glioma is de2-7EGFR (or EGFRvIII). Glioma cells expressing contain an intracellular pool with high levels mannose glycosylation, which consistent delayed processing. We now show that this delay occurs Golgi complex. Low were also seen within mitochondria. Src activation dramatically increased amount mitochondrial de2-7EGFR, whereas its pharmacological inhibition caused a significant reduction. Because phosphorylated by at Y845, we...
The oncoprotein Cancerous Inhibitor of Protein Phosphatase 2A (CIP2A) is overexpressed in most malignancies and an obvious candidate target protein for future cancer therapies. However, the physiological importance CIP2A-mediated PP2A inhibition largely unknown. As regulates immune responses, we investigated role CIP2A normal system development during response vivo. We show that CIP2A-deficient mice (CIP2AHOZ) present a function unchallenged conditions. However when challenged with Listeria...
Kaposi's sarcoma herpesvirus (KSHV)-encoded v-cyclin, a homolog of cellular cyclin D2, activates CDK6, promotes G1-S transition the cell cycle, induces DNA damage, apoptosis, autophagy and is reported to have oncogenic potential. Here we show that in vivo expression v-cyclin B- T-cell lymphocyte compartments results markedly low survival due high penetrance early-onset lymphoma pancarditis. The transgenic mice smaller pre-tumorigenic lymphoid organs, showing decreased cellularity, increased...
Abstract Identification of ovarian cancer patient subpopulations with increased sensitivity to targeted therapies could offer significant clinical benefit. We report that 22% the high-grade tumors at diagnosis express CIP2A oncoprotein low levels. Furthermore, regardless their significantly lower likelihood disease relapse after standard chemotherapy, a portion relapsed retain CIP2A-deficient phenotype. Through screen for therapeutics would preferentially kill cells, we identified reactive...
Abstract Despite saturated genetic profiling of breast cancers, oncogenic drivers for the clinically challenging basal-like cancer (BLBC) subtype are still poorly understood. Here, we demonstrate that CIP2A is selectively essential DNA damage-induced initiation mouse BLBC tumors, but not other types. Mechanistically, was discovered genome-widely closest functional homologue DNA-damage proteins TopBP1, RHNO, POLQ, NBN and PARP1. directly interacts with ATR-activation domain dampens both,...
Supplementary Data from CIP2A Interacts with TopBP1 and Drives Basal-Like Breast Cancer Tumorigenesis
Supplementary Data from CIP2A Interacts with TopBP1 and Drives Basal-Like Breast Cancer Tumorigenesis
<div>Abstract<p>Basal-like breast cancers (BLBC) are characterized by defects in homologous recombination (HR), deficient mitotic checkpoint, and high-proliferation activity. Here, we discover CIP2A as a candidate driver of BLBC. was essential for DNA damage–induced initiation mouse BLBC-like mammary tumors survival HR–defective BLBC cells. dispensable normal gland development unperturbed mitosis, but selectively progression damaged A direct interaction between repair scaffold...
Supplementary Figures 1-6 from Fyn and Src Are Effectors of Oncogenic Epidermal Growth Factor Receptor Signaling in Glioblastoma Patients
Supplementary Data from CIP2A Interacts with TopBP1 and Drives Basal-Like Breast Cancer Tumorigenesis
Supplementary Data from CIP2A Interacts with TopBP1 and Drives Basal-Like Breast Cancer Tumorigenesis
Supplementary Methods and Materials from Fyn Src Are Effectors of Oncogenic Epidermal Growth Factor Receptor Signaling in Glioblastoma Patients
Supplementary Methods and Materials from Fyn Src Are Effectors of Oncogenic Epidermal Growth Factor Receptor Signaling in Glioblastoma Patients
<div>Abstract<p>Basal-like breast cancers (BLBC) are characterized by defects in homologous recombination (HR), deficient mitotic checkpoint, and high-proliferation activity. Here, we discover CIP2A as a candidate driver of BLBC. was essential for DNA damage–induced initiation mouse BLBC-like mammary tumors survival HR–defective BLBC cells. dispensable normal gland development unperturbed mitosis, but selectively progression damaged A direct interaction between repair scaffold...
Supplementary Data from CIP2A Interacts with TopBP1 and Drives Basal-Like Breast Cancer Tumorigenesis
Supplementary Data from CIP2A Interacts with TopBP1 and Drives Basal-Like Breast Cancer Tumorigenesis
Supplementary Data from CIP2A Interacts with TopBP1 and Drives Basal-Like Breast Cancer Tumorigenesis
Supplementary Data from CIP2A Interacts with TopBP1 and Drives Basal-Like Breast Cancer Tumorigenesis
Supplementary Data from CIP2A Interacts with TopBP1 and Drives Basal-Like Breast Cancer Tumorigenesis
Supplementary Data from CIP2A Interacts with TopBP1 and Drives Basal-Like Breast Cancer Tumorigenesis