LMW-E/CDK2 deregulates acinar morphogenesis, induces tumorigenesis, and associates with the activated b-Raf-ERK1/2-mTOR pathway in breast cancer patients (Q34220979)

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English	LMW-E/CDK2 deregulates acinar morphogenesis, induces tumorigenesis, and associates with the activated b-Raf-ERK1/2-mTOR pathway in breast cancer patients	scientific article

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scholarly article

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Europe PubMed Central

31 July 2017

LMW-E/CDK2 deregulates acinar morphogenesis, induces tumorigenesis, and associates with the activated b-Raf-ERK1/2-mTOR pathway in breast cancer patients (English)

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Europe PubMed Central

31 July 2017

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based on heuristic

inferred from title

9

object named as

Kelly K Hunt

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Europe PubMed Central

31 July 2017

Gordon B. Mills

8

object named as

Gordon B Mills

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Europe PubMed Central

31 July 2017

author name string

MyLinh T Duong

1

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Europe PubMed Central

31 July 2017

Said Akli

2

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Europe PubMed Central

31 July 2017

Caimiao Wei

3

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Europe PubMed Central

31 July 2017

Hannah F Wingate

4

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Europe PubMed Central

31 July 2017

Wenbin Liu

5

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Europe PubMed Central

31 July 2017

Yiling Lu

6

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Europe PubMed Central

31 July 2017

Min Yi

7

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Europe PubMed Central

31 July 2017

Khandan Keyomarsi

10

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Europe PubMed Central

31 July 2017

publication date

29 March 2012

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Europe PubMed Central

31 July 2017

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Europe PubMed Central

31 July 2017

8

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Europe PubMed Central

31 July 2017

3

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Europe PubMed Central

31 July 2017

e1002538

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Europe PubMed Central

31 July 2017

copyright license

Creative Commons Attribution 4.0 International

29 March 2012

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April 2022 Public Data File from Crossref

copyright status

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Targeting low molecular weight cyclin E (LMW-E) in breast cancer.

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Cdk2 is required for breast cancer mediated by the low-molecular-weight isoform of cyclin E

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Low molecular weight cyclin E overexpression shortens mitosis, leading to chromosome missegregation and centrosome amplification

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A novel interaction between HER2/neu and cyclin E in breast cancer

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Low-molecular-weight cyclin E can bypass letrozole-induced G1 arrest in human breast cancer cells and tumors

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HER2 signaling pathway activation and response of breast cancer cells to HER2-targeting agents is dependent strongly on the 3D microenvironment

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Characterization of a naturally occurring breast cancer subset enriched in epithelial-to-mesenchymal transition and stem cell characteristics

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Low molecular weight cyclin E is specific in breast cancer and is associated with mechanisms of tumor progression

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The MAPK(ERK-1,2) pathway integrates distinct and antagonistic signals from TGFalpha and FGF7 in morphogenesis of mouse mammary epithelium

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Gene expression signature in organized and growth-arrested mammary acini predicts good outcome in breast cancer

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Beta1 integrin inhibitory antibody induces apoptosis of breast cancer cells, inhibits growth, and distinguishes malignant from normal phenotype in three dimensional cultures and in vivo

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Seliciclib (CYC202, R-Roscovitine) induces cell death in multiple myeloma cells by inhibition of RNA polymerase II-dependent transcription and down-regulation of Mcl-1

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Bim regulation of lumen formation in cultured mammary epithelial acini is targeted by oncogenes.

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The tumor-specific hyperactive forms of cyclin E are resistant to inhibition by p21 and p27.

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Tumor-specific low molecular weight forms of cyclin E induce genomic instability and resistance to p21, p27, and antiestrogens in breast cancer

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Morphogenesis and oncogenesis of MCF-10A mammary epithelial acini grown in three-dimensional basement membrane cultures

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Cyclin E and survival in patients with breast cancer

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beta4 integrin-dependent formation of polarized three-dimensional architecture confers resistance to apoptosis in normal and malignant mammary epithelium

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Normal and tumor-derived myoepithelial cells differ in their ability to interact with luminal breast epithelial cells for polarity and basement membrane deposition

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ErbB2, but not ErbB1, reinitiates proliferation and induces luminal repopulation in epithelial acini

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Tumor-specific proteolytic processing of cyclin E generates hyperactive lower-molecular-weight forms

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Novel splice variants of cyclin E with altered substrate specificity

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Differential abilities of the Raf family of protein kinases to abrogate cytokine dependency and prevent apoptosis in murine hematopoietic cells by a MEK1-dependent mechanism

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Processing of cyclin E differs between normal and tumor breast cells

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Nonparametric Estimation from Incomplete Observations

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Deregulation of cyclin E in breast cancer

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10.1371/JOURNAL.PGEN.1002538

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Europe PubMed Central

31 July 2017

1 reference

Europe PubMed Central

31 July 2017

1 reference

Europe PubMed Central

31 July 2017

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