DNA alterations in cancer

genetic and epigenetic changes

Publisher: Eaton Pub. in Natick, MA

Written in English
Cover of: DNA alterations in cancer |
Published: Pages: 508 Downloads: 339
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Subjects:

  • Cancer -- Genetic aspects

Edition Notes

Includes bibliographical references and index.

Statementedited by Melanie Ehrlich.
ContributionsEhrlich, Melanie, 1945-
Classifications
LC ClassificationsRC268.4 .D63 2000
The Physical Object
Paginationxvii, 508 p. :
Number of Pages508
ID Numbers
Open LibraryOL20701805M
ISBN 101881299198
LC Control Number99056013
OCLC/WorldCa42771514

Alterations in DNA damage response (DDR) is one of the several hallmarks of cancer. Genomic instability resulting from a disrupted DDR mechanism is known to contribute to cancer progression, and are subjected to radiation, cytotoxic, or more recently targeted therapies with limited success. Synthetic lethality (SL), which is a condition where simultaneous loss-of-function of the genes from.   Prostate cancer is the most common cancer in men and the second leading cause of cancer death. Furthermore, many men with notably advanced disease have been found to have abnormalities in DNA repair. The purpose of this research is to study the role of a DNA repair pathway in prostate cancer, specifically in response to administration of radium.   Possible alterations in the DNA involved in cancer Date: December 5, Source: University of Seville Summary: The study shows the role of the protein PIF1, capable of . BACKGROUND. Emerging evidence has suggested that DNA repair gene alterations may be important in prostate cancer pathogenesis. In the current study, the authors sought to characterize alterations in DNA repair pathway genes in both primary and metastatic prostate tumors with attention to tissue distribution as well as specific genomic alterations.

  Distinct genetic alterations. In a study, published in Molecular Cancer Research, researchers sequenced 39 genes of interest in tumours and matched normal tissue, from 77 African American patients with prostate cancer. The team found that over 35% of patients’ tumours harboured potentially damaging mutations in several genes. Raeker MÖ, Carethers JM. Immunological Features with DNA Microsatellite Alterations in Patients with Colorectal Cancer. J Cancer Immunol. ; 2(3): J Cancer Immunol. Volume 2, Issue 3 Loss of any component of MMR will cause frameshift mutations at . The development of solid tumors is associated with the acquisition of genetic and epigenetic alterations. Although these changes may be brought about at the genomic level in a variety of ways, genomic DNA copy number aberrations are particularly frequent in solid tumors and are expected to contribute to tumor evolution by copy number induced alterations in gene expression. DNA damage repair (DDR) alterations, specifically those resulting in homologous recombination repair deficiency (HRD). It has been known for at least two decades that germline alterations in BRCA genes are associated with an increased risk of prostate cancer. Dr.

pathway alterations has not been extensively analyzed in localized disease. Thus far two prior studies suggested the incidence to range 8–20% [8, 9]. Therefore, in the present study, we analyzed the largest publically available version of The Cancer Genome Atlas (TCGA) to assess the rate of altered DNA damage repair machinery in. Prostate cancer tumors from African American men had higher frequencies of certain genetic alterations that may be associated with aggressive disease, compared with prostate cancer tumors from. Cancer is a disease driven by mutations arising within our DNA, caused by environmental factors or ageing. It is less studied how these alterations in the genome change our RNA. More research is required to understand which of the alterations in RNA are a consequence of the mutations and which contribute to cancer progression. Screening prostate biopsy samples (formalin-fixed paraffin-embedded tissue) were analyzed for alteration in DNA damage repair genes using the Foundation Medicine Inc FoundationOne assay. Germline sequencing was carried about using the Ambry Genetics CustomNext-Cancer panel.

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DNA Alterations in Cancer: Genetic and Epigenetic Changes: Medicine & Health Science Books @   : DNA Alterations in Cancer: Genetic and Epigenetic Changes: Former Library book. Shows some signs of DNA alterations in cancer book, and may have some markings on the inside.

An estima of diagnosed colorectal cancer cases worldwide are attributed to Lynch syndrome each year. Intensive cancer screening, with early initiation and frequent follow-up, can reduce colorectal cancer incidence and mortality in LS patients.

This book provides an up-to-date overview on the genetic and epigenetic basis of Lynch syndrome. The content of the book is considerably broadened and enhanced by addressing topics such as the possible use of alterations in DNA as predictive biomarkers and the role of DNA damage and its repair in neurotoxicity associated with cancer Edition: 1.

An estima of diagnosed colorectal cancer cases worldwide are attributed to Lynch syndrome each year. Intensive cancer screening, with early initiation and frequent follow-up, can reduce colorectal cancer incidence and mortality in LS patients.

This book provides an up-to-date overview on the genetic DNA alterations in cancer book epigenetic basis of Lynch syndrome.4/5(1). The authors studied the distribution and type of alterations in 24 genes that are considered important for DNA repair in prostate cancers harvested from localized and metastatic tumors.

Tumor DNA underwent hybrid capture for all coding exons of or cancer‐related genes plus select introns from 19 or 31 genes frequently rearranged. Precision Medicine and Imaging Alterations in DNA Damage Repair Genes in Primary Liver Cancer JianzhenLin1,JunpingShi2,HonglinGuo2,XuYang1,YanJiang2,JunyuLong1,YiBai1, Dongxu Wang1, Xiaobo Yang1, Xueshuai Wan1, Lei Zhang1, Jie Pan3,KeHu4, Mei Guan5, Li Huo6, Xinting Sang1, Kai Wang2,7, and Haitao Zhao1,8 Abstract Purpose: Alterations in DNA damage repair (DDR) genes.

(Messenger RNA in turn is translated to produce the proteins encoded by the DNA.) In general, cancer cells have more genetic changes than normal cells.

But each person’s cancer has a unique combination of genetic alterations. Some of these changes may be the result of cancer, rather than the cause.

Alterations that are benign or of unknown significance do not aid patient care. Tumor DNA sequencing tests may also uncover the presence of inherited alterations that increase cancer risk (hereditary cancer syndromes) or that are associated with diseases or conditions other than cancer.

These are known as incidental, or secondary, findings. Transcript alterations often result from somatic changes in cancer genomes s forms of RNA alterations have been described in cancer, including overexpression 2, altered splicing 3 and gene fusions 4; however, it is difficult to attribute these to underlying genomic changes owing to heterogeneity among patients and tumour types, and the relatively small cohorts of patients for whom.

Structural chromosomal alterations are common in many cancer types and presumably reflect the consequences of DNA double-strand breaks and nonhomologous end joining to generate chromosomal deletions, inversions, and translocations, with biologic selection acting on the variant cells with the structural alterations.

DNA damage appears to be a fundamental problem for life. In this chapter we review evidence indicating that DNA damages are a major primary cause of cancer. DNA damages give rise to mutations and epimutations that, by a process of natural selection, can cause progression to cancer.

To facilitate discussion of complex clinical data it also provides a brief overview of essential DNA repair pathways that operate in man. Several recent reviews are available for a detailed discussion of individual biochemical pathways.

DNA repair alterations in cancer have the potential to direct personalized cancer. Otto Warburg’s discovery in the s that tumor cells took up more glucose and produced more lactate than normal cells provided the first clues that cancer cells reprogrammed their metabolism.

For many years, however, it was unclear as to whether these metabolic alterations were a consequence of tumor growth or an adaptation that provided a survival advantage to these cells. In. Results: At least % of the differentially methylated DNA loci (DM loci) observed in peripheral whole blood/leukocytes and serum of cancer patients overlapped with DM loci that distinguish between myeloid and lymphoid cells and >% of the overlapped DM loci had consistent alteration states (hyper- or hypomethylation) in cancer samples compared to normal controls with those in.

But other alterations to longer stretches of DNA can aid and abet cancer growth, too. These changes include rearrangements, deletions, duplications and fusions of segments of DNA.

The terms driver mutation, driver gene and driver oncogene also describe these gene alterations that help cancer. The book is well written and well illustrated, with schematic diagrams and actual research data to demonstrate points made in the text.

There is also an extensive, up-to-date bibliography, making the book valuable to scientists, and to physicians, students, and nurses interested in the field of cancer Reviews: 1. Read "DNA Alterations in Lynch Syndrome Advances in molecular diagnosis and genetic counselling" by available from Rakuten Kobo.

Lynch syndrome (LS) is the most common cause of inherited colorectal cancer, a disease with a high mortality rate. An es. Chapter 1 DNA/RNA Hypomethylation in Cancer Cells and Tissues Authors: Dr. Burong Hu, Dr. Dong Pan. Evidence demonstrates that epigenetic alterations, such as DNA/RNA methylation alterations, chromatin remodeling and difference in microRNA expression, play key roles in a wide range of cellular processes and : Burong Hu, Dong Pan.

Precision medicine in cancer is the idea that the recognition and targeting of key genetic drivers of a patient’s tumor can permit more effective and less toxic outcomes. Point mutations that alter protein function have been primary targets. Yet in ovarian cancer, unique genetic mutations have been identified only in adult granulosa cell tumors, with a number of other point mutations present Author: Joe R.

Delaney, Dwayne G. Stupack. Epigenetic alterations are as important as genetic mutations in a cell’s transformation to cancer. Mechanisms of epigenetic silencing of tumor suppressor genes and activation of oncogenes include: alteration in CpG island methylation patterns, histone modifications, and dysregulation of DNA.

Additional Physical Format: Online version: DNA alterations in cancer. Natick, MA: Eaton Pub., © (OCoLC) Online version: DNA alterations in cancer.

Genomic alterations in plasma DNA from patients with metastasized prostate cancer receiving abiraterone or enzalutamide Int J Cancer.

Sep 1;(5) doi: /ijc The purpose of this book is to provide an up to date review of the nature and consequences of epigenetic changes in cancer. Epigenetics literally means “above” genetics, and consists of heritable gene expression or other phenotypic states not accounted for by DNA base sequence.

This new book is an essential reference, as well as introduction to the field of chemical carcinogenesis, with particular focus on DNA damage as a critical link between exposure and disease, and emphasis on biomarkers associated with cancer risk in humans. In addition to DNA damage, related topics covered include metabolism of selected chemical.

Somatic mutations of DNA damage response (DDR) genes are frequently found in urothelial cancer and appear to play an important role in tumorigenesis, progression, treatment response, and outcomes. In a set of DDR genes, ATM alterations were associated with worse survival, while other alterations were associated with better survival in advanced.

The central role of DNA damage in progression to cancer is indicated at the second level of the figure. The central elements of DNA damage, epigenetic alterations and deficient DNA repair in progression to cancer are shown in red.

A deficiency in DNA repair would cause more DNA damage to accumulate, and increase the risk for cancer.

This pioneering book is a unique compilation of mitochondrial genome alterations in cancer. While primarily focused on the emerging role of mitochondrial genome changes, bioenergetics and signaling pathways, attention is also given to the metabolic transformations of the cancer cell, as well as the established altered cell death processes that.

HRD in cancer results in a distinctive pattern of genomic instability due to the deficiency in error-free DNA double strand break repair by HR.(10–12) Therefore, biomarkers based on genomic landscape ‘scars’ or ‘footprints’ (i.e.

patterns of somatic genetic alterations assessed by large-scale state transitions (LST), telomeric regions. Epigenetic alterations are able to modulate gene activ-ity without affecting their nucleotide sequence. Aberrant methylation has been recognized as a hallmark of hu-man cancer, and DNA methylation patterns are altered in all types of cancers analyzed, affecting virtually all cellular pathways trough methylation-mediated silencing.

Precision Medicine has particular relevance in oncology Precision Medicine in oncology is the use of therapeutic interventions to identify and treat patients based on specific molecular or cellular features of their cancer, such as genomic alterations or protein expression levels.

1 Advancements in testing have led to the identification of multiple genomic alterations, changing the approach to.Most bladder tumors have complex genomes characterized by a high mutation burden as well as frequent copy number alterations and chromosomal rearrangements.

Alterations in DNA repair pathways—including the double-strand break (DSB) and nucleotide excision repair (NER) pathways—are present in bladder tumors and may contribute to genomic instability and drive the tumor phenotype.The aim of this study was to analyze plasma DNA from primary and metastatic breast cancer cases for tumor-specific alterations and to compare these findings with immunocytochemistry and estimation of cytokeratin 19 (CK19) mRNA for detection of micrometastases.

DNA was extracted from plasma, lymphocytes, and microdissected tumor tissue sections obtained from 71 patients with breast cancer .