Robert A. Finch

1.4k total citations
36 papers, 1.1k citations indexed

About

Robert A. Finch is a scholar working on Molecular Biology, Health, Toxicology and Mutagenesis and Surgery. According to data from OpenAlex, Robert A. Finch has authored 36 papers receiving a total of 1.1k indexed citations (citations by other indexed papers that have themselves been cited), including 10 papers in Molecular Biology, 10 papers in Health, Toxicology and Mutagenesis and 6 papers in Surgery. Recurrent topics in Robert A. Finch's work include Effects and risks of endocrine disrupting chemicals (9 papers), Animal testing and alternatives (4 papers) and Pluripotent Stem Cells Research (3 papers). Robert A. Finch is often cited by papers focused on Effects and risks of endocrine disrupting chemicals (9 papers), Animal testing and alternatives (4 papers) and Pluripotent Stem Cells Research (3 papers). Robert A. Finch collaborates with scholars based in United States, Canada and Germany. Robert A. Finch's co-authors include John A. Bantle, James N. Dumont, David C. Whitcomb, M. Michael Barmada, Andrew P. J. Brunskill, Roland H. Pfützer, John P. Neoptolemos, William Furey, P. Suzanne Hart and Douglas J. Fort and has published in prestigious journals such as Nature, Gastroenterology and Environmental Health Perspectives.

In The Last Decade

Robert A. Finch

36 papers receiving 1.0k citations

Peers

Robert A. Finch
Robert A. Finch
Citations per year, relative to Robert A. Finch Robert A. Finch (= 1×) peers Federica Battaglia

Countries citing papers authored by Robert A. Finch

Since Specialization
Citations

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

Fields of papers citing papers by Robert A. Finch

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Robert A. Finch. 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 Robert A. Finch. The network helps show where Robert A. Finch may publish in the future.

Co-authorship network of co-authors of Robert A. Finch

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

All Works

20 of 20 papers shown
1.
Tward, Jonathan D., Alexander Gutin, Chelsea R. Kasten, et al.. (2024). Using the Cell-Cycle Risk Score to Predict the Benefit of Androgen-Deprivation Therapy Added to Radiation Therapy in Patients With Newly Diagnosed Prostate Cancer. JCO Precision Oncology. 8(8). e2300722–e2300722. 2 indexed citations
2.
Iliev, Diana, Chelsea R. Kasten, Howard Korman, et al.. (2024). Active surveillance selection and 3-year durability in intermediate-risk prostate cancer following genomic testing. Prostate Cancer and Prostatic Diseases. 28(2). 427–434. 2 indexed citations
3.
Yusuf, Kamran, et al.. (2011). Ionized calcium levels in umbilical cord blood of women with preeclampsia and normotensive pregnancies. The Journal of Maternal-Fetal & Neonatal Medicine. 25(2). 203–205. 6 indexed citations
5.
Finch, Robert A., Harvey G. Moore, Noralane M. Lindor, et al.. (2005). Familial Adenomatous Polyposis and Mental Retardation Caused by a de novo Chromosomal Deletion at 5q15-q22: Report of a Case. Diseases of the Colon & Rectum. 48(11). 2148–2152. 16 indexed citations
6.
Orenstein, Susan R., et al.. (2002). Autosomal dominant infantile gastroesophageal reflux disease: exclusion of a 13q14 locus in five well characterized families. The American Journal of Gastroenterology. 97(11). 2725–2732. 14 indexed citations
7.
Rogers, Robert L., et al.. (2001). OPTIMIZATION OF AN EXOGENOUS METABOLIC ACTIVATION SYSTEM FOR FETAX. I. POST-ISOLATION RAT LIVER MICROSOME MIXTURES. Drug and Chemical Toxicology. 24(2). 103–115. 7 indexed citations
8.
Fort, Douglas J., Enos L. Stover, John A. Bantle, James N. Dumont, & Robert A. Finch. (2001). Evaluation of a reproductive toxicity assay using Xenopus laevis: boric acid, cadmium and ethylene glycol monomethyl ether. Journal of Applied Toxicology. 21(1). 41–52. 29 indexed citations
9.
Orenstein, Susan R., Theresa M. Shalaby, M. Michael Barmada, et al.. (2001). Autosomal dominant infant GERD: Exclusion of a 13q14 locus in 6 well-characterized families suggests genetic heterogeneity. Gastroenterology. 120(5). A211–A211. 5 indexed citations
10.
Fort, Douglas J., et al.. (2001). OPTIMIZATION OF AN EXOGENOUS METABOLIC ACTIVATION SYSTEM FOR FETAX. II. PRELIMINARY EVALUATION. Drug and Chemical Toxicology. 24(2). 117–127. 5 indexed citations
11.
Fort, Douglas J., Enos L. Stover, John A. Bantle, & Robert A. Finch. (2000). Evaluation of the developmental toxicity of thalidomide using frog embryo teratogenesis assay?Xenopus (FETAX): biotransformation and detoxification. Teratogenesis Carcinogenesis and Mutagenesis. 20(1). 35–47. 23 indexed citations
12.
Pfützer, Roland H., M. Michael Barmada, Andrew P. J. Brunskill, et al.. (2000). SPINK1/PSTI polymorphisms act as disease modifiers in familial and idiopathic chronic pancreatitis. Gastroenterology. 119(3). 615–623. 381 indexed citations
13.
Bantle, John A., et al.. (1999). Phase III interlaboratory study of FETAX part 3. FETAX validation using 12 compounds with and without an exogenous metabolic activation system. Journal of Applied Toxicology. 19(6). 447–472. 2 indexed citations
14.
Fort, Douglas J., Enos L. Stover, John A. Bantle, et al.. (1998). Phase III Interlaboratory Study of Fetax, Part 2: Interlaboratory Validation of an Exogenous Metabolic Activation System for Frog Embryo TeratogenesisAssay-Xenopus(Fetax). Drug and Chemical Toxicology. 21(1). 1–14. 28 indexed citations
15.
Bantle, John A., Robert A. Finch, Dennis T. Burton, et al.. (1996). FETAX Interlaboratory Validation Study: Phase III-Part 1 Testing. Journal of Applied Toxicology. 16(6). 517–528. 28 indexed citations
16.
Bantle, John A., James R. Rayburn, Dennis T. Burton, et al.. (1994). Initial interlaboratory validation study of FETAX: Phase I testing. Journal of Applied Toxicology. 14(3). 213–223. 32 indexed citations
17.
Rayburn, James R., John A. Bantle, Dennis T. Burton, et al.. (1994). Fetax interlaboratory validation study: Phase II testing. Environmental Toxicology and Chemistry. 13(10). 1629–1637. 41 indexed citations
18.
Finch, Robert A., et al.. (1992). Teratogenic assessment of four solvents using the frog embryo teratogenesis assay—xenopus (FETAX). Journal of Applied Toxicology. 12(1). 49–56. 41 indexed citations
19.
Finch, Robert A. & Mark S. Henry. (1985). An Interindustry Approach to Financing Small Port Development and Maintenance. Growth and Change. 16(2). 26–33. 1 indexed citations
20.
Finch, Robert A.. (1969). The influence of the nerve on lower jaw regeneration in the adult newt, Triturus viridescens,. Journal of Morphology. 129(4). 401–413. 8 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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