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Article ; Online: Conditional in vivo deletion of LYN kinase has little effect on a BRCA1 loss-of-function-associated mammary tumour model.

Tornillo, Giusy / Warrington, Lauren / Kendrick, Howard / Higgins, Adam T / Hay, Trevor / Beck, Sam / Smalley, Matthew J

Disease models & mechanisms

2024 Volume 17, Issue 1

Abstract: LYN kinase is expressed in BRCA1 loss-of-function-dependent mouse mammary tumours, in the cells of origin of such tumours, and in human breast cancer. Suppressing LYN kinase activity in BRCA1-defective cell lines as well as in in vitro cultures of Brca1- ... ...

Abstract	LYN kinase is expressed in BRCA1 loss-of-function-dependent mouse mammary tumours, in the cells of origin of such tumours, and in human breast cancer. Suppressing LYN kinase activity in BRCA1-defective cell lines as well as in in vitro cultures of Brca1-null mouse mammary tumours is deleterious to their growth. Here, we examined the interaction between LYN kinase and BRCA1 loss-of-function in an in vivo mouse mammary tumour model, using conditional knockout Brca1 and Lyn alleles. Comparison of Brca1 tumour cohorts showed little difference in mammary tumour formation between animals that were wild type, heterozygous or homozygous for the conditional Lyn allele, although this was confounded by factors including incomplete Lyn recombination in some tumours. RNA-sequencing analysis demonstrated that tumours with high levels of Lyn gene expression had a slower doubling time, but this was not correlated with levels of LYN staining in tumour cells themselves. Rather, high Lyn expression and slower tumour growth were likely a result of B-cell infiltration. The multifaceted role of LYN indicates that it is likely to present difficulties as a therapeutic target in breast cancer.
MeSH term(s)	Animals ; Female ; Humans ; Mice ; BRCA1 Protein/genetics ; Breast/pathology ; Breast Neoplasms/genetics ; Cell Line ; Mammary Neoplasms, Animal/genetics ; Mammary Neoplasms, Animal/pathology ; Mice, Knockout
Chemical Substances	BRCA1 Protein ; BRCA1 protein, human ; lyn protein-tyrosine kinase (EC 2.7.10.2) ; Brca1 protein, mouse
Language	English
Publishing date	2024-01-25
Publishing country	England
Document type	Journal Article
ZDB-ID	2451104-3
ISSN	1754-8411 ; 1754-8403
ISSN (online)	1754-8411
ISSN	1754-8403
DOI	10.1242/dmm.050211
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Article: NOTCH and AKT Signalling Interact to Drive Mammary Tumour Heterogeneity.

Ordonez, Liliana / Tornillo, Giusy / Kendrick, Howard / Hay, Trevor / Smalley, Matthew John

Cancers

2023 Volume 15, Issue 17

Abstract: A better understanding of the mechanisms generating tumour heterogeneity will allow better targeting of current therapies, identify potential resistance mechanisms and highlight new approaches for therapy. We have previously shown that in genetically ... ...

Abstract	A better understanding of the mechanisms generating tumour heterogeneity will allow better targeting of current therapies, identify potential resistance mechanisms and highlight new approaches for therapy. We have previously shown that in genetically modified mouse models carrying conditional oncogenic alleles, mammary tumour histotype varies depending on the combination of alleles, the cell type to which they are targeted and, in some cases, reproductive history. This suggests that tumour heterogeneity is not a purely stochastic process; rather, differential activation of signalling pathways leads to reproducible differences in tumour histotype. We propose the NOTCH signalling pathway as one such pathway. Here, we have crossed conditional knockout
Language	English
Publishing date	2023-08-29
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers15174324
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Article ; Online: See One, Do One, Teach One: A Practical Course on Methods in Mammary Gland Biology.

Jechlinger, Martin / Kendrick, Howard / Smalley, Matthew / Vivanco, Maria dM

Journal of mammary gland biology and neoplasia

2018 Volume 22, Issue 4, Page(s) 215–219

MeSH term(s)	Animals ; Female ; Humans ; Mammary Glands, Animal/physiology ; Mammary Glands, Human/physiology ; Mice
Language	English
Publishing date	2018-02-14
Publishing country	United States
Document type	Editorial
ZDB-ID	1327345-0
ISSN	1573-7039 ; 1083-3021
ISSN (online)	1573-7039
ISSN	1083-3021
DOI	10.1007/s10911-017-9387-6
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Article ; Online: Reproductive history determines Erbb2 locus amplification, WNT signalling and tumour phenotype in a murine breast cancer model.

Ordonez, Liliana D / Melchor, Lorenzo / Greenow, Kirsty R / Kendrick, Howard / Tornillo, Giusy / Bradford, James / Giles, Peter / Smalley, Matthew J

Disease models & mechanisms

2021 Volume 14, Issue 5

Abstract: Understanding the mechanisms underlying tumour heterogeneity is key to the development of treatments that can target specific tumour subtypes. We have previously targeted CRE recombinase-dependent conditional deletion of the tumour suppressor genes Brca1, ...

Abstract	Understanding the mechanisms underlying tumour heterogeneity is key to the development of treatments that can target specific tumour subtypes. We have previously targeted CRE recombinase-dependent conditional deletion of the tumour suppressor genes Brca1, Brca2, p53 (also known as Trp53) and/or Pten to basal or luminal oestrogen receptor-negative (ER-) cells of the mouse mammary epithelium. We demonstrated that both the cell-of-origin and the tumour-initiating genetic lesions cooperate to influence mammary tumour phenotype. Here, we use a CRE-activated HER2 orthologue to specifically target HER2/ERBB2 oncogenic activity to basal or luminal ER- mammary epithelial cells and perform a detailed analysis of the tumours that develop. We find that, in contrast to our previous studies, basal epithelial cells are less sensitive to transformation by the activated NeuKI allele, with mammary epithelial tumour formation largely confined to luminal ER- cells. Histologically, most tumours that developed were classified as either adenocarcinomas of no special type or as metaplastic adenosquamous tumours. The former were typically characterized by amplification of the NeuNT/Erbb2 locus; in contrast, tumours displaying squamous metaplasia were enriched in animals that had been through at least one pregnancy and typically had lower levels of NeuNT/Erbb2 locus amplification but had activated canonical WNT signalling. Squamous changes in these tumours were associated with activation of the epidermal differentiation cluster. Thus, in this model of HER2 breast cancer, cell-of-origin, reproductive history, NeuNT/Erbb2 locus amplification and the activation of specific branches of the WNT signalling pathway all interact to drive inter-tumour heterogeneity.
MeSH term(s)	Alleles ; Animals ; Carcinogenesis/pathology ; Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/pathology ; Disease Models, Animal ; Epithelium/pathology ; Female ; Gene Amplification ; Gene Dosage ; Gene Expression Regulation, Neoplastic ; Genetic Loci ; Integrases/metabolism ; Kaplan-Meier Estimate ; Mammary Glands, Animal/pathology ; Mammary Neoplasms, Animal/genetics ; Mammary Neoplasms, Animal/pathology ; Metaplasia ; Mice, Transgenic ; Phenotype ; Receptor, ErbB-2/genetics ; Reproduction/physiology ; Wnt Signaling Pathway/genetics
Chemical Substances	Receptor, ErbB-2 (EC 2.7.10.1) ; Cre recombinase (EC 2.7.7.-) ; Integrases (EC 2.7.7.-)
Language	English
Publishing date	2021-05-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2451104-3
ISSN	1754-8411 ; 1754-8403
ISSN (online)	1754-8411
ISSN	1754-8403
DOI	10.1242/dmm.048736
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Article ; Online: Lect2

Greenow, Kirsty R / Zverev, Matthew / May, Stephanie / Kendrick, Howard / Williams, Geraint T / Phesse, Toby / Parry, Lee

Oncotarget

2018 Volume 9, Issue 92, Page(s) 36430–36443

Abstract: Leukocyte cell-derived chemotaxin 2 (Lect2) is a chemokine-like chemotactic factor that has been identified as a downstream target of the Wnt signalling pathway. Whilst the primary function of Lect2 is thought to be in modulating the inflammatory process, ...

Abstract	Leukocyte cell-derived chemotaxin 2 (Lect2) is a chemokine-like chemotactic factor that has been identified as a downstream target of the Wnt signalling pathway. Whilst the primary function of Lect2 is thought to be in modulating the inflammatory process, it has recently been implicated as a potential inhibitor of the Wnt pathway. Deregulation of the Wnt pathway, often due to loss of the negative regulator
Language	English
Publishing date	2018-11-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.26335
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Article ; Online: Immune Remodeling of the Extracellular Matrix Drives Loss of Cancer Stem Cells and Tumor Rejection.

Pires, Ana / Greenshields-Watson, Alexander / Jones, Emma / Smart, Kathryn / Lauder, Sarah N / Somerville, Michelle / Milutinovic, Stefan / Kendrick, Howard / Hindley, James P / French, Rhiannon / Smalley, Matthew J / Watkins, William J / Andrews, Robert / Godkin, Andrew / Gallimore, Awen

Cancer immunology research

2020 Volume 8, Issue 12, Page(s) 1520–1531

Abstract: The nature of the tumor microenvironment (TME) influences the ability of tumor-specific T cells to control tumor growth. In this study, we performed an unbiased comparison of the TME of regulatory T-cell (Treg)-replete and Treg-depleted carcinogen- ... ...

Abstract	The nature of the tumor microenvironment (TME) influences the ability of tumor-specific T cells to control tumor growth. In this study, we performed an unbiased comparison of the TME of regulatory T-cell (Treg)-replete and Treg-depleted carcinogen-induced tumors, including Treg-depleted responding (regressing) and non-responding (growing) tumors. This analysis revealed an inverse relationship between extracellular matrix (ECM) and T-cell infiltrates where responding tumors were T-cell rich and ECM poor, whereas the converse was observed in non-responder tumors. For this reason, we hypothesized that the ECM acted as a barrier to successful T-cell infiltration and tumor rejection. However, further experiments revealed that this was not the case but instead showed that an effective T-cell response dramatically altered the density of ECM in the TME. Along with loss of ECM and high numbers of infiltrating T cells, responder tumors were distinguished by the development of lymphatic and blood vessel networks with specialized immune function. ECM-rich tumors exhibited a stem cell-like gene expression profile and superior tumor-initiating capacity, whereas such features were absent in responder tumors. Overall, these findings define an extended role for an effective immune response, not just in direct killing of tumor cells but in widescale remodeling of the TME to favor loss of ECM, elimination of cancer stem cells, and propagation of adaptive immunity.
MeSH term(s)	Animals ; Cell Line, Tumor ; Extracellular Matrix ; Female ; Humans ; Mice ; Mice, Inbred BALB C ; Neoplasms/etiology ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplastic Stem Cells/metabolism ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism ; Tumor Microenvironment/genetics ; Tumor Microenvironment/immunology
Language	English
Publishing date	2020-10-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2732489-8
ISSN	2326-6074 ; 2326-6066
ISSN (online)	2326-6074
ISSN	2326-6066
DOI	10.1158/2326-6066.CIR-20-0070
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Article ; Online: Dual Mechanisms of LYN Kinase Dysregulation Drive Aggressive Behavior in Breast Cancer Cells.

Tornillo, Giusy / Knowlson, Catherine / Kendrick, Howard / Cooke, Joe / Mirza, Hasan / Aurrekoetxea-Rodríguez, Iskander / Vivanco, Maria D M / Buckley, Niamh E / Grigoriadis, Anita / Smalley, Matthew J

Cell reports

2018 Volume 25, Issue 13, Page(s) 3674–3692.e10

Abstract: The SRC-family kinase LYN is highly expressed in triple-negative/basal-like breast cancer (TNBC) and in the cell of origin of these tumors, c-KIT-positive luminal progenitors. Here, we demonstrate LYN is a downstream effector of c-KIT in normal mammary ... ...

Abstract	The SRC-family kinase LYN is highly expressed in triple-negative/basal-like breast cancer (TNBC) and in the cell of origin of these tumors, c-KIT-positive luminal progenitors. Here, we demonstrate LYN is a downstream effector of c-KIT in normal mammary cells and protective of apoptosis upon genotoxic stress. LYN activity is modulated by PIN1, a prolyl isomerase, and in BRCA1 mutant TNBC PIN1 upregulation activates LYN independently of c-KIT. Furthermore, the full-length LYN splice isoform (as opposed to the Δaa25-45 variant) drives migration and invasion of aggressive TNBC cells, while the ratio of splice variants is informative for breast cancer-specific survival across all breast cancers. Thus, dual mechanisms-uncoupling from upstream signals and splice isoform ratios-drive the activity of LYN in aggressive breast cancers.
MeSH term(s)	Adolescent ; Adult ; Animals ; BRCA1 Protein/deficiency ; BRCA1 Protein/metabolism ; Breast Neoplasms/enzymology ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Female ; Gene Expression Regulation, Neoplastic ; HEK293 Cells ; Humans ; Isoenzymes/metabolism ; Mice ; NIMA-Interacting Peptidylprolyl Isomerase/metabolism ; Neoplasm Invasiveness ; Proto-Oncogene Proteins c-kit/metabolism ; RNA Splicing/genetics ; Survival Analysis ; Up-Regulation ; Young Adult ; src-Family Kinases/genetics ; src-Family Kinases/metabolism
Chemical Substances	BRCA1 Protein ; BRCA1 protein, human ; Isoenzymes ; NIMA-Interacting Peptidylprolyl Isomerase ; Proto-Oncogene Proteins c-kit (EC 2.7.10.1) ; lyn protein-tyrosine kinase (EC 2.7.10.2) ; src-Family Kinases (EC 2.7.10.2) ; PIN1 protein, human (EC 5.2.1.8)
Language	English
Publishing date	2018-12-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2018.11.103
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Article ; Online: The receptor protein tyrosine phosphatase PTPRB negatively regulates FGF2-dependent branching morphogenesis.

Soady, Kelly J / Tornillo, Giusy / Kendrick, Howard / Meniel, Valerie / Olijnyk-Dallis, Daria / Morris, Joanna S / Stein, Torsten / Gusterson, Barry A / Isacke, Clare M / Smalley, Matthew J

Development (Cambridge, England)

2017 Volume 144, Issue 20, Page(s) 3777–3788

Abstract: PTPRB is a transmembrane protein tyrosine phosphatase known to regulate blood vessel remodelling and angiogenesis. Here, we demonstrate that PTPRB negatively regulates branching morphogenesis in the mouse mammary epithelium. We show ... ...

Abstract	PTPRB is a transmembrane protein tyrosine phosphatase known to regulate blood vessel remodelling and angiogenesis. Here, we demonstrate that PTPRB negatively regulates branching morphogenesis in the mouse mammary epithelium. We show that
MeSH term(s)	Animals ; Body Patterning ; Epithelial Cells/cytology ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Female ; Fibroblast Growth Factor 2/pharmacology ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Green Fluorescent Proteins/metabolism ; Mammary Glands, Animal/growth & development ; Mice ; Morphogenesis ; Neovascularization, Physiologic ; Oligonucleotide Array Sequence Analysis ; Organoids/growth & development ; Phosphorylation ; RNA, Small Interfering/metabolism ; Receptor-Like Protein Tyrosine Phosphatases, Class 3/genetics ; Receptor-Like Protein Tyrosine Phosphatases, Class 3/metabolism ; Receptors, Estrogen/metabolism ; Receptors, Fibroblast Growth Factor/metabolism ; Signal Transduction ; Stem Cells/cytology ; Transgenes
Chemical Substances	RNA, Small Interfering ; Receptors, Estrogen ; Receptors, Fibroblast Growth Factor ; Fibroblast Growth Factor 2 (103107-01-3) ; Green Fluorescent Proteins (147336-22-9) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; Ptprb protein, mouse (EC 3.1.3.48) ; Receptor-Like Protein Tyrosine Phosphatases, Class 3 (EC 3.1.3.48)
Language	English
Publishing date	2017-09-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	90607-4
ISSN	1477-9129 ; 0950-1991
ISSN (online)	1477-9129
ISSN	0950-1991
DOI	10.1242/dev.149120
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Article ; Online: Wnt and Neuregulin1/ErbB signalling extends 3D culture of hormone responsive mammary organoids.

Jardé, Thierry / Lloyd-Lewis, Bethan / Thomas, Mairian / Kendrick, Howard / Melchor, Lorenzo / Bougaret, Lauriane / Watson, Peter D / Ewan, Kenneth / Smalley, Matthew J / Dale, Trevor C

Nature communications

2016 Volume 7, Page(s) 13207

Abstract: The development of in vitro culture systems quantitatively and qualitatively recapitulating normal breast biology is key to the understanding of mammary gland biology. Current three-dimensional mammary culture systems have not demonstrated concurrent ... ...

Abstract	The development of in vitro culture systems quantitatively and qualitatively recapitulating normal breast biology is key to the understanding of mammary gland biology. Current three-dimensional mammary culture systems have not demonstrated concurrent proliferation and functional differentiation ex vivo in any system for longer than 2 weeks. Here, we identify conditions including Neuregulin1 and R-spondin 1, allowing maintenance and expansion of mammary organoids for 2.5 months in culture. The organoids comprise distinct basal and luminal compartments complete with functional steroid receptors and stem/progenitor cells able to reconstitute a complete mammary gland in vivo. Alternative conditions are also described that promote enrichment of basal cells organized into multiple layers surrounding a keratinous core, reminiscent of structures observed in MMTV-Wnt1 tumours. These conditions comprise a unique tool that should further understanding of normal mammary gland development, the molecular mechanism of hormone action and signalling events whose deregulation leads to breast tumourigenesis.
MeSH term(s)	Animals ; Female ; Gene Expression Regulation, Developmental ; Karyotyping ; Mammary Glands, Animal/growth & development ; Mammary Glands, Animal/metabolism ; Mice, Inbred C57BL ; Microscopy, Confocal ; Neuregulin-1/genetics ; Neuregulin-1/metabolism ; Organoids/growth & development ; Organoids/metabolism ; Receptor, ErbB-3/genetics ; Receptor, ErbB-3/metabolism ; Receptor, ErbB-4/genetics ; Receptor, ErbB-4/metabolism ; Time-Lapse Imaging/methods ; Tissue Culture Techniques/methods ; Wnt Signaling Pathway
Chemical Substances	Neuregulin-1 ; ErbB3 protein, mouse (EC 2.7.10.1) ; Erbb4 protein, mouse (EC 2.7.10.1) ; Receptor, ErbB-3 (EC 2.7.10.1) ; Receptor, ErbB-4 (EC 2.7.10.1)
Language	English
Publishing date	2016-10-26
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/ncomms13207
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Article: Drug sensitivity of Leishmania species: some unresolved problems.

Croft, Simon L / Yardley, Vanessa / Kendrick, Howard

Transactions of the Royal Society of Tropical Medicine and Hygiene

2002 Volume 96 Suppl 1, Page(s) S127–9

Abstract: Leishmania species show a significant variation in their sensitivity to established and experimental drugs. Molecular techniques to identify species in clinical infections rapidly could be used to guide treatment. Molecular markers are required to detect ...

Abstract	Leishmania species show a significant variation in their sensitivity to established and experimental drugs. Molecular techniques to identify species in clinical infections rapidly could be used to guide treatment. Molecular markers are required to detect and monitor acquired resistance to antimonial drugs. Reporter genes and the polymerase chain reaction will improve assays both in vitro and in vivo for the identification and evaluation of new drugs.
MeSH term(s)	Animals ; Antiprotozoal Agents/pharmacology ; Drug Evaluation, Preclinical/methods ; Drug Resistance ; Humans ; Leishmania/classification ; Leishmania/drug effects ; Parasitic Sensitivity Tests
Chemical Substances	Antiprotozoal Agents
Language	English
Publishing date	2002-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	441375-1
ISSN	1878-3503 ; 0035-9203
ISSN (online)	1878-3503
ISSN	0035-9203
DOI	10.1016/s0035-9203(02)90063-5
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