David B. Solit

84.6k citations
365 papers · 26.2k · 13 hit papers · h-index 82

Impact in

  • Oncology top 0.05%
    • Colorectal Cancer Treatments and Studies
    • Cancer Immunotherapy and Biomarkers
    • Cancer Genomics and Diagnostics

Papers in

    • Colorectal Cancer Treatments and Studies 47
    • HER2/EGFR in Cancer Research 30
    • Melanoma and MAPK Pathways 45
    • Heat shock proteins research 30

David B. Solit

344 papers receiving 25.8k citations

David B. Solit's Hit Papers

BRAF — a tumour-agnostic drug target with lineage-specific dependencies 2024 · 57 citations
570+8+16Years since publication50010001.5k2.0k

Peers

David B. Solit
Comparison fields: 5 of 163
  • Oncology 10.6k
  • Cancer Research 4.8k
  • Molecular Biology 15.6k
  • Pathology and Forensic Medicine 3.5k
  • Pulmonary and Respiratory Medicine 5.6k
Replace Neal Rosen with:
Neal Rosen United States
William R. Sellers United States
P. Andrew Futreal United States
Grant A. McArthur Australia
Jeffrey A. Sosman United States
Geoffrey I. Shapiro United States
Levi A. Garraway United States
Carlos L. Arteaga United States
Patricia LoRusso United States
Keith T. Flaherty United States
David B. Solit relative to Neal Rosen United States Neal Rosen's profile →
Citations per field
00.5×1.5×
Neal Rosen · 1×
Citations per year

Countries citing papers authored by David B. Solit

Since Specialization
Citations

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

Fields of papers citing papers by David B. Solit

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by David B. Solit. 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 David B. Solit. The network helps show where David B. Solit may publish in the future.

Co-authors

The 25 scholars most cited alongside David B. Solit, linked wherever they have co-authored with each other. Click a name or a connecting line to browse the papers they share.

Border = papers with David B. Solit Line = papers co-authored together David B. Solit links everyone, so they are left out of the graph.

All Works

20 of 20 papers shown

Showing the 20 most-cited of 365 papers — load more, or switch the sort, to bring in the rest.

#Work
1
mTOR Inhibition Induces Upstream Receptor Tyrosine Kinase Signaling and Activates Akt
Hit paper breakdown →
20062037
2
Tumour micro-environment elicits innate resistance to RAF inhibitors through HGF secretion
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20121378
3
BRAF mutation predicts sensitivity to MEK inhibition
Hit paper breakdown →
20051013
4
Patient HLA class I genotype influences cancer response to checkpoint blockade immunotherapy
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2017738
5
Akt Forms an Intracellular Complex with Heat Shock Protein 90 (Hsp90) and Cdc37 and Is Destabilized by Inhibitors of Hsp90 Function
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2002524
6
Therapy-Related Clonal Hematopoiesis in Patients with Non-hematologic Cancers Is Common and Associated with Adverse Clinical Outcomes
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2017521
7
Identifying recurrent mutations in cancer reveals widespread lineage diversity and mutational specificity
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2015492
8
Genome Sequencing Identifies a Basis for Everolimus Sensitivity
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2012480
9 2009455
10 2009420
11
Tumor adaptation and resistance to RAF inhibitors
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2013417
12
Alterations in DNA Damage Response and Repair Genes as Potential Marker of Clinical Benefit From PD-1/PD-L1 Blockade in Advanced Urothelial Cancers
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2018374
13
Comprehensive Molecular Profiling of Intrahepatic and Extrahepatic Cholangiocarcinomas: Potential Targets for Intervention
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2018369
14 2015358
15
17-Allylamino-17-demethoxygeldanamycin induces the degradation of androgen receptor and HER-2/neu and inhibits the growth of prostate cancer xenografts.
2002354
16 2005352
17 2017349
18 2010349
19
Genome doubling shapes the evolution and prognosis of advanced cancers
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2018343
20 2011328

About David B. Solit

David B. Solit is a scholar working on Oncology, Molecular Biology, Pulmonary and Respiratory Medicine, Surgery and Cancer Research, having authored 365 papers that have together received 26.2k indexed citations. Recurring topics across this work include Cancer Genomics and Diagnostics (84 papers), Bladder and Urothelial Cancer Treatments (79 papers), Colorectal Cancer Treatments and Studies (47 papers), Lung Cancer Treatments and Mutations (47 papers), Melanoma and MAPK Pathways (45 papers), Genetic factors in colorectal cancer (39 papers), HER2/EGFR in Cancer Research (30 papers) and Heat shock proteins research (30 papers). The work is most often cited by research in Oncology (10.6k citations), Cancer Research (4.8k citations), Molecular Biology (15.6k citations), Pathology and Forensic Medicine (3.5k citations) and Pulmonary and Respiratory Medicine (5.6k citations). David B. Solit has collaborated with scholars based in United States, Spain and Canada. Frequent co-authors include Neal Rosen, Michael F. Berger, Andrea Basso, Qing‐Bai She, Christine A. Pratilas, Gabriela Chiosis, Barry S. Taylor, José Baselga, Qing Ye and Marc Ladanyi. Their work appears in journals such as Journal of Clinical Oncology, Cancer Research, Clinical Cancer Research, The Journal of Urology and Cancer.

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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