What is she best known for?
The fields of study she is best known for:
The scientist’s investigation covers issues in Genetics, Neurofibromatosis, Mutation, Neurofibromin 1 and Pathology.
Her study in Genetics concentrates on Germline mutation, Exon, Genotype, Missense mutation and Gene.
Her Neurofibromatosis research incorporates elements of Cancer research, Neurooncology, Germline, Molecular genetics and Human genetics.
Her Mutation study combines topics in areas such as Mitosis, Microsatellite instability, Neurofibroma and Somatic cell.
Meena Upadhyaya has included themes like Etiology, Medical diagnosis and Intensive care medicine in her Neurofibromin 1 study.
Her research integrates issues of Myeloid and Gene expression profiling in her study of Pathology.
Her most cited work include:
- Guidelines for the diagnosis and management of individuals with neurofibromatosis 1 (613 citations)
- Blind analysis of denaturing high-performance liquid chromatography as a tool for mutation detection (331 citations)
- Genetic linkage of von Recklinghausen neurofibromatosis to the nerve growth factor receptor gene (314 citations)
What are the main themes of her work throughout her whole career to date?
Meena Upadhyaya mostly deals with Genetics, Neurofibromatosis, Gene, Mutation and Pathology.
Her research links Molecular biology with Genetics.
Neurofibromin 1 is the focus of her Neurofibromatosis research.
Her Neurofibromin 1 research is multidisciplinary, incorporating elements of Tumor suppressor gene and Gene product.
Her biological study spans a wide range of topics, including Genotype, Germline and Somatic cell.
Her Germline mutation study integrates concerns from other disciplines, such as Gene mutation, Neurofibroma and Loss of heterozygosity.
She most often published in these fields:
- Genetics (62.62%)
- Neurofibromatosis (42.72%)
- Gene (21.36%)
What were the highlights of her more recent work (between 2010-2019)?
- Neurofibromatosis (42.72%)
- Genetics (62.62%)
- Cancer research (10.68%)
In recent papers she was focusing on the following fields of study:
Meena Upadhyaya focuses on Neurofibromatosis, Genetics, Cancer research, Missense mutation and Carcinogenesis.
Her study on Neurofibromatosis is covered under Pathology.
Her study in Mutation, Neurofibromin 1, Gene, Breakpoint and Gene mutation falls within the category of Genetics.
While the research belongs to areas of Gene, Meena Upadhyaya spends her time largely on the problem of Molecular biology, intersecting her research to questions surrounding Nonsynonymous substitution.
Meena Upadhyaya has researched Cancer research in several fields, including Bromodomain and Nerve sheath neoplasm.
Her Missense mutation study incorporates themes from Noonan syndrome, Proband, Neurofibromatosis type I and Spinal neurofibromas.
Between 2010 and 2019, her most popular works were:
- PRC2 loss amplifies Ras-driven transcription and confers sensitivity to BRD4-based therapies (272 citations)
- The NF1 somatic mutational landscape in sporadic human cancers (97 citations)
- Inter-individual differences in CpG methylation at D4Z4 correlate with clinical variability in FSHD1 and FSHD2 (97 citations)
In her most recent research, the most cited papers focused on:
Meena Upadhyaya mainly focuses on Neurofibromatosis, Genetics, Cancer research, Bioinformatics and Missense mutation.
As a member of one scientific family, she mostly works in the field of Neurofibromatosis, focusing on Legius syndrome and, on occasion, Noonan syndrome and RASopathy.
By researching both Genetics and Non-allelic homologous recombination, Meena Upadhyaya produces research that crosses academic boundaries.
Her Cancer research research integrates issues from Carcinogenesis, Neurofibromin 1 and Loss of heterozygosity.
Her work focuses on many connections between Bioinformatics and other disciplines, such as Epigenetics, that overlap with her field of interest in Transcription factor, Chromatin and Nerve sheath neoplasm.
The study incorporates disciplines such as Proband and Spinal neurofibromas in addition to Missense mutation.
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