D-Index & Metrics Best Publications

D-Index & Metrics D-index (Discipline H-index) only includes papers and citation values for an examined discipline in contrast to General H-index which accounts for publications across all disciplines.

Discipline name D-index D-index (Discipline H-index) only includes papers and citation values for an examined discipline in contrast to General H-index which accounts for publications across all disciplines. Citations Publications World Ranking National Ranking
Biology and Biochemistry D-index 54 Citations 15,176 107 World Ranking 7942 National Ranking 628

Overview

What is he best known for?

The fields of study he is best known for:

  • Gene
  • Enzyme
  • Cancer

John A. Hickman focuses on Apoptosis, Programmed cell death, Cell biology, Cancer research and Cell. John A. Hickman interconnects Molecular biology, Small intestine and Stem cell in the investigation of issues within Apoptosis. His studies in Programmed cell death integrate themes in fields like Cytotoxic T cell, DNA damage and Drug resistance.

His work in Cell biology tackles topics such as Autophagy which are related to areas like Gene knockdown and Protein structure. John A. Hickman has researched Cancer research in several fields, including Gene expression profiling, Radioresistance, Cytotoxicity, Tumor suppressor gene and Clonogenic assay. His work deals with themes such as Mammary gland involution, Immunology, Drug and Basement membrane, which intersect with Cell.

His most cited work include:

  • Apoptotic death in epithelial cells: cleavage of DNA to 300 and/or 50 kb fragments prior to or in the absence of internucleosomal fragmentation. (1041 citations)
  • Functional and physical interaction between Bcl‐XL and a BH3‐like domain in Beclin‐1 (888 citations)
  • Apoptosis induced by anticancer drugs. (750 citations)

What are the main themes of his work throughout his whole career to date?

His primary areas of study are Apoptosis, Cell biology, Programmed cell death, Molecular biology and Stereochemistry. His Apoptosis research is multidisciplinary, relying on both Cell, Cancer research, Cell culture, Small intestine and Immunology. His work in Cell biology covers topics such as Bcl-2-associated X protein which are related to areas like Etoposide.

His Programmed cell death study combines topics in areas such as DNA damage, Mechanism of action, Toxicity, Cytotoxic T cell and Clonogenic assay. His study explores the link between Molecular biology and topics such as In vivo that cross with problems in Pharmacology. His research integrates issues of Biochemistry, Aryl, Alkoxy group, Alkyl and Chemical synthesis in his study of Stereochemistry.

He most often published in these fields:

  • Apoptosis (32.13%)
  • Cell biology (23.08%)
  • Programmed cell death (18.55%)

What were the highlights of his more recent work (between 2007-2021)?

  • Alkyl (12.22%)
  • Group (8.14%)
  • Medicinal chemistry (9.50%)

In recent papers he was focusing on the following fields of study:

John A. Hickman mainly focuses on Alkyl, Group, Medicinal chemistry, Stereochemistry and Aryl. His Medicinal chemistry research incorporates themes from Nitrogen atom and Hydrogen. His Stereochemistry research incorporates elements of Imide and Chemical synthesis.

His Aryl research includes themes of Ring, Alkoxy group and Tricyclic. The concepts of his Toxicity study are interwoven with issues in Cell culture, Apoptosis and In vivo. In his work, John A. Hickman performs multidisciplinary research in Apoptosis and RNA interference.

Between 2007 and 2021, his most popular works were:

  • The MCL1 inhibitor S63845 is tolerable and effective in diverse cancer models (499 citations)
  • Limits to Personalized Cancer Medicine (218 citations)
  • Three-dimensional models of cancer for pharmacology and cancer cell biology: capturing tumor complexity in vitro/ex vivo (190 citations)

In his most recent research, the most cited papers focused on:

  • Gene
  • Enzyme
  • Cancer

The scientist’s investigation covers issues in Cell biology, Pharmacology, Cancer cell, Cancer and Bcl-xL. His work blends Cell biology and Biphenyl compound studies together. His Biphenyl compound study spans across into areas like Programmed cell death, Plasma protein binding, BCL-2 Gene Family, Apoptosis and Puma.

His Pharmacology study combines topics in areas such as Bevacizumab, Myeloid Cell Leukemia Sequence 1 Protein and Receptor tyrosine kinase. His Cancer cell research is multidisciplinary, incorporating elements of Bcl-2 Homologous Antagonist-Killer Protein, Tumor progression, Leukemia, MCL1 and Drug discovery. His studies in Cancer integrate themes in fields like Ex vivo, Stromal cell, Stem cell and Kinase.

This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.

Best Publications

Apoptotic death in epithelial cells: cleavage of DNA to 300 and/or 50 kb fragments prior to or in the absence of internucleosomal fragmentation.

F. Oberhammer;J.W. Wilson;C. Dive;I.D. Morris.
The EMBO Journal (1993)

1408 Citations

Functional and physical interaction between Bcl‐XL and a BH3‐like domain in Beclin‐1

M Chiara Maiuri;Gaëtane Le Toumelin;Alfredo Criollo;Alfredo Criollo;Alfredo Criollo;Jean-Christophe Rain.
The EMBO Journal (2007)

1228 Citations

Apoptosis induced by anticancer drugs.

John A. Hickman.
Cancer and Metastasis Reviews (1992)

1191 Citations

The role of p53 in spontaneous and radiation-induced apoptosis in the gastrointestinal tract of normal and p53-deficient mice.

Anita J. Merritt;Christopher S. Potten;Christopher J. Kemp;John A. Hickman.
Cancer Research (1994)

758 Citations

The MCL1 inhibitor S63845 is tolerable and effective in diverse cancer models

András Kotschy;Zoltán Szlavik;James Murray;James Davidson.
Nature (2016)

623 Citations

Cell Damage-induced Conformational Changes of the Pro-Apoptotic Protein Bak In Vivo Precede the Onset of Apoptosis

Gareth J. Griffiths;Laurence Dubrez;Clive P. Morgan;Neil A. Jones.
Journal of Cell Biology (1999)

599 Citations

Drug-target interactions: only the first step in the commitment to a programmed cell death?

C. Dive;J. A. Hickman.
British Journal of Cancer (1991)

560 Citations

BH3-only proteins and BH3 mimetics induce autophagy by competitively disrupting the interaction between Beclin 1 and Bcl-2/Bcl-X(L).

Maria Chiara Maiuri;Alfredo Criollo;Ezgi Tasdemir;Jose Miguel Vicencio.
Autophagy (2007)

479 Citations

Antitumor Activity and Pharmacokinetics in Mice of 8-Carbamoyl-3-methyl-imidazo[5,1-d]-1,2,3,5-tetrazin-4(3H)-one (CCRG 81045; M & B 39831), a Novel Drug with Potential as an Alternative to Dacarbazine

Malcolm F. G. Stevens;John A. Hickman;Simon P. Langdon;David Chubb.
Cancer Research (1987)

409 Citations

Differential expression of bcl-2 in intestinal epithelia. Correlation with attenuation of apoptosis in colonic crypts and the incidence of colonic neoplasia.

Anita J Merritt;Christopher S Potten;A J Watson;D Y Loh.
Journal of Cell Science (1995)

385 Citations

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