Francesco Hofmann

14.2k total citations · 1 hit paper
56 papers, 5.9k citations indexed

About

Francesco Hofmann is a scholar working on Molecular Biology, Oncology and Cancer Research. According to data from OpenAlex, Francesco Hofmann has authored 56 papers receiving a total of 5.9k indexed citations (citations by other indexed papers that have themselves been cited), including 37 papers in Molecular Biology, 22 papers in Oncology and 9 papers in Cancer Research. Recurrent topics in Francesco Hofmann's work include PI3K/AKT/mTOR signaling in cancer (12 papers), Cancer-related Molecular Pathways (11 papers) and Growth Hormone and Insulin-like Growth Factors (8 papers). Francesco Hofmann is often cited by papers focused on PI3K/AKT/mTOR signaling in cancer (12 papers), Cancer-related Molecular Pathways (11 papers) and Growth Hormone and Insulin-like Growth Factors (8 papers). Francesco Hofmann collaborates with scholars based in Switzerland, United States and United Kingdom. Francesco Hofmann's co-authors include Daniel J. Hicklin, Qing‐Bai She, José Baselga, Debra L. Smith, Heidi A. Lane, David B. Solit, Gordon B. Mills, Kathryn O’Reilly, Neal Rosen and Dale L. Ludwig and has published in prestigious journals such as Proceedings of the National Academy of Sciences, Blood and Molecular Cell.

In The Last Decade

Francesco Hofmann

54 papers receiving 5.7k citations

Hit Papers

align trajectories sort by overperformance

What are hit papers?

Hit papers significantly outperform the citation benchmark for their cohort. A paper qualifies if it has ≥500 total citations, achieves ≥1.5× the top-1% citation threshold for papers in the same subfield and year (this is the minimum needed to enter the top 1%, not the average within it), or reaches the top citation threshold in at least one of its specific research topics.

mTOR Inhibition Induces Upstream Receptor Tyrosine Kinase Signaling and Activates Akt

2006 2.0k citations Kathryn O’Reilly, Qing‐Bai She et al. Cancer Research profile →

Peers — A (Enhanced Table)

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

Name	h						Papers	Cites
Francesco Hofmann Switzerland	30	4.2k	1.4k	1.0k	900	882	56	5.9k
Dale L. Ludwig United States	36	4.4k 1.0×	1.6k 1.1×	993 1.0×	850 0.9×	854 1.0×	91	5.9k
Jonathan A. Pachter United States	32	2.4k 0.6×	1.7k 1.2×	664 0.6×	507 0.6×	583 0.7×	137	4.4k
Christine A. Pratilas United States	30	3.6k 0.9×	2.0k 1.4×	625 0.6×	933 1.0×	218 0.2×	95	5.0k
Pnina Brodt Canada	46	3.2k 0.8×	2.5k 1.8×	2.2k 2.1×	689 0.8×	1.3k 1.5×	115	6.8k
Bijoyesh Mookerjee United States	30	4.1k 1.0×	3.7k 2.5×	2.3k 2.2×	2.2k 2.5×	447 0.5×	85	7.4k
Paul D. Smith United Kingdom	45	5.1k 1.2×	2.4k 1.7×	1.4k 1.3×	1.4k 1.6×	124 0.1×	120	7.5k
Judith S. Sebolt–Leopold United States	33	4.9k 1.2×	2.7k 1.9×	790 0.8×	591 0.7×	156 0.2×	67	6.8k
Eliot M. Rosen United States	57	4.7k 1.1×	1.8k 1.2×	1.2k 1.2×	999 1.1×	166 0.2×	145	7.9k
Dennie T. Frederick United States	32	3.8k 0.9×	3.2k 2.2×	1.1k 1.0×	618 0.7×	184 0.2×	79	6.2k
Poulikos I. Poulikakos United States	27	4.7k 1.1×	2.2k 1.5×	719 0.7×	670 0.7×	154 0.2×	46	6.0k

Countries citing papers authored by Francesco Hofmann

Since Specialization

Citations

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

Fields of papers citing papers by Francesco Hofmann

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Francesco Hofmann. 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 Francesco Hofmann. The network helps show where Francesco Hofmann may publish in the future.

Co-authorship network of co-authors of Francesco Hofmann

This figure shows the co-authorship network connecting the top 25 collaborators of Francesco Hofmann. A scholar is included among the top collaborators of Francesco Hofmann 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 Francesco Hofmann. Francesco Hofmann 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

Baltschukat, Sabrina, Barbara Schacher Engstler, Alan Huang, et al.. (2019). Capmatinib (INC280) Is Active Against Models of Non–Small Cell Lung Cancer and Other Cancer Types with Defined Mechanisms of MET Activation. Clinical Cancer Research. 25(10). 3164–3175. 105 indexed citations

Weiss, Andreas, Diana Graus Porta, Christelle Stamm, et al.. (2017). Abstract 2103: NVP-FGF401: Cellular and in vivo profile of a novel highly potent and selective FGFR4 inhibitor for the treatment of FGF19/FGFR4/KLB+ tumors. Cancer Research. 77(13_Supplement). 2103–2103. 5 indexed citations

Ebel, Nicolas, Vincent Romanet, Rita Andraos, et al.. (2013). JAK1/2 and Pan-Deacetylase Inhibitor Combination Therapy Yields Improved Efficacy in Preclinical Mouse Models of JAK2V617F-Driven Disease. Clinical Cancer Research. 19(22). 6230–6241. 59 indexed citations

Wöhrle, Simon, Andreas Weiss, Moriko Ito, et al.. (2013). Fibroblast Growth Factor Receptors as Novel Therapeutic Targets in SNF5-Deleted Malignant Rhabdoid Tumors. PLoS ONE. 8(10). e77652–e77652. 39 indexed citations

Cortés-Cros, Marta, Tobias Schmelzle, Volker M. Stucke, & Francesco Hofmann. (2013). The Path to Oncology Drug Target Validation: An Industry Perspective. Methods in molecular biology. 986. 3–13. 4 indexed citations

Michaloglou, Chrysiis, Typhaine Martin, Clara Delaunay, et al.. (2013). The Tyrosine Phosphatase PTPN14 Is a Negative Regulator of YAP Activity. PLoS ONE. 8(4). e61916–e61916. 69 indexed citations

Zumsteg, Adrian, Laura Pisarsky, Karin Strittmatter, et al.. (2012). Repression of Malignant Tumor Progression upon Pharmacologic IGF1R Blockade in a Mouse Model of Insulinoma. Molecular Cancer Research. 10(6). 800–809. 6 indexed citations

Schnell, Christian, Stéphanie Barbé, Giorgio Caravatti, et al.. (2012). Abstract 3743: NVP-BYL719, a selective inhibitor of the class Ia PI3K isoform alpha impairs angiogenesis and microvascular permeability.. Cancer Research. 72(8_Supplement). 3743–3743.

Fritsch, Christine, Christian Schnell, Christian Chatenay‐Rivauday, et al.. (2012). Abstract 3748: NVP-BYL719, a novel PI3Kalpha selective inhibitor with all the characteristics required for clinical development as an anti-cancer agent. Cancer Research. 72(8_Supplement). 3748–3748. 15 indexed citations

10.

Tiedt, Ralph, Pascal Furet, B.A. Appleton, et al.. (2011). A Drug Resistance Screen Using a Selective MET Inhibitor Reveals a Spectrum of Mutations That Partially Overlap with Activating Mutations Found in Cancer Patients. Cancer Research. 71(15). 5255–5264. 99 indexed citations

11.

Bielen, Aleksandra, Lara Perryman, Gary Box, et al.. (2011). Enhanced Efficacy of IGF1R Inhibition in Pediatric Glioblastoma by Combinatorial Targeting of PDGFRα/β. Molecular Cancer Therapeutics. 10(8). 1407–1418. 41 indexed citations

12.

Hägerstrand, Daniel, Maja Bradic Lindh, Cristina Peña, et al.. (2010). PI3K/PTEN/Akt pathway status affects the sensitivity of high-grade glioma cell cultures to the insulin-like growth factor-1 receptor inhibitor NVP-AEW541. Neuro-Oncology. 12(9). 967–975. 30 indexed citations

13.

O’Reilly, Kathryn, Qing‐Bai She, David B. Solit, et al.. (2006). mTOR Inhibition Induces Upstream Receptor Tyrosine Kinase Signaling and Activates Akt. Cancer Research. 66(3). 1500–1508. 2037 indexed citations breakdown →

14.

Hofmann, Francesco & Carlos Garcı́a-Echeverrı́a. (2005). Blocking the insulin-like growth factor-I receptor as a strategy for targeting cancer. Drug Discovery Today. 10(15). 1041–1047. 118 indexed citations

15.

Ruetz, Stephan, François Natt, Jonathan Hall, et al.. (2004). The human ubiquitin-conjugating enzyme Cdc34 controls cellular proliferation through regulation of p27Kip1 protein levels. Experimental Cell Research. 303(2). 482–493. 22 indexed citations

16.

Ozaki, Hiroaki, Man‐Seong Seo, Keiko Ozaki, et al.. (2000). Blockade of Vascular Endothelial Cell Growth Factor Receptor Signaling Is Sufficient to Completely Prevent Retinal Neovascularization. American Journal Of Pathology. 156(2). 697–707. 302 indexed citations

17.

Rösel, Johannes, et al.. (1999). Mechanisms and kinetics of procathepsin D activation. European Journal of Biochemistry. 265(1). 384–393. 43 indexed citations

18.

Fabbro, Doriano, Elisabeth Buchdunger, Jürgen Mestan, et al.. (1999). Inhibitors of Protein KinasesCGP 41251, a Protein Kinase Inhibitor with Potential as an Anticancer Agent. Pharmacology & Therapeutics. 82(2-3). 293–301. 122 indexed citations

19.

Anagli, John, Francesco Hofmann, Manfredo Quadroni, Thomas Vorherr, & Ernesto Carafoli. (1995). The Calmodulin‐binding Domain of the Inducible (Macrophage) Nitric Oxide Synthase. European Journal of Biochemistry. 233(3). 701–708. 32 indexed citations

20.

Vorherr, Thomas, Lea Knoepfel, Francesco Hofmann, et al.. (1993). The calmodulin binding domain of nitric oxide synthase and adenylyl cyclase. Biochemistry. 32(23). 6081–6088. 139 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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