José A. Pellicer

734 total citations
18 papers, 633 citations indexed

About

José A. Pellicer is a scholar working on Molecular Biology, Biochemistry and Cancer Research. According to data from OpenAlex, José A. Pellicer has authored 18 papers receiving a total of 633 indexed citations (citations by other indexed papers that have themselves been cited), including 9 papers in Molecular Biology, 8 papers in Biochemistry and 4 papers in Cancer Research. Recurrent topics in José A. Pellicer's work include Sulfur Compounds in Biology (6 papers), Genomics, phytochemicals, and oxidative stress (5 papers) and Amino Acid Enzymes and Metabolism (4 papers). José A. Pellicer is often cited by papers focused on Sulfur Compounds in Biology (6 papers), Genomics, phytochemicals, and oxidative stress (5 papers) and Amino Acid Enzymes and Metabolism (4 papers). José A. Pellicer collaborates with scholars based in Spain and United States. José A. Pellicer's co-authors include Elena Obrador, José M. Estrela, Julián Carretero, Miguel Asensi, Ángel Ortega, José Navarro, María Benlloch, Soraya L. Vallés, Vicente Rodilla and Antonio Pascual and has published in prestigious journals such as Journal of Biological Chemistry, Nature Medicine and PLoS ONE.

In The Last Decade

José A. Pellicer

18 papers receiving 620 citations

Peers

José A. Pellicer

BIOCH

ONCOL

IMMUN

Federica Vannini United States

Peter J. Bungay United Kingdom

Juan M. Esteve Spain

Kristell Le Gal Sweden

Yinlin Ge China

Hitoshi Akedo Japan

Soyeon Shin South Korea

Tim Prozorovski Germany

Jon Peñarando Spain

Federica Vannini United States

José A. Pellicer

222 ×0.6

72 ×0.5

BIOCH

143 ×1.2

78 ×0.9

ONCOL

108 ×1.4

IMMUN

Citations per year, relative to José A. Pellicer José A. Pellicer (= 1×) peers Federica Vannini

Countries citing papers authored by José A. Pellicer

Since Specialization

Citations

This map shows the geographic impact of José A. Pellicer's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by José A. Pellicer with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites José A. Pellicer more than expected).

Fields of papers citing papers by José A. Pellicer

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by José A. Pellicer. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by José A. Pellicer. The network helps show where José A. Pellicer may publish in the future.

Co-authorship network of co-authors of José A. Pellicer

This figure shows the co-authorship network connecting the top 25 collaborators of José A. Pellicer. A scholar is included among the top collaborators of José A. Pellicer based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with José A. Pellicer. José A. Pellicer is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

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18 of 18 papers shown

Obrador, Elena, Rosario Salvador‐Palmer, Rafael López‐Blanch, et al.. (2020). Melanoma in the liver: Oxidative stress and the mechanisms of metastatic cell survival. Seminars in Cancer Biology. 71. 109–121. 17 indexed citations

Estrela, José M., Rosario Salvador‐Palmer, Patricia Marchio, et al.. (2019). Glucocorticoid receptor antagonism overcomes resistance to BRAF inhibition in BRAF^V600E-mutated metastatic melanoma.. PubMed. 9(12). 2580–2598. 15 indexed citations

Benlloch, María, Soraya L. Vallés, María L. Rodríguez, et al.. (2016). Abstract 2810: Pterostilbene, a natural phytoalexin, weakens the antioxidant defenses of aggressive cancer cells in vivo: a pituitary gland- and Nrf2-dependent mechanism. Cancer Research. 76(14_Supplement). 2810–2810. 1 indexed citations

Benlloch, María, Elena Obrador, Soraya L. Vallés, et al.. (2015). Pterostilbene Decreases the Antioxidant Defenses of Aggressive Cancer Cells In Vivo : A Physiological Glucocorticoids- and Nrf2-Dependent Mechanism. Antioxidants and Redox Signaling. 24(17). 974–990. 56 indexed citations

Obrador, Elena, Soraya L. Vallés, María Benlloch, et al.. (2014). Glucocorticoid Receptor Knockdown Decreases the Antioxidant Protection of B16 Melanoma Cells: An Endocrine System-Related Mechanism that Compromises Metastatic Cell Resistance to Vascular Endothelium-Induced Tumor Cytotoxicity. PLoS ONE. 9(5). e96466–e96466. 24 indexed citations

Vallés, Soraya L., María Benlloch, María L. Rodríguez, et al.. (2013). Stress hormones promote growth of B16-F10 melanoma metastases: an interleukin 6- and glutathione-dependent mechanism. Journal of Translational Medicine. 11(1). 72–72. 54 indexed citations

Obrador, Elena, María Benlloch, José A. Pellicer, Miguel Asensi, & José M. Estrela. (2011). Intertissue Flow of Glutathione (GSH) as a Tumor Growth-promoting Mechanism. Journal of Biological Chemistry. 286(18). 15716–15727. 24 indexed citations

Benlloch, María, Salvador Mena, Paula Ferrer, et al.. (2005). Bcl-2 and Mn-SOD Antisense Oligodeoxynucleotides and a Glutamine-enriched Diet Facilitate Elimination of Highly Resistant B16 Melanoma Cells by Tumor Necrosis Factor-α and Chemotherapy. Journal of Biological Chemistry. 281(1). 69–79. 39 indexed citations

Ortega, Ángel, Paula Ferrer, Julián Carretero, et al.. (2003). Down-regulation of Glutathione and Bcl-2 Synthesis in Mouse B16 Melanoma Cells Avoids Their Survival during Interaction with the Vascular Endothelium. Journal of Biological Chemistry. 278(41). 39591–39599. 43 indexed citations

10.

Obrador, Elena, Julián Carretero, Ángel Ortega, et al.. (2002). γ-Glutamyl transpeptidase overexpression increases metastatic growth of B16 melanoma cells in the mouse liver. Hepatology. 35(1). 74–81. 78 indexed citations

11.

Obrador, Elena, Julián Carretero, Juan M. Esteve, et al.. (2001). Glutamine potentiates TNF-α-induced tumor cytotoxicity. Free Radical Biology and Medicine. 31(5). 642–650. 31 indexed citations

12.

Carretero, Julián, Elena Obrador, Juan M. Esteve, et al.. (2001). Tumoricidal Activity of Endothelial Cells. Journal of Biological Chemistry. 276(28). 25775–25782. 43 indexed citations

13.

Carretero, Julián, Elena Obrador, José A. Pellicer, Antonio Pascual, & José M. Estrela. (2000). Mitochondrial glutathione depletion by glutamine in growing tumor cells. Free Radical Biology and Medicine. 29(9). 913–923. 36 indexed citations

14.

Obrador, Elena, et al.. (1998). Regulation of tumour cell sensitivity to TNF‐induced oxidative stress and cytotoxicity: Role of glutathione. BioFactors. 8(1-2). 23–26. 23 indexed citations

15.

Obrador, Elena, et al.. (1997). Glutathione and the rate of cellular proliferation determine tumour cell sensitivity to tumour necrosis factor in vivo. Biochemical Journal. 325(1). 183–189. 70 indexed citations

16.

Estrela, José M., et al.. (1995). Elimination of Ehrlich tumours by ATP-induced growth inhibition, glutathione depletion and X-rays. Nature Medicine. 1(1). 84–88. 60 indexed citations

17.

Rodilla, Vicente, et al.. (1990). Induction of micronucleated and binucleate cells in Chinese hamster ovary (CHO) cells by cis-diamminedichloroplatinum (II): a morphological and morphometric study. Mutation Research/Genetic Toxicology. 241(2). 115–124. 15 indexed citations

18.

Pellicer, José A., et al.. (1989). Binucleate cells in the Ehrlich ascites tumor. Autoradiographic labeling. Biology of the Cell. 65(1). 75–77. 4 indexed citations

Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.

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