Ricardo M. Attar

4.9k total citations
72 papers, 3.2k citations indexed

About

Ricardo M. Attar is a scholar working on Molecular Biology, Endocrinology, Diabetes and Metabolism and Oncology. According to data from OpenAlex, Ricardo M. Attar has authored 72 papers receiving a total of 3.2k indexed citations (citations by other indexed papers that have themselves been cited), including 39 papers in Molecular Biology, 28 papers in Endocrinology, Diabetes and Metabolism and 19 papers in Oncology. Recurrent topics in Ricardo M. Attar's work include Growth Hormone and Insulin-like Growth Factors (17 papers), Monoclonal and Polyclonal Antibodies Research (17 papers) and Hormonal and reproductive studies (11 papers). Ricardo M. Attar is often cited by papers focused on Growth Hormone and Insulin-like Growth Factors (17 papers), Monoclonal and Polyclonal Antibodies Research (17 papers) and Hormonal and reproductive studies (11 papers). Ricardo M. Attar collaborates with scholars based in United States, Germany and Belgium. Ricardo M. Attar's co-authors include Marco M. Gottardis, Joan M. Carboni, Chris H. Takimoto, Mark Salvati, Roberto Weinmann, Michael Gilman, Stanley R. Krystek, John S. Sack, Chihuei Wang and Kevin Kish and has published in prestigious journals such as Proceedings of the National Academy of Sciences, Nucleic Acids Research and Journal of Biological Chemistry.

In The Last Decade

Ricardo M. Attar

72 papers receiving 3.1k citations

Peers — A (Enhanced Table)

Peers by citation overlap · career bar shows stage (early→late) cites · hero ref

Name	h						Papers	Cites
Ricardo M. Attar United States	30	1.7k	877	864	827	652	72	3.2k
Junichi Kurebayashi Japan	37	1.8k 1.0×	1.9k 2.2×	497 0.6×	425 0.5×	999 1.5×	157	3.8k
Vivek Arora United States	21	2.0k 1.1×	931 1.1×	803 0.9×	3.3k 4.0×	1.3k 2.0×	38	4.8k
Jeffrey H. Hager United States	17	1.2k 0.7×	647 0.7×	230 0.3×	631 0.8×	705 1.1×	29	2.4k
Robert A. Sikes United States	31	1.6k 0.9×	956 1.1×	299 0.3×	1.3k 1.5×	608 0.9×	71	3.3k
Michael C. Haffner United States	34	2.8k 1.6×	1.2k 1.4×	310 0.4×	2.5k 3.0×	1.5k 2.4×	120	5.3k
Barry R. Davies United Kingdom	33	2.1k 1.2×	1.0k 1.1×	217 0.3×	735 0.9×	584 0.9×	99	3.4k
Susan S. Leong United States	16	1.4k 0.8×	627 0.7×	392 0.5×	1.1k 1.3×	395 0.6×	26	2.9k
David O. Azorsa United States	27	2.6k 1.5×	769 0.9×	226 0.3×	523 0.6×	584 0.9×	58	4.0k
Joan M. Carboni United States	34	2.4k 1.4×	1.4k 1.6×	1.0k 1.2×	361 0.4×	804 1.2×	75	4.0k
Jacek Pinski United States	31	1.1k 0.6×	727 0.8×	247 0.3×	1.1k 1.4×	415 0.6×	114	2.9k

Countries citing papers authored by Ricardo M. Attar

Since Specialization

Citations

This map shows the geographic impact of Ricardo M. Attar'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 Ricardo M. Attar with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Ricardo M. Attar more than expected).

Fields of papers citing papers by Ricardo M. Attar

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Ricardo M. Attar. 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 Ricardo M. Attar. The network helps show where Ricardo M. Attar may publish in the future.

Co-authorship network of co-authors of Ricardo M. Attar

This figure shows the co-authorship network connecting the top 25 collaborators of Ricardo M. Attar. A scholar is included among the top collaborators of Ricardo M. Attar 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 Ricardo M. Attar. Ricardo M. Attar is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

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20 of 20 papers shown

Yang, Danlin, Jianhong Yao, Melissa Smith, et al.. (2023). Characterization of JNJ-79635322, a Novel BCMAxGPRC5DxCD3 T-Cell Redirecting Trispecific Antibody, for the Treatment of Multiple Myeloma. Blood. 142(Supplement 1). 456–456. 19 indexed citations

Rudnick, Stephen I., Leopoldo Luistro, Melissa Smith, et al.. (2020). Blockade of VLA4 sensitizes leukemic and myeloma tumor cells to CD3 redirection in the bone marrow microenvironment. Blood Cancer Journal. 10(6). 65–65. 23 indexed citations

Moores, Sheri L., Mark L. Chiu, Barbara S. Bushey, et al.. (2016). A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors. Cancer Research. 76(13). 3942–3953. 188 indexed citations

Pillarisetti, Kodandaram, Eric T. Baldwin, Alexander Babich, et al.. (2016). Development of a New BCMAxCD3 Duobody® Antibody for Multiple Myeloma. Blood. 128(22). 2116–2116. 8 indexed citations

Dinchuk, Joseph, Carolyn Cao, Fei Huang, et al.. (2010). Insulin Receptor (IR) Pathway Hyperactivity in IGF-IR Null Cells and Suppression of Downstream Growth Signaling Using the Dual IGF-IR/IR Inhibitor, BMS-754807. Endocrinology. 151(9). 4123–4132. 32 indexed citations

Attar, Ricardo M., Maria Jure–Kunkel, Aaron Balog, et al.. (2009). Discovery of BMS-641988, a Novel and Potent Inhibitor of Androgen Receptor Signaling for the Treatment of Prostate Cancer. Cancer Research. 69(16). 6522–6530. 38 indexed citations

Carboni, Joan M., Mark D. Wittman, Zheng Yang, et al.. (2009). BMS-754807, a small molecule inhibitor of insulin-like growth factor-1R/IR. Molecular Cancer Therapeutics. 8(12). 3341–3349. 218 indexed citations

Hendrickson, Andrea E. Wahner, Paul Haluska, Paula A. Schneider, et al.. (2009). Expression of Insulin Receptor Isoform A and Insulin-like Growth Factor-1 Receptor in Human Acute Myelogenous Leukemia: Effect of the Dual-Receptor Inhibitor BMS-536924 In vitro. Cancer Research. 69(19). 7635–7643. 43 indexed citations

Haluska, Paul, Joan M. Carboni, Cynthia J. TenEyck, et al.. (2008). HER receptor signaling confers resistance to the insulin-like growth factor-I receptor inhibitor, BMS-536924. Molecular Cancer Therapeutics. 7(9). 2589–2598. 85 indexed citations

10.

Huang, Fei, Ann Greer, Warren Hurlburt, et al.. (2008). The Mechanisms of Differential Sensitivity to an Insulin-like Growth Factor-1 Receptor Inhibitor (BMS-536924) and Rationale for Combining with EGFR/HER2 Inhibitors. Cancer Research. 69(1). 161–170. 137 indexed citations

11.

Ross‐Macdonald, Petra, Heshani de Silva, Qi Guo, et al.. (2008). Identification of a nonkinase target mediating cytotoxicity of novel kinase inhibitors. Molecular Cancer Therapeutics. 7(11). 3490–3498. 102 indexed citations

12.

Litzenburger, Beate C., Isere Kuiatse, Joan M. Carboni, et al.. (2008). BMS-536924 Reverses IGF-IR-Induced Transformation of Mammary Epithelial Cells and Causes Growth Inhibition and Polarization of MCF7 Cells. Clinical Cancer Research. 15(1). 226–237. 33 indexed citations

13.

Zimmermann, Kurt, Mark D. Wittman, Mark G. Saulnier, et al.. (2008). Balancing oral exposure with Cyp3A4 inhibition in benzimidazole-based IGF-IR inhibitors. Bioorganic & Medicinal Chemistry Letters. 18(14). 4075–4080. 17 indexed citations

14.

Saulnier, Mark G., David B. Frennesson, Mark D. Wittman, et al.. (2008). 2-(1H-Imidazol-4-yl)ethanamine and 2-(1H-pyrazol-1-yl)ethanamine side chain variants of the IGF-1R inhibitor BMS-536924. Bioorganic & Medicinal Chemistry Letters. 18(5). 1702–1707. 20 indexed citations

15.

Kim, Hyun Jung, Beate C. Litzenburger, Xiaojiang Cui, et al.. (2007). Constitutively Active Type I Insulin-Like Growth Factor Receptor Causes Transformation and Xenograft Growth of Immortalized Mammary Epithelial Cells and Is Accompanied by an Epithelial-to-Mesenchymal Transition Mediated by NF-κB and Snail. Molecular and Cellular Biology. 27(8). 3165–3175. 196 indexed citations

16.

Huang, Fei, Warren Hurlburt, J. Chen, et al.. (2007). Identification of sensitivity markers for BMS-536924, an inhibitor for insulin-like growth factor-1 receptor. Journal of Clinical Oncology. 25(18_suppl). 3506–3506. 4 indexed citations

17.

Wittman, Mark D., Balu Balasubramanian, Upender Velaparthi, et al.. (2006). Novel 1H-(benzimidazol-2-yl)-1H-pyridin-2-one inhibitors of insulin-like growth factor I (IGF-1R) kinase. Bioorganic & Medicinal Chemistry Letters. 17(4). 974–977. 19 indexed citations

18.

Haluska, Paul, Joan M. Carboni, David A. Loegering, et al.. (2005). BMS-554417, an inhibitor of the insulin-like growth factor I receptor and insulin receptor, inhibits proliferation and induces mitochondrial pathway-mediated apoptosis in cancer cell lines. Cancer Research. 65. 1191–1191. 2 indexed citations

19.

Spires, Thomas, Brian E. Fink, Ellen K. Kick, et al.. (2005). Identification of novel functional inhibitors of 17β-hydroxysteroid dehydrogenase type III (17β-HSD3). The Prostate. 65(2). 159–170. 22 indexed citations

20.

Attar, Ricardo M., Heather Macdonald-Bravo, Carmen Raventós-Suárez, Stephen K. Durham, & Rodrigo Bravo. (1998). Expression of Constitutively Active IκBβ in T Cells of Transgenic Mice: Persistent NF-κB Activity Is Required for T-Cell Immune Responses. Molecular and Cellular Biology. 18(1). 477–487. 48 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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