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Loss of Kmt2c in vivo leads to EMT, mitochondrial dysfunction and improved response to lapatinib in...

Loss of Kmt2c in vivo leads to EMT, mitochondrial dysfunction and improved response to lapatinib in...

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_10024673

Loss of Kmt2c in vivo leads to EMT, mitochondrial dysfunction and improved response to lapatinib in breast cancer

About this item

Full title

Loss of Kmt2c in vivo leads to EMT, mitochondrial dysfunction and improved response to lapatinib in breast cancer

Publisher

Cham: Springer International Publishing

Journal title

Cellular and molecular life sciences : CMLS, 2023-04, Vol.80 (4), p.100-100, Article 100

Language

English

Formats

Publication information

Publisher

Cham: Springer International Publishing

More information

Scope and Contents

Contents

Deep sequencing of human tumours has uncovered a previously unappreciated role for epigenetic regulators in tumorigenesis. H3K4 methyltransferase
KMT2C/MLL3
is mutated in several solid malignancies, including more than 10% of breast tumours. To study the tumour suppressor role of KMT2C in breast cancer, we generated mouse models of Erbb2/Neu,...

Alternative Titles

Full title

Loss of Kmt2c in vivo leads to EMT, mitochondrial dysfunction and improved response to lapatinib in breast cancer

Identifiers

Primary Identifiers

Record Identifier

TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_10024673

Permalink

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_10024673

Other Identifiers

ISSN

1420-682X

E-ISSN

1420-9071

DOI

10.1007/s00018-023-04734-7

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