Correction to: FAK activates AKT-mTOR signaling to promote the growth and progression of MMTV-Wnt1-driven basal-like mammary tumors

to related objects

Location: Deutsche Nationalbibliothek Frankfurt am Main

ISSN: 1465-542X

Extent: Online-Ressource

Language: Englisch

Notes: online resource.

Bibliographic citation: Correction to: FAK activates AKT-mTOR signaling to promote the growth and progression of MMTV-Wnt1-driven basal-like mammary tumors ; volume:22 ; number:1 ; day:29 ; month:6 ; year:2020 ; pages:1-2 ; date:12.2020
Breast cancer research ; 22, Heft 1 (29.6.2020), 1-2, 12.2020

Creator: Paul, Ritama
Luo, Ming
Mo, Xueying
Lu, Jason
Yeo, Syn Kok
Guan, Jun-Lin

Contributor: SpringerLink (Online service)

DOI: 10.1186/s13058-020-01310-w

URN: urn:nbn:de:101:1-2020082420071710630242

Rights: Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.

Last update: 14.08.2025, 10:56 AM CEST

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Paul, Ritama
Luo, Ming
Mo, Xueying
Lu, Jason
Yeo, Syn Kok
Guan, Jun-Lin
SpringerLink (Online service)

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FAK activates AKT-mTOR signaling to promote the growth and progression of MMTV-Wnt1-driven basal-like mammary tumors

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

Embryonic mammary signature subsets are activated in Brca1 -/- and basal-like breast cancers

Human basal-like breast cancer is represented by one of the two mammary tumor subtypes in dogs

A mouse model featuring tissue-specific deletion of p53 and Brca1 gives rise to mammary tumors with genomic and transcriptomic similarities to human basal-like breast cancer

C-terminally phosphorylated p27 activates self-renewal driver genes to program cancer stem cell expansion, mammary hyperplasia and cancer

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

ERβ1 represses basal-like breast cancer epithelial to mesenchymal transition by destabilizing EGFR

Claudin 1 expression in basal-like breast cancer is related to patient age

RNF40 epigenetically modulates glycolysis to support the aggressiveness of basal-like breast cancer

FAK activates AKT-mTOR signaling to promote the growth and progression of MMTV-Wnt1-driven basal-like mammary tumors

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

TRIM44 activates the AKT/mTOR signal pathway to induce melanoma progression by stabilizing TLR4

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

Embryonic mammary signature subsets are activated in Brca1 -/- and basal-like breast cancers

Human basal-like breast cancer is represented by one of the two mammary tumor subtypes in dogs

A mouse model featuring tissue-specific deletion of p53 and Brca1 gives rise to mammary tumors with genomic and transcriptomic similarities to human basal-like breast cancer

C-terminally phosphorylated p27 activates self-renewal driver genes to program cancer stem cell expansion, mammary hyperplasia and cancer

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

ERβ1 represses basal-like breast cancer epithelial to mesenchymal transition by destabilizing EGFR

Claudin 1 expression in basal-like breast cancer is related to patient age

RNF40 epigenetically modulates glycolysis to support the aggressiveness of basal-like breast cancer

FAK activates AKT-mTOR signaling to promote the growth and progression of MMTV-Wnt1-driven basal-like mammary tumors

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

TRIM44 activates the AKT/mTOR signal pathway to induce melanoma progression by stabilizing TLR4

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

Embryonic mammary signature subsets are activated in Brca1 -/- and basal-like breast cancers

Human basal-like breast cancer is represented by one of the two mammary tumor subtypes in dogs

A mouse model featuring tissue-specific deletion of p53 and Brca1 gives rise to mammary tumors with genomic and transcriptomic similarities to human basal-like breast cancer

C-terminally phosphorylated p27 activates self-renewal driver genes to program cancer stem cell expansion, mammary hyperplasia and cancer

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

ERβ1 represses basal-like breast cancer epithelial to mesenchymal transition by destabilizing EGFR

Claudin 1 expression in basal-like breast cancer is related to patient age

RNF40 epigenetically modulates glycolysis to support the aggressiveness of basal-like breast cancer

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Correction to: FAK activates AKT-mTOR signaling to promote the growth and progression of MMTV-Wnt1-driven basal-like mammary tumors

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Other Objects (12)

FAK activates AKT-mTOR signaling to promote the growth and progression of MMTV-Wnt1-driven basal-like mammary tumors

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

TRIM44 activates the AKT/mTOR signal pathway to induce melanoma progression by stabilizing TLR4

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

Embryonic mammary signature subsets are activated in Brca1 -/- and basal-like breast cancers

Human basal-like breast cancer is represented by one of the two mammary tumor subtypes in dogs

A mouse model featuring tissue-specific deletion of p53 and Brca1 gives rise to mammary tumors with genomic and transcriptomic similarities to human basal-like breast cancer

C-terminally phosphorylated p27 activates self-renewal driver genes to program cancer stem cell expansion, mammary hyperplasia and cancer

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

ERβ1 represses basal-like breast cancer epithelial to mesenchymal transition by destabilizing EGFR

Claudin 1 expression in basal-like breast cancer is related to patient age

RNF40 epigenetically modulates glycolysis to support the aggressiveness of basal-like breast cancer

FAK activates AKT-mTOR signaling to promote the growth and progression of MMTV-Wnt1-driven basal-like mammary tumors

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

TRIM44 activates the AKT/mTOR signal pathway to induce melanoma progression by stabilizing TLR4

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

Embryonic mammary signature subsets are activated in Brca1 -/- and basal-like breast cancers

Human basal-like breast cancer is represented by one of the two mammary tumor subtypes in dogs

A mouse model featuring tissue-specific deletion of p53 and Brca1 gives rise to mammary tumors with genomic and transcriptomic similarities to human basal-like breast cancer

C-terminally phosphorylated p27 activates self-renewal driver genes to program cancer stem cell expansion, mammary hyperplasia and cancer

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

ERβ1 represses basal-like breast cancer epithelial to mesenchymal transition by destabilizing EGFR

Claudin 1 expression in basal-like breast cancer is related to patient age

RNF40 epigenetically modulates glycolysis to support the aggressiveness of basal-like breast cancer

FAK activates AKT-mTOR signaling to promote the growth and progression of MMTV-Wnt1-driven basal-like mammary tumors

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

TRIM44 activates the AKT/mTOR signal pathway to induce melanoma progression by stabilizing TLR4

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

Embryonic mammary signature subsets are activated in Brca1 -/- and basal-like breast cancers

Human basal-like breast cancer is represented by one of the two mammary tumor subtypes in dogs

A mouse model featuring tissue-specific deletion of p53 and Brca1 gives rise to mammary tumors with genomic and transcriptomic similarities to human basal-like breast cancer

C-terminally phosphorylated p27 activates self-renewal driver genes to program cancer stem cell expansion, mammary hyperplasia and cancer

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

ERβ1 represses basal-like breast cancer epithelial to mesenchymal transition by destabilizing EGFR

Claudin 1 expression in basal-like breast cancer is related to patient age

RNF40 epigenetically modulates glycolysis to support the aggressiveness of basal-like breast cancer

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