Author

B. Sainz

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Cancer Biology· 5

Signature Assays, Organisms & Methods

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Research Focus:cancer & tumor microenvironment· 5 Approach:experimental assay· 5 Organism:human· 4 Assay:bulk RNA-seq· 2 Research Focus:cell type annotation· 2 Research Focus:drug response / drug discovery· 2 Research Focus:benchmarking· 1 Research Focus:cell signaling & trafficking· 1

Frequent Co-Authors

C. Heeschen· 3 shared B. Parejo-Alonso· 2 shared L. Penin-Peyta· 2 shared P. Jagust· 2 shared P. Sancho· 2 shared S. Courtois· 2 shared A. Berninger· 1 shared A. Bosma· 1 shared

Activity by Year

2020-2022 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 23 mutual co-author links

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3 shared papersCancer Biology

C. Heeschen

Mutual co-authors in cluster

Author profile →

5 papers

Recent·Most cited

LAMC2 marks a tumor-initiating cell population with an aggressive signature in pancreatic cancer

D. Delle Cave, S. Buonaiuto, M. Mangini, B. Sainz, A. Di Domenico, T. Teresa Iavazzo, G. Andolfi, C. Cortina Duran, M. Sevillano, C. Heeschen, V. Colonna, M. Corona, A. Cucciardi, M. Di Guida, E. Batlle, , E. Lonardo

This study identifies LAMC2-positive cells as tumor-initiating cells in pancreatic cancer with aggressive properties and shows that targeting TGF-β signaling inhibits metastasis.

bioRxiv · Mar 24, 2022Cancer Biology

Combined SHP2 and ERK inhibition for the treatment of KRAS-driven Pancreatic Ductal Adenocarcinoma

K. J. Ciecielski, A. Mulero-Sanchez, A. Berninger, L. R. Canas, A. Bosma, K. Gorgulu, N. Wu, K. N. Diakopoulos, E. Kaya-Aksoy, D. A. Ruess, D. Kabacaoglu, F. Schmidt, L. Heinemann, Y. Fan, B. Thijssen, , S. Mainardi

This paper investigates the combination of SHP2 and ERK inhibition as a treatment for KRAS-driven pancreatic ductal adenocarcinoma, showing synergistic anticancer effects and tumor regression in mouse models.

bioRxiv · Dec 14, 2021 · PreprintCancer Biology

PPAR-delta acts as a metabolic master checkpoint for metastasis in pancreatic cancer

B. Parejo-Alonso, D. Barneda, S. M. Trabulo, S. Courtois, S. Compte-Sancerni, L. Ruiz-Canas, Q. Zheng, J. Tang, M. Chen, Z. Guo, U. Schmitz, P. Irun, L. Penin-Peyta, S. M. Crusz, A. Cano-Galiano, , P. Sancho

This study shows PPAR-delta drives metabolic reprogramming in pancreatic cancer, promoting metastasis, and its inhibition reduces invasiveness.

bioRxiv · Nov 15, 2021 · PreprintCancer Biology

Inhibition of mitochondrial dynamics preferentially targets pancreatic cancer cells with enhanced tumorigenic and invasive potential

S. Courtois, B. de Luxan-Delgado, L. Penin-Peyta, A. Royo-Garcia, B. Parejo-Alonso, P. Jagust, S. Alcala, J. A. Rubiolo, L. Sanchez, B. Sainz, C. Heeschen, P. Sancho

This study shows that inhibiting mitochondrial fission with mDivi-1 selectively kills pancreatic cancer stem cells by causing mitochondrial dysfunction and energy crisis.

bioRxiv · Jan 17, 2021Cancer Biology

A feedback-loop between telomerase activity and stemness factors regulates PDAC stem cells

K. Walter, E. Rodriguez-Aznar, M. S. Ventura-Ferreira, P. O. Frappant, T. Dittrich, K. Tiwary, S. Meessen, L. Lerma, N. Daiss, L. A. Schulte, F. Arnold, N. Azoitei, M. Erkan, A. Lehel, T. Bruemmendorf, , P. C. Hermann

This study shows that telomerase activity and stemness factors form a feedback loop that maintains pancreatic cancer stem cells, and disrupting this loop reduces their tumorigenic potential.

bioRxiv · Nov 2, 2020 · PreprintCancer Biology