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GD3 synthase regulates epithelial-mesenchymal transition and metastasis in breast cancer

Oncogene, 2015-06, Vol.34 (23), p.2958-2967

2015

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Inhibition of FOXC2 restores epithelial phenotype and drug sensitivity in prostate cancer cells with stem-cell properties

Oncogene, 2016-11, Vol.35 (46), p.5963-5976

2016

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Phosphorylation of serine 367 of FOXC2 by p38 regulates ZEB1 and breast cancer metastasis, without impacting primary tumor growth

Oncogene, 2016-11, Vol.35 (46), p.5977-5988

2016

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pIgR: Frenemy of Inflammation, EMT, and HCC Progression

JNCI : Journal of the National Cancer Institute, 2011-11, Vol.103 (22), p.1644-1645

2011

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Mutational analysis of the Ricinus lectin B-chains: galactose-binding ability of the 2 gamma subdomain of Ricinus communis agglutinin B-chain

The Journal of biological chemistry, 1995-09, Vol.270 (35), p.20292-20297

1995

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p73α is a candidate effector in the p53 independent apoptosis pathway of cisplatin damaged primary murine colonocytes

Journal of clinical pathology, 2004-05, Vol.57 (5), p.492-498

2004

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p53 deficiency exacerbates pleiotropic mitotic defects, changes in nuclearity and polyploidy in transdifferentiating pancreatic acinar cells

Oncogene, 2005-03, Vol.24 (13), p.2184-2194

2005

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Improved retention of zymogen granules in cultured murine pancreatic acinar cells and induction of acinar-ductal transdifferentiation in vitro

Pancreas, 2005-03, Vol.30 (2), p.148-157

2005

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Induction of p21 and nuclear accumulation of TAp73α and c-abl during apoptosis of cisplatin-treated primary pancreatic acinar cells

International journal of oncology, 2004-12

2004

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p73[alpha] is a candidate effector in the p53 independent apoptosis pathway of cisplatin damaged primary murine colonocytes

Journal of clinical pathology, 2004-05, Vol.57 (5), p.492

2004

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p73alpha is a candidate effector in the p53 independent apoptosis pathway of cisplatin damaged primary murine colonocytes

Journal of clinical pathology, 2004-05, Vol.57 (5), p.492

2004

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Glutathione and p53 independently mediate responses against oxidative stress in ES cells

Free radical biology & medicine, 2002-01, Vol.32 (2), p.187-196

2002

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Apoptosis in vivo and in vitro: conflict or complementarity?

Molecular medicine today (Regul. ed.), 1996-05, Vol.2 (5), p.189-191

1996

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The H3K27me3-demethylase KDM6A is suppressed in breast cancer stem-like cells, and enables the resolution of bivalency during the mesenchymal-epithelial transition

Oncotarget, 2017-09, Vol.8 (39), p.65548-65565

2017

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GD3 synthase regulates epithelial-mesenchymal transition and metastasis in breast cancer

Inhibition of FOXC2 restores epithelial phenotype and drug sensitivity in prostate cancer cells with stem-cell properties

Phosphorylation of serine 367 of FOXC2 by p38 regulates ZEB1 and breast cancer metastasis, without impacting primary tumor growth

NOTUM from Apc-mutant cells biases clonal competition to initiate cancer

pIgR: Frenemy of Inflammation, EMT, and HCC Progression

Mutational analysis of the Ricinus lectin B-chains: galactose-binding ability of the 2 gamma subdomain of Ricinus communis agglutinin B-chain

p73α is a candidate effector in the p53 independent apoptosis pathway of cisplatin damaged primary murine colonocytes

p53 deficiency exacerbates pleiotropic mitotic defects, changes in nuclearity and polyploidy in transdifferentiating pancreatic acinar cells

Improved retention of zymogen granules in cultured murine pancreatic acinar cells and induction of acinar-ductal transdifferentiation in vitro

Induction of p21 and nuclear accumulation of TAp73α and c-abl during apoptosis of cisplatin-treated primary pancreatic acinar cells

p73[alpha] is a candidate effector in the p53 independent apoptosis pathway of cisplatin damaged primary murine colonocytes

p73alpha is a candidate effector in the p53 independent apoptosis pathway of cisplatin damaged primary murine colonocytes

Glutathione and p53 independently mediate responses against oxidative stress in ES cells

Apoptosis in vivo and in vitro: conflict or complementarity?

The H3K27me3-demethylase KDM6A is suppressed in breast cancer stem-like cells, and enables the resolution of bivalency during the mesenchymal-epithelial transition

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