What is he best known for?
The fields of study he is best known for:
His primary areas of study are Cancer research, RNA interference, Small hairpin RNA, Cell biology and Carcinogenesis.
His studies in Cancer research integrate themes in fields like DNA damage, Tumor suppressor gene, Regulation of gene expression, Drug resistance and Adenocarcinoma.
His research in Regulation of gene expression intersects with topics in Gene silencing and microRNA.
The study incorporates disciplines such as Haematopoiesis and Lymphoma in addition to microRNA.
His study in Small hairpin RNA is interdisciplinary in nature, drawing from both Cancer cell, Pharmacology and In vivo.
The concepts of his Cell biology study are interwoven with issues in Phenotype, Cell cycle checkpoint and Transcription factor.
His most cited work include:
- A microRNA polycistron as a potential human oncogene (3197 citations)
- Disrupting the Pairing Between let-7 and Hmga2 Enhances Oncogenic Transformation (987 citations)
- The Shortest Telomere, Not Average Telomere Length, Is Critical for Cell Viability and Chromosome Stability (931 citations)
What are the main themes of his work throughout his whole career to date?
Cancer research, Cancer, Cell biology, Cancer cell and RNA interference are his primary areas of study.
His Cancer research study incorporates themes from Leukemia, Immunology, Chemotherapy and DNA damage.
He combines subjects such as Homologous recombination, Pharmacology, Bioinformatics and DNA repair with his study of Cancer.
His biological study spans a wide range of topics, including Carcinogenesis, Cell cycle checkpoint, Cell and Programmed cell death.
Michael T. Hemann studied Cancer cell and Apoptosis that intersect with Cell culture.
His RNA interference research is multidisciplinary, relying on both Molecular biology, Small hairpin RNA, In vivo and Suppressor.
He most often published in these fields:
- Cancer research (44.39%)
- Cancer (24.60%)
- Cell biology (20.86%)
What were the highlights of his more recent work (between 2017-2021)?
- Cancer research (44.39%)
- Cancer (24.60%)
- Chemotherapy (6.95%)
In recent papers he was focusing on the following fields of study:
His main research concerns Cancer research, Cancer, Chemotherapy, RNA interference and Cell biology.
His studies deal with areas such as Cell culture, DNA damage, Cisplatin, Cancer cell and Senescence as well as Cancer research.
The Cancer study combines topics in areas such as Cytotoxic T cell, Antibiotics and Cell growth.
His RNA interference study integrates concerns from other disciplines, such as Functional genomics, In vivo and Phenotypic screening.
He has included themes like Endogeny and Creatine kinase in his Cell biology study.
His Regulation of gene expression research is multidisciplinary, incorporating perspectives in Transcription and Computational biology.
Between 2017 and 2021, his most popular works were:
- A Small Molecule Targeting Mutagenic Translesion Synthesis Improves Chemotherapy (45 citations)
- Exploiting an Asp-Glu "switch" in glycogen synthase kinase 3 to design paralog-selective inhibitors for use in acute myeloid leukemia. (38 citations)
- The primary mechanism of cytotoxicity of the chemotherapeutic agent CX-5461 is topoisomerase II poisoning (27 citations)
In his most recent research, the most cited papers focused on:
The scientist’s investigation covers issues in Cancer research, Cell biology, Wnt signaling pathway, Chemotherapy and Cell culture.
His work on Stromal cell is typically connected to Stroma as part of general Cancer research study, connecting several disciplines of science.
His Cell biology research integrates issues from Carcinogenesis, Endogeny and Creatine kinase.
Michael T. Hemann has researched Wnt signaling pathway in several fields, including Haematopoiesis, Myeloid, GSK-3, Myeloid leukemia and Leukemia.
His work on Cisplatin as part of general Chemotherapy research is frequently linked to Aiding and abetting, bridging the gap between disciplines.
His Cell culture research incorporates themes from PI3K/AKT/mTOR pathway, MAPK/ERK pathway and Effector.
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