Výsledky vyhledávání - "Madoz-Gurpide J"

CIP2A as a Key Regulator for AKT Phosphorylation Has Partial Impact Determining Clinical Outcome in Breast Cancer

Autor: Luque M, Cristobal I, Sanz-Alvarez M, Santos A, Zazo S, Eroles P, Arpi O, Rovira A, Albanell J, Madoz-Gurpide J, Garcia-Foncillas J, Rojo F

Publikováno v: Journal of Clinical Medicine
r-INCLIVA. Repositorio Institucional de Producción Científica de INCLIVA
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Together with its reported ability to modulate AKT phosphorylation (p-AKT) status in several tumor types, the oncoprotein CIP2A has been described to induce breast cancer progression and drug resistance. However, the clinical and therapeutic relevanc

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=RECOLECTA___::ab00d7a98822bbfbeaae82a79cd5c177
https://www.fundanet.incliva.es/publicaciones/ProdCientif/PublicacionFrw.aspx?id=16697

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Expression of Phosphorylated BRD4 Is Markedly Associated with the Activation Status of the PP2A Pathway and Shows a Strong Prognostic Value in Triple Negative Breast Cancer Patients

Autor: Sanz-Alvarez M, Cristobal I, Luque M, Santos A, Zazo S, Madoz-Gurpide J, Carames C, Chiang C, Garcia-Foncillas J, Eroles P, Albanell J, Rojo F

Publikováno v: Cancers
r-INCLIVA. Repositorio Institucional de Producción Científica de INCLIVA
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Simple Summary The use of BRD4 inhibitors has emerged as a novel therapeutic approach in a wide variety of tumors including the triple negative breast cancer. Moreover, PP2A has been proposed as the phosphatase involved in regulating BRD4 phosphoryla

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=RECOLECTA___::99b8dd740e2e09c19196da59d0bacb22
https://www.fundanet.incliva.es/publicaciones/ProdCientif/PublicacionFrw.aspx?id=16173

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Targeted Therapy Modulates the Secretome of Cancer-Associated Fibroblasts to Induce Resistance in HER2-Positive Breast Cancer

Autor: Luque M, Sanz-Alvarez M, Santamaria A, Zazo S, Cristobal I, de la Fuente L, Minguez P, Eroles P, Rovira A, Albanell J, Madoz-Gurpide J, Rojo F

Publikováno v: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
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The combination of trastuzumab plus pertuzumab plus docetaxel as a first-line therapy in patients with HER2-positive metastatic breast cancer has provided significant clinical benefits compared to trastuzumab plus docetaxel alone. However, despite th

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=RECOLECTA___::29179f1eeaff0884dbff6b3125c0e76f
https://www.fundanet.incliva.es/publicaciones/ProdCientif/PublicacionFrw.aspx?id=16385

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The Hippo Pathway Transducers YAP1/TEAD Induce Acquired Resistance to Trastuzumab in HER2-Positive Breast Cancer

Publikováno v: Cancers
r-INCLIVA. Repositorio Institucional de Producción Científica de INCLIVA
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Trastuzumab is the first-line targeted therapeutic drug for HER2-positive breast cancer, leading to improved overall survival. However, acquired resistance inevitably occurs. We aimed to identify, quantify, and assess the mechanisms of acquired resis

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=RECOLECTA___::ccfd1d5399c893609b303d2859eee706
https://www.fundanet.incliva.es/publicaciones/ProdCientif/PublicacionFrw.aspx?id=4236

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Autocrine CCL5 effect mediates trastuzumab resistance by ERK pathway activation in HER2-positive breast cancer

Autor: Zazo S, Gonzalez-Alonso P, Martin-Aparicio E, Chamizo C, Luque M, Sanz-Alvarez M, Minguez P, Gomez-Lopez G, Cristobal I, Carames C, Garcia-Foncillas J, Eroles P, Lluch A, Arpi O, Rovira A, Albanell J, Madoz-Gurpide J, Rojo F

Publikováno v: MOLECULAR CANCER THERAPEUTICS
r-INCLIVA. Repositorio Institucional de Producción Científica de INCLIVA
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HER2-positive breast cancer is currently managed with chemotherapy in combination with specific anti-HER2 therapies, including trastuzumab. However, a high percentage of patients with HER2-positive tumors do not respond to trastuzumab (primary resist

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=RECOLECTA___::d3a0ae64ea01e1c92d9da343bed95c2d
https://www.fundanet.incliva.es/publicaciones/ProdCientif/PublicacionFrw.aspx?id=4444

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