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Start Over Author "Höland K" Publisher international institute of anticancer research
2 results on '"Höland K"'

1. Republication: Targeting PI3KC2β Impairs Proliferation and Survival in Acute Leukemia, Brain Tumours and Neuroendocrine Tumours.

Author

Boller D, Doepfner KT, Laurentiis A, Guerreiro AS, Marinov M, Shalaby T, Depledge P, Robson A, Saghir N, Hayakawa M, Kaizawa H, Koizumi T, Ohishi T, Fattet S, Delattre O, Schweri-Olac A, Höland K, Grotzer MA, Frei K, Spertini O, Waterfield MD, and Arcaro A

Subjects
Acute Disease, Cell Line, Tumor, Cell Proliferation, Humans, Isoenzymes genetics, Isoenzymes metabolism, Lung Neoplasms, Phosphatidylinositol 3-Kinases metabolism, Brain Neoplasms drug therapy, Brain Neoplasms genetics, Cerebellar Neoplasms drug therapy, Cerebellar Neoplasms genetics, Leukemia, Myeloid, Acute drug therapy, Leukemia, Myeloid, Acute genetics, Neuroendocrine Tumors drug therapy, Neuroendocrine Tumors genetics
Abstract

Background: Eight human catalytic phosphoinositide 3-kinase (PI3K) isoforms exist which are subdivided into three classes. While class I isoforms have been well-studied in cancer, little is known about the functions of class II PI3Ks., Materials and Methods: The expression pattern and functions of the class II PI3KC2β isoform were investigated in a panel of tumour samples and cell lines., Results: Overexpression of PI3KC2β was found in subsets of tumours and cell lines from acute myeloid leukemia (AML), glioblastoma multiforme (GBM), medulloblastoma (MB), neuroblastoma (NB), and small cell lung cancer (SCLC). Specific pharmacological inhibitors of PI3KC2β or RNA interference impaired proliferation of a panel of human cancer cell lines and primary cultures. Inhibition of PI3KC2β also induced apoptosis and sensitised the cancer cells to chemotherapeutic agents., Conclusion: Together, these data show that PI3KC2β contributes to proliferation and survival in AML, brain tumours and neuroendocrine tumours, and may represent a novel target in these malignancies., (Copyright © 2022 International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.)

Published
2022
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2. Targeting PI3KC2β impairs proliferation and survival in acute leukemia, brain tumours and neuroendocrine tumours.

Author

Boller D, Doepfner KT, De Laurentiis A, Guerreiro AS, Marinov M, Shalaby T, Depledge P, Robson A, Saghir N, Hayakawa M, Kaizawa H, Koizumi T, Ohishi T, Fattet S, Delattre O, Schweri-Olac A, Höland K, Grotzer MA, Frei K, Spertini O, Waterfield MD, and Arcaro A

Subjects
Animals, Cell Line, Tumor, Electrophoresis, Polyacrylamide Gel, Enzyme Inhibitors pharmacology, Humans, Inhibitory Concentration 50, Mice, Oligonucleotide Array Sequence Analysis, Phosphoinositide-3 Kinase Inhibitors, Brain Neoplasms pathology, Cell Proliferation, Isoenzymes metabolism, Leukemia, Myeloid, Acute pathology, Neuroendocrine Tumors pathology, Phosphatidylinositol 3-Kinases metabolism, Survival Rate
Abstract

Background: Eight human catalytic phosphoinositide 3-kinase (PI3K) isoforms exist which are subdivided into three classes. While class I isoforms have been well-studied in cancer, little is known about the functions of class II PI3Ks., Materials and Methods: The expression pattern and functions of the class II PI3KC2β isoform were investigated in a panel of tumour samples and cell lines., Results: Overexpression of PI3KC2β was found in subsets of tumours and cell lines from acute myeloid leukemia (AML), glioblastoma multiforme (GBM), medulloblastoma (MB), neuroblastoma (NB), and small cell lung cancer (SCLC). Specific pharmacological inhibitors of PI3KC2β or RNA interference impaired proliferation of a panel of human cancer cell lines and primary cultures. Inhibition of PI3KC2β also induced apoptosis and sensitised the cancer cells to chemotherapeutic agents., Conclusion: Together, these data show that PI3KC2β contributes to proliferation and survival in AML, brain tumours and neuroendocrine tumours, and may represent a novel target in these malignancies.

Published
2012

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