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Proteogenomic analysis of Inhibitor of Differentiation 4 (ID4) in basal-like breast cancer

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Proteogenomic analysis of Inhibitor of Differentiation 4 (ID4) in basal-like breast cancer. / Baker, Laura A; Holliday, Holly; Roden, Daniel; Krisp, Christoph; Wu, Sunny Z; Junankar, Simon; Serandour, Aurelien A; Mohammed, Hisham; Nair, Radhika; Sankaranarayanan, Geetha; Law, Andrew M K; McFarland, Andrea; Simpson, Peter T; Lakhani, Sunil; Dodson, Eoin; Selinger, Christina; Anderson, Lyndal; Samimi, Goli; Hacker, Neville F; Lim, Elgene; Ormandy, Christopher J; Naylor, Matthew J; Simpson, Kaylene; Nikolic, Iva; O'Toole, Sandra; Kaplan, Warren; Cowley, Mark J; Carroll, Jason S; Molloy, Mark; Swarbrick, Alexander.

in: BREAST CANCER RES, Jahrgang 22, Nr. 1, 11.06.2020, S. 63.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Baker, LA, Holliday, H, Roden, D, Krisp, C, Wu, SZ, Junankar, S, Serandour, AA, Mohammed, H, Nair, R, Sankaranarayanan, G, Law, AMK, McFarland, A, Simpson, PT, Lakhani, S, Dodson, E, Selinger, C, Anderson, L, Samimi, G, Hacker, NF, Lim, E, Ormandy, CJ, Naylor, MJ, Simpson, K, Nikolic, I, O'Toole, S, Kaplan, W, Cowley, MJ, Carroll, JS, Molloy, M & Swarbrick, A 2020, 'Proteogenomic analysis of Inhibitor of Differentiation 4 (ID4) in basal-like breast cancer', BREAST CANCER RES, Jg. 22, Nr. 1, S. 63. https://doi.org/10.1186/s13058-020-01306-6

APA

Baker, L. A., Holliday, H., Roden, D., Krisp, C., Wu, S. Z., Junankar, S., Serandour, A. A., Mohammed, H., Nair, R., Sankaranarayanan, G., Law, A. M. K., McFarland, A., Simpson, P. T., Lakhani, S., Dodson, E., Selinger, C., Anderson, L., Samimi, G., Hacker, N. F., ... Swarbrick, A. (2020). Proteogenomic analysis of Inhibitor of Differentiation 4 (ID4) in basal-like breast cancer. BREAST CANCER RES, 22(1), 63. https://doi.org/10.1186/s13058-020-01306-6

Vancouver

Baker LA, Holliday H, Roden D, Krisp C, Wu SZ, Junankar S et al. Proteogenomic analysis of Inhibitor of Differentiation 4 (ID4) in basal-like breast cancer. BREAST CANCER RES. 2020 Jun 11;22(1):63. https://doi.org/10.1186/s13058-020-01306-6

Bibtex

@article{ef222e74811f457a9a2ba11763fd0e90,
title = "Proteogenomic analysis of Inhibitor of Differentiation 4 (ID4) in basal-like breast cancer",
abstract = "BACKGROUND: Basal-like breast cancer (BLBC) is a poorly characterised, heterogeneous disease. Patients are diagnosed with aggressive, high-grade tumours and often relapse with chemotherapy resistance. Detailed understanding of the molecular underpinnings of this disease is essential to the development of personalised therapeutic strategies. Inhibitor of differentiation 4 (ID4) is a helix-loop-helix transcriptional regulator required for mammary gland development. ID4 is overexpressed in a subset of BLBC patients, associating with a stem-like poor prognosis phenotype, and is necessary for the growth of cell line models of BLBC through unknown mechanisms.METHODS: Here, we have defined unique molecular insights into the function of ID4 in BLBC and the related disease high-grade serous ovarian cancer (HGSOC), by combining RIME proteomic analysis, ChIP-seq mapping of genomic binding sites and RNA-seq.RESULTS: These studies reveal novel interactions with DNA damage response proteins, in particular, mediator of DNA damage checkpoint protein 1 (MDC1). Through MDC1, ID4 interacts with other DNA repair proteins (γH2AX and BRCA1) at fragile chromatin sites. ID4 does not affect transcription at these sites, instead binding to chromatin following DNA damage. Analysis of clinical samples demonstrates that ID4 is amplified and overexpressed at a higher frequency in BRCA1-mutant BLBC compared with sporadic BLBC, providing genetic evidence for an interaction between ID4 and DNA damage repair deficiency.CONCLUSIONS: These data link the interactions of ID4 with MDC1 to DNA damage repair in the aetiology of BLBC and HGSOC.",
author = "Baker, {Laura A} and Holly Holliday and Daniel Roden and Christoph Krisp and Wu, {Sunny Z} and Simon Junankar and Serandour, {Aurelien A} and Hisham Mohammed and Radhika Nair and Geetha Sankaranarayanan and Law, {Andrew M K} and Andrea McFarland and Simpson, {Peter T} and Sunil Lakhani and Eoin Dodson and Christina Selinger and Lyndal Anderson and Goli Samimi and Hacker, {Neville F} and Elgene Lim and Ormandy, {Christopher J} and Naylor, {Matthew J} and Kaylene Simpson and Iva Nikolic and Sandra O'Toole and Warren Kaplan and Cowley, {Mark J} and Carroll, {Jason S} and Mark Molloy and Alexander Swarbrick",
year = "2020",
month = jun,
day = "11",
doi = "10.1186/s13058-020-01306-6",
language = "English",
volume = "22",
pages = "63",
journal = "BREAST CANCER RES",
issn = "1465-5411",
publisher = "BioMed Central Ltd.",
number = "1",

}

RIS

TY - JOUR

T1 - Proteogenomic analysis of Inhibitor of Differentiation 4 (ID4) in basal-like breast cancer

AU - Baker, Laura A

AU - Holliday, Holly

AU - Roden, Daniel

AU - Krisp, Christoph

AU - Wu, Sunny Z

AU - Junankar, Simon

AU - Serandour, Aurelien A

AU - Mohammed, Hisham

AU - Nair, Radhika

AU - Sankaranarayanan, Geetha

AU - Law, Andrew M K

AU - McFarland, Andrea

AU - Simpson, Peter T

AU - Lakhani, Sunil

AU - Dodson, Eoin

AU - Selinger, Christina

AU - Anderson, Lyndal

AU - Samimi, Goli

AU - Hacker, Neville F

AU - Lim, Elgene

AU - Ormandy, Christopher J

AU - Naylor, Matthew J

AU - Simpson, Kaylene

AU - Nikolic, Iva

AU - O'Toole, Sandra

AU - Kaplan, Warren

AU - Cowley, Mark J

AU - Carroll, Jason S

AU - Molloy, Mark

AU - Swarbrick, Alexander

PY - 2020/6/11

Y1 - 2020/6/11

N2 - BACKGROUND: Basal-like breast cancer (BLBC) is a poorly characterised, heterogeneous disease. Patients are diagnosed with aggressive, high-grade tumours and often relapse with chemotherapy resistance. Detailed understanding of the molecular underpinnings of this disease is essential to the development of personalised therapeutic strategies. Inhibitor of differentiation 4 (ID4) is a helix-loop-helix transcriptional regulator required for mammary gland development. ID4 is overexpressed in a subset of BLBC patients, associating with a stem-like poor prognosis phenotype, and is necessary for the growth of cell line models of BLBC through unknown mechanisms.METHODS: Here, we have defined unique molecular insights into the function of ID4 in BLBC and the related disease high-grade serous ovarian cancer (HGSOC), by combining RIME proteomic analysis, ChIP-seq mapping of genomic binding sites and RNA-seq.RESULTS: These studies reveal novel interactions with DNA damage response proteins, in particular, mediator of DNA damage checkpoint protein 1 (MDC1). Through MDC1, ID4 interacts with other DNA repair proteins (γH2AX and BRCA1) at fragile chromatin sites. ID4 does not affect transcription at these sites, instead binding to chromatin following DNA damage. Analysis of clinical samples demonstrates that ID4 is amplified and overexpressed at a higher frequency in BRCA1-mutant BLBC compared with sporadic BLBC, providing genetic evidence for an interaction between ID4 and DNA damage repair deficiency.CONCLUSIONS: These data link the interactions of ID4 with MDC1 to DNA damage repair in the aetiology of BLBC and HGSOC.

AB - BACKGROUND: Basal-like breast cancer (BLBC) is a poorly characterised, heterogeneous disease. Patients are diagnosed with aggressive, high-grade tumours and often relapse with chemotherapy resistance. Detailed understanding of the molecular underpinnings of this disease is essential to the development of personalised therapeutic strategies. Inhibitor of differentiation 4 (ID4) is a helix-loop-helix transcriptional regulator required for mammary gland development. ID4 is overexpressed in a subset of BLBC patients, associating with a stem-like poor prognosis phenotype, and is necessary for the growth of cell line models of BLBC through unknown mechanisms.METHODS: Here, we have defined unique molecular insights into the function of ID4 in BLBC and the related disease high-grade serous ovarian cancer (HGSOC), by combining RIME proteomic analysis, ChIP-seq mapping of genomic binding sites and RNA-seq.RESULTS: These studies reveal novel interactions with DNA damage response proteins, in particular, mediator of DNA damage checkpoint protein 1 (MDC1). Through MDC1, ID4 interacts with other DNA repair proteins (γH2AX and BRCA1) at fragile chromatin sites. ID4 does not affect transcription at these sites, instead binding to chromatin following DNA damage. Analysis of clinical samples demonstrates that ID4 is amplified and overexpressed at a higher frequency in BRCA1-mutant BLBC compared with sporadic BLBC, providing genetic evidence for an interaction between ID4 and DNA damage repair deficiency.CONCLUSIONS: These data link the interactions of ID4 with MDC1 to DNA damage repair in the aetiology of BLBC and HGSOC.

U2 - 10.1186/s13058-020-01306-6

DO - 10.1186/s13058-020-01306-6

M3 - SCORING: Journal article

C2 - 32527287

VL - 22

SP - 63

JO - BREAST CANCER RES

JF - BREAST CANCER RES

SN - 1465-5411

IS - 1

ER -