Manasa Ramakrishna
A5028292065- Cancer Genomics and Diagnostics
- Genetic factors in colorectal cancer
- Genomics and Chromatin Dynamics
- RNA modifications and cancer
- RNA and protein synthesis mechanisms
- Epigenetics and DNA Methylation
- RNA Research and Splicing
- DNA Repair Mechanisms
- Genomic variations and chromosomal abnormalities
- Genomics and Phylogenetic Studies
- Chromosomal and Genetic Variations
- Cancer-related molecular mechanisms research
- Mitochondrial Function and Pathology
- Ovarian cancer diagnosis and treatment
- Nutrition, Genetics, and Disease
- Biotin and Related Studies
- Evolution and Genetic Dynamics
- Genetics, Bioinformatics, and Biomedical Research
- Genomics and Rare Diseases
- Lung Cancer Treatments and Mutations
- CRISPR and Genetic Engineering
- Cancer-related gene regulation
- Bioinformatics and Genomic Networks
- BRCA gene mutations in cancer
- Cellular transport and secretion
Queen's University Belfast
2025
Manipal Academy of Higher Education
2024
Visvesvaraya Technological University
2024
Wellcome Sanger Institute
2013-2023
Adikavi Nannaya University
2022
MRC Toxicology Unit
2018-2020
University of Cambridge
2018-2020
Medical Research Council
2018-2020
MNJ Institute Of Oncology and Regional Cancer Centre
2015-2020
Prostate Cancer Research
2016
Introduction The human genome is peppered with mobile repetitive elements called long interspersed nuclear element–1 (L1) retrotransposons. Propagating through RNA and cDNA intermediates, these molecular parasites copy insert themselves throughout the genome, potentially disruptive effects on neighboring genes or regulatory sequences. In germ line, unique sequence downstream of L1 can also be retrotransposed if transcription continues beyond repeat, a process known as 3′ transduction. There...
Abstract Somatic mutations in human cancers show unevenness genomic distribution that correlate with aspects of genome structure and function. These are, however, generated by multiple mutational processes operating through the cellular lineage between fertilized egg cancer cell, each composed specific DNA damage repair components leaving its own characteristic signature on genome. Using somatic mutation catalogues from 560 breast whole-genome sequences, here we 12 base substitution, 2...
Abstract Ionizing radiation is a potent carcinogen, inducing cancer through DNA damage. The signatures of mutations arising in human tissues following vivo exposure to ionizing have not been documented. Here, we searched for 12 radiation-associated second malignancies different tumour types. Two somatic mutation characterize irrespective type. Compared with 319 radiation-naive tumours, tumours carry median extra 201 deletions genome-wide, sized 1–100 base pairs often microhomology at the...
Ovarian cancer is a disease characterised by complex genomic rearrangements but the majority of genes that are target these alterations remain unidentified. Cataloguing will provide useful insights into etiology and may an opportunity to develop novel diagnostic therapeutic interventions. High resolution genome wide copy number matching expression data from 68 primary epithelial ovarian carcinomas various histotypes was integrated identify in regions most frequent amplification with...
Ovarian cancer is a heterogeneous disease displaying complex genomic alterations, and consequently, it has been difficult to determine the most relevant copy number alterations with scale of studies date. We obtained genome-wide alteration (CNA) data from four different SNP array platforms, final set 398 ovarian tumours, mostly serous histological subtype. Frequent CNA aberrations targeted many thousands genes. However, high-level amplicons homozygous deletions enabled filtering this list...
Mitochondrial genomes are separated from the nuclear genome for most of cell cycle by double membrane, intervening cytoplasm, and mitochondrial membrane. Despite these physical barriers, we show that somatically acquired mitochondrial-nuclear fusion sequences present in cancer cells. Most occur conjunction with intranuclear genomic rearrangements, features fragments indicate nonhomologous end joining and/or replication-dependent DNA double-strand break repair dominant mechanisms involved....
Abstract Global loss of DNA methylation and CpG island (CGI) hypermethylation are key epigenomic aberrations in cancer. manifests itself partially methylated domains (PMDs) which extend up to megabases. However, the distribution PMDs within between tumor types, their effects on functional genomic elements including CGIs poorly defined. We comprehensively show that occurs a large fraction genome represents prime source variation. hypervariable level, size distribution, display elevated...
Chromodomain, helicase, DNA binding 5 (CHD5) is a member of subclass the chromatin remodeling Swi/Snf proteins and has recently been proposed as tumor suppressor in diverse range human cancers. We analyzed all 41 coding exons CHD5 for somatic mutations 123 primary ovarian cancers well 60 breast using high-resolution melt analysis. also examined methylation promoter 48 cancer samples by methylation-specific single-stranded conformation polymorphism bisulfite sequencing. In contrast to...
Abstract Ovarian cancer is characterized by complex genetic alterations, including copy number loss and number‐neutral of heterozygosity (LOH). These alterations are assumed to represent the “second hit” underlying tumor suppressor gene (TSG), however, relative LOH hotspots reported, few ovarian TSGs have been identified. We conducted a high‐resolution analysis using SNP arrays (500K SNP6.0) 106 primary tumors various histological subtypes together with matching normal DNA. was detected in...