Metabolic biomarkers for response to PI3K inhibition in basal-like breast cancer

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Location: Deutsche Nationalbibliothek Frankfurt am Main

ISSN: 1465-542X

Extent: Online-Ressource

Language: Englisch

Notes: online resource.

Bibliographic citation: Metabolic biomarkers for response to PI3K inhibition in basal-like breast cancer ; volume:15 ; number:1 ; day:28 ; month:2 ; year:2013 ; pages:1-18 ; date:2.2013
Breast cancer research ; 15, Heft 1 (28.2.2013), 1-18, 2.2013

Creator: Moestue, Siver A.

Contributor: Dam, Cornelia G.
Gorad, Saurabh S.
Kristian, Alexandr
Bofin, Anna
Mælandsmo, Gunhild M.
Engebråten, Olav
Gribbestad, Ingrid S.
Bjørkøy, Geir
SpringerLink (Online service)

DOI: 10.1186/bcr3391

URN: urn:nbn:de:1111-2016032417075

Rights: Der Zugriff auf das Objekt ist unbeschränkt möglich.

Last update: 14.08.2025, 10:48 AM CEST

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Moestue, Siver A.
Dam, Cornelia G.
Gorad, Saurabh S.
Kristian, Alexandr
Bofin, Anna
Mælandsmo, Gunhild M.
Engebråten, Olav
Gribbestad, Ingrid S.
Bjørkøy, Geir
SpringerLink (Online service)

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Metabolic biomarkers for response to PI3K inhibition in basal-like breast cancer

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Other Objects (12)

Feline mammary basal-like adenocarcinomas: a potential model for human triple-negative breast cancer (TNBC) with basal-like subtype

SRC inhibition prevents P-cadherin mediated signaling and function in basal-like breast cancer cells

Inactivation of LATS1/2 drives luminal-basal plasticity to initiate basal-like mammary carcinomas

Weight loss reduces basal-like breast cancer through kinome reprogramming

CCL3 predicts exceptional response to TGFβ inhibition in basal-like pancreatic cancer enriched in LIF-producing macrophages

Integrated molecular pathway analysis informs a synergistic combination therapy targeting PTEN/PI3K and EGFR pathways for basal-like breast cancer

Targeting BCL-2–expressing basal-like breast cancer with BH3-mimetics

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The CD44+/CD24-phenotype is enriched in basal-like breast tumors

Inhibition of basal-like breast cancer growth by FTY720 in combination with epidermal growth factor receptor kinase blockade

Inhibition of SHP2 in basal-like and triple-negative breast cells induces basal-to-luminal transition, hormone dependency, and sensitivity to anti-hormone treatment

Gene expression signatures of morphologically normal breast tissue identify basal-like tumors

Feline mammary basal-like adenocarcinomas: a potential model for human triple-negative breast cancer (TNBC) with basal-like subtype

SRC inhibition prevents P-cadherin mediated signaling and function in basal-like breast cancer cells

Inactivation of LATS1/2 drives luminal-basal plasticity to initiate basal-like mammary carcinomas

Weight loss reduces basal-like breast cancer through kinome reprogramming

CCL3 predicts exceptional response to TGFβ inhibition in basal-like pancreatic cancer enriched in LIF-producing macrophages

Integrated molecular pathway analysis informs a synergistic combination therapy targeting PTEN/PI3K and EGFR pathways for basal-like breast cancer

Targeting BCL-2–expressing basal-like breast cancer with BH3-mimetics

Basal-like breast cancer: molecular profiles, clinical features and survival outcomes

The CD44+/CD24-phenotype is enriched in basal-like breast tumors

Inhibition of basal-like breast cancer growth by FTY720 in combination with epidermal growth factor receptor kinase blockade

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Gene expression signatures of morphologically normal breast tissue identify basal-like tumors

Feline mammary basal-like adenocarcinomas: a potential model for human triple-negative breast cancer (TNBC) with basal-like subtype

SRC inhibition prevents P-cadherin mediated signaling and function in basal-like breast cancer cells

Inactivation of LATS1/2 drives luminal-basal plasticity to initiate basal-like mammary carcinomas

Weight loss reduces basal-like breast cancer through kinome reprogramming

CCL3 predicts exceptional response to TGFβ inhibition in basal-like pancreatic cancer enriched in LIF-producing macrophages

Integrated molecular pathway analysis informs a synergistic combination therapy targeting PTEN/PI3K and EGFR pathways for basal-like breast cancer

Targeting BCL-2–expressing basal-like breast cancer with BH3-mimetics

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Inhibition of SHP2 in basal-like and triple-negative breast cells induces basal-to-luminal transition, hormone dependency, and sensitivity to anti-hormone treatment

Gene expression signatures of morphologically normal breast tissue identify basal-like tumors

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