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  • 1
    Keywords: Oncology ; Human Genetics ; Medicine ; Biomedical Engineering ; Medical laboratories ; Cancer Research ; Human Genetics ; Molecular Medicine ; Biomedical Engineering/Biotechnology ; Laboratory Medicine ; Springer eBooks
    Description / Table of Contents: 1. Section 1. RNome: Evolution and nature -- Chapter. 1.1. RNA world hypothesis -- Chapter.1.2. Various classes of RNAs (coding as well non-coding), their biosynthesis and basic functions -- 2. Section 2. Cellular RNome: Chromatin dynamics -- Chapter. 2.1. Chromatin modifications & transcription -- Chapter. 2.2. RNA modifications and epitranscriptomics -- Chapter. 2.3. Cellular RNome: Contribution of non-coding RNA -- 3. Section 3. Cancer RNome: Evolution and Sustenance.(How is cancer RNome different from RNome of healthy cell? How does the cancer RNome regulate the evolution as well as the sustenance of cancer?) -- Chapter. 3.1. Genome instability and mutation -- Chapter. 3.2. Tumor-promoting inflammation -- Chapter. 3.3. DNA methylation addiction -- Chapter. 3.4. Oncoviruses -- Chapter. 3.5. Sustained proliferative signaling -- Chapter. 3.6. Evasion of growth suppressors -- Chapter. 3.7. Replicative immortality -- Chapter. 3.8. Resisting Cell death -- Chapter. 3.9. Invasion and metastasis -- Chapter. 3.10. Angiogenesis induction.-Chapter. 3.11. Deregulated cellular energetics/Molecular sweet tooth -- Chapter. 3.12. Tumor Immune-evasion -- Chapter. 3.13. Cancer stem cells and tumor cell plasticity -- 4. Section 4. Cancer RNome: Therapeutic implications(Translational implications of the cancer RNome). Chapter. 4.1. RNAs as diagnostic/prognostic biomarkers -- Chapter. 4.2. RNAs in cancer therapy & chemo-resistance
    Abstract: In the last decade, researchers working in the field of cancer biology have shifted their focus from genetic defects to epigenetic dysregulation, especially that of non-coding RNAs (ncRNAs). This book encompasses a comprehensive review of the transcriptional landscape of the cell and its involvement in the cancer pathophysiology. The first two chapters elucidate the basics of biosynthesis, mechanism of action and modulation of the epigenetic regulation of gene expression by coding as well as non-coding RNAs. The third chapter discusses the aberrant expression of the cellular RNome in the cancer cells and highlights its role in the orchestration of processes involved in evolution as well as the sustenance of cancer cells. The fourth chapter describes the recent advances in the field of translating the transcriptome into diagnostic/prognostic biomarkers and as targets for novel anti-cancer therapies. The final chapter then reviews the emerging experimental approaches to screen, identify and explore the functions of ncRNAs. Providing valuable insights into the field of RNome in the context of cancer, this book is helpful to students, researchers and clinicians
    Pages: XII, 313 p. 51 illus., 50 illus. in color. : online resource.
    ISBN: 9789811315688
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  • 2
    ISSN: 1574-6968
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: Recent reports have indicated that cholesterol-dependent association of tryptophan-aspartate containing coat protein (TACO) plays a crucial role in the entry/survival of Mycobacterium tuberculosis within human macrophages. Keeping this in view, the present study explored whether the molecules that have the ability to downregulate TACO gene transcription could also restrict entry/survival of mycobacteria within human macrophages. The study revealed that chenodeoxycholic acid (CDCA), either alone or in combination with retinoic acid (RA), had the inherent capacity to downregulate TACO gene transcription in a dose-dependent fashion. This result was in conformity with the existence of a functional FXR/RXR binding site analyzed in the regulatory region of the TACO gene. Furthermore, we demonstrate that the entry and intracellular survival of M. tuberculosis is significantly restricted in THP-1 macrophages exposed to CDCA/RA. On the basis of these findings, we propose that the CDCA/RA-dependent pathway may open a new possibility for the treatment of tuberculosis.
    Type of Medium: Electronic Resource
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