Relevant bibliographies by topics / Chromosomal Instability (CIN)

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Chromosomal Instability (CIN)'

Author: Grafiati
Published: 4 June 2021
Last updated: 28 January 2023

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Journal articles on the topic "Chromosomal Instability (CIN)"

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Xiao, Yajuan, Yuanlu Huang, Na Xu, et al. "Chromosomal Instability: A Probable Unfavorable Prognostic Factor For Patients Of Myeloidysplastic Syndromes." Blood 122, no. 21 (2013): 5243. http://dx.doi.org/10.1182/blood.v122.21.5243.5243.

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Abstract Objective Myelodysplastic syndromes (MDS) are a group of heterogeneous hematopoetic stem cell clonal disorders with a high frequency of karyotypic abnormalities (40-60%). Among karyotypic abnormalities, abnormal chromosome numbers (aneuploidy) occurs frequently. In aneuploidy, chromosomal instability (CIN) is defined as persistent mis-segregation of whole chromosomes and is caused by defects during mitosis with an odd number of chromosomes. CIN is associated with tumor heterogenesis, multidrug resistance and aggressiveness in solid tumor. Hence, we performed a one-center study on MDS
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Thompson, Sarah L., and Duane A. Compton. "Examining the link between chromosomal instability and aneuploidy in human cells." Journal of Cell Biology 180, no. 4 (2008): 665–72. http://dx.doi.org/10.1083/jcb.200712029.

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Solid tumors can be highly aneuploid and many display high rates of chromosome missegregation in a phenomenon called chromosomal instability (CIN). In principle, aneuploidy is the consequence of CIN, but the relationship between CIN and aneuploidy has not been clearly defined. In this study, we use live cell imaging and clonal cell analyses to evaluate the fidelity of chromosome segregation in chromosomally stable and unstable human cells. We show that improper microtubule–chromosome attachment (merotely) is a cause of chromosome missegregation in unstable cells and that increasing chromosome
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McClelland, Sarah E. "Role of chromosomal instability in cancer progression." Endocrine-Related Cancer 24, no. 9 (2017): T23—T31. http://dx.doi.org/10.1530/erc-17-0187.

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Cancer cells often displaychromosomal instability(CIN), a defect that involves loss or rearrangement of the cell’s genetic material – chromosomes – during cell division. This process results in the generation of aneuploidy, a deviation from the haploid number of chromosomes, and structural alterations of chromosomes in over 90% of solid tumours and many haematological cancers. This trait is unique to cancer cells as normal cells in the body generally strictly maintain the correct number and structure of chromosomes. This key difference between cancer and normal cells has led to two important h
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Wilhelm, Therese, Maha Said, and Valeria Naim. "DNA Replication Stress and Chromosomal Instability: Dangerous Liaisons." Genes 11, no. 6 (2020): 642. http://dx.doi.org/10.3390/genes11060642.

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Chromosomal instability (CIN) is associated with many human diseases, including neurodevelopmental or neurodegenerative conditions, age-related disorders and cancer, and is a key driver for disease initiation and progression. A major source of structural chromosome instability (s-CIN) leading to structural chromosome aberrations is “replication stress”, a condition in which stalled or slowly progressing replication forks interfere with timely and error-free completion of the S phase. On the other hand, mitotic errors that result in chromosome mis-segregation are the cause of numerical chromoso
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Bendre, Shweta, Arnaud Rondelet, Conrad Hall, et al. "GTSE1 tunes microtubule stability for chromosome alignment and segregation by inhibiting the microtubule depolymerase MCAK." Journal of Cell Biology 215, no. 5 (2016): 631–47. http://dx.doi.org/10.1083/jcb.201606081.

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The dynamic regulation of microtubules (MTs) during mitosis is critical for accurate chromosome segregation and genome stability. Cancer cell lines with hyperstabilized kinetochore MTs have increased segregation errors and elevated chromosomal instability (CIN), but the genetic defects responsible remain largely unknown. The MT depolymerase MCAK (mitotic centromere-associated kinesin) can influence CIN through its impact on MT stability, but how its potent activity is controlled in cells remains unclear. In this study, we show that GTSE1, a protein found overexpressed in aneuploid cancer cell
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Yuen, Karen W., and Arshad Desai. "The wages of CIN." Journal of Cell Biology 180, no. 4 (2008): 661–63. http://dx.doi.org/10.1083/jcb.200801030.

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Aneuploidy and chromosome instability (CIN) are hallmarks of the majority of solid tumors, but the relationship between them is not well understood. In this issue, Thompson and Compton (Thompson, S.L., and D.A. Compton. 2008. Examining the link between chromosomal instability and aneuploidy in human cells. J. Cell. Biol. 180:665–672) investigate the mechanism of CIN in cancer cells and find that CIN arises primarily from defective kinetochore–spindle attachments that evade detection by the spindle checkpoint and persist into anaphase. They also explore the consequences of artificially elevatin
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de Oliveira Lisboa, Mateus, Paulo Roberto Slud Brofman, Ana Teresa Schmid-Braz, Aline Rangel-Pozzo, and Sabine Mai. "Chromosomal Instability in Acute Myeloid Leukemia." Cancers 13, no. 11 (2021): 2655. http://dx.doi.org/10.3390/cancers13112655.

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Chromosomal instability (CIN), the increasing rate in which cells acquire new chromosomal alterations, is one of the hallmarks of cancer. Many studies highlighted CIN as an important mechanism in the origin, progression, and relapse of acute myeloid leukemia (AML). The ambivalent feature of CIN as a cancer-promoting or cancer-suppressing mechanism might explain the prognostic variability. The latter, however, is described in very few studies. This review highlights the important CIN mechanisms in AML, showing that CIN signatures can occur largely in all the three major AML types (de novo AML,
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Michor, Franziska. "Chromosomal instability and human cancer." Philosophical Transactions of the Royal Society B: Biological Sciences 360, no. 1455 (2005): 631–35. http://dx.doi.org/10.1098/rstb.2004.1617.

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Genetic instability is a defining feature of human cancer. The main type of genetic instability, chromosomal instability (CIN), enhances the rate of gross chromosomal changes during cell division. CIN is brought about by mutations of CIN genes, i.e. genes that are involved in maintaining the genomic integrity of the cell. A major question in cancer genetics is whether genetic instability is a cause and hence a driving force of tumorigenesis. A mathematical framework for studying the somatic evolution of cancer sheds light onto the causal relations between CIN and human cancer.
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Siri, Sebastián Omar, Julieta Martino, and Vanesa Gottifredi. "Structural Chromosome Instability: Types, Origins, Consequences, and Therapeutic Opportunities." Cancers 13, no. 12 (2021): 3056. http://dx.doi.org/10.3390/cancers13123056.

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Chromosomal instability (CIN) refers to an increased rate of acquisition of numerical and structural changes in chromosomes and is considered an enabling characteristic of tumors. Given its role as a facilitator of genomic changes, CIN is increasingly being considered as a possible therapeutic target, raising the question of which variables may convert CIN into an ally instead of an enemy during cancer treatment. This review discusses the origins of structural chromosome abnormalities and the cellular mechanisms that prevent and resolve them, as well as how different CIN phenotypes relate to e
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Weiss, Johannes G., Filip Gallob, Patricia Rieder, and Andreas Villunger. "Apoptosis as a Barrier against CIN and Aneuploidy." Cancers 15, no. 1 (2022): 30. http://dx.doi.org/10.3390/cancers15010030.

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Aneuploidy is the gain or loss of entire chromosomes, chromosome arms or fragments. Over 100 years ago, aneuploidy was described to be a feature of cancer and is now known to be present in 68–90% of malignancies. Aneuploidy promotes cancer growth, reduces therapy response and frequently worsens prognosis. Chromosomal instability (CIN) is recognized as the main cause of aneuploidy. CIN itself is a dynamic but stochastic process consisting of different DNA content-altering events. These can include impaired replication fidelity and insufficient clearance of DNA damage as well as chromosomal mis-
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Dissertations / Theses on the topic "Chromosomal Instability (CIN)"

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Joy, Jery 1992. "Chromosomal instability : interplay between proteotoxic and metabolic stress." Doctoral thesis, Universitat Pompeu Fabra, 2020. http://hdl.handle.net/10803/668516.

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Chromosomal Instability (CIN) and associated aneuploidy are salient features of the majority of human solid tumors. In the Drosophila epithelial model of CIN, the generation of highly aneuploid karyotypes drive cell delamination and c-Jun N-terminal Kinase (JNK) dependent cell death. Aneuploidy associated generation of Reactive Oxygen Species (ROS) plays a key role in the activation of JNK. When delaminating cells are maintained in the tissue by apoptosis inhibition, aberrant karyotypes promote a cell-autonomous malignant behavior. Here we have dissected the molecular mechanisms under
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Shaukat, Zeeshan. "Targeting chromosomal instability: screening and characterization of CIN killers." Thesis, 2014. http://hdl.handle.net/2440/85191.

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Chromosomal INstability (CIN), a hallmark of cancer cells, refers to a state in which cells have an increased rate of gain or loss of whole chromosomes or large chromosomal fractions. CIN is linked to the progression of tumours with poor clinical outcomes such as drug resistance and metastasis. Chromosomal instability is mainly caused by defective chromosomal segregation during mitosis and normally prevented by cellular checkpoints. As CIN is not found in normal cells, it offers a cancer-specific target for therapy, which may be particularly valuable because CIN is common in advanced tumours t
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Hussain, Rashid. "Exploring metabolic interventions for CIN cancer therapy." Thesis, 2017. http://hdl.handle.net/2440/119191.

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Chromosomal instability (CIN) has been established as one of the hallmarks of cancer, which is prevalent in most of the solid and advanced tumours. CIN enhances genetic heterogeneity in cancer cells. This heterogeneity provides selective advantages to cancer cells against the drugs and the therapies, which are linked to poor prognosis and relapse of cancer. Altered metabolism is another hallmark of cancer, which is being targeted for cancer therapy. In this thesis, I have discussed the therapeutic effect of targeting metabolism in CIN cells and CIN tumours. Chapter 1 is my introduction in whic
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Lüddecke, Sina. "CEP72 represents a putative Oncogene that negatively regulates the mitotic Function of Brca1 and induces Chromosomal Instability." Doctoral thesis, 2015. http://hdl.handle.net/11858/00-1735-0000-0023-965A-C.

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Books on the topic "Chromosomal Instability (CIN)"

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Al-Romaih, Khaldoun Ibraheem. Chromosomal instability (CIN) in osteosarcoma and its association with centrosome abnormalities and/or p53 mutation. National Library of Canada, 2002.

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Book chapters on the topic "Chromosomal Instability (CIN)"

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Nübel, M., S. Kraus, A. Rehders, et al. "Molecular characterization of disseminated tumor cells from colorectal cancer: nuclear beta-catenin defines subpopulation with higher chromosomal instability (CIN)." In Deutsche Gesellschaft für Chirurgie. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00625-8_25.

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Iourov, Ivan Y., Svetlana G. Vorsanova, and Yuri B. Yurov. "FISH—Interphase Applications Including Detection of Chromosome Instability (CIN)." In Cytogenetics and Molecular Cytogenetics. CRC Press, 2022. http://dx.doi.org/10.1201/9781003223658-16.

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"Chromosomal Instability (CIN)." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics. Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_2951.

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Cheng, Tracie T., Sujani M. K. Gamage, Sharmin Aktar, Vinod Gopalan, and Farhadul Islam. "Karyotyping and Chromosomal Aberrations in Cancer: Molecular and Diagnostic Biomarkers." In Current Cancer Biomarkers. BENTHAM SCIENCE PUBLISHERS, 2023. http://dx.doi.org/10.2174/9789815079364123010007.

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Chromosomal abnormalities induce genomic instability and are associated with cancer hallmarks. Chromosomal abnormalities can be categorised into structural and numerical aberrations and are seen under a light microscope. Given the ease of detecting and observing such changes using karyotyping, chromosomal aberrations may be a useful diagnostic tool. For example, the discovery of the Philadelphia chromosome was a cytogenetic hallmark of chronic myeloid leukaemia and acute lymphoblastic leukaemia. Thus, this chapter explores potential aberrations which have the potential to be used as cancer markers in a clinical setting. Recurrent structural aberrations with known genetic mutations are observed in cancers of the bones, lungs, salivary glands, soft tissue, stomach, thyroid, and uterus. The association of these genetic alterations with various cancers suggests a causative role of structural aberrations in carcinogenesis and is characteristic of some cancers. Additionally, mono- and tri-somies, known as aneuploidy, are common to all cancer types, however, their roles as a cause or consequence are difficult to establish due to the sheer loss or gain of genetic material, respectively. Cancers with the most frequent trisomies, include Ewing’s sarcoma of the bone, astrocytoma of the brain, and renal adenocarcinoma. Common cancer monosomies include meningioma of the brain and ovarian adenocarcinoma. These chromosomal aberrations forge the path to a better understanding of cancer genetics. Though there are potential chromosome markers in cancer, the heterogeneity of cancer genetics makes this a challenging tool to incorporate into current oncological diagnostic guidelines.
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Yurekli, Nazlıcan, Elif Cansu Abay, Merve Tutar, et al. "Molecular Mechanisms of Breast Cancer Metastasis." In Cancer Metastasis - Molecular Mechanism and Clinical Therapy [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.108424.

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Breast cancer (BC) is one of the most frequently occurring diseases with high morbidity and mortality rates in the world today. BC cells live under stress with altered pathway signaling, chromosome and microsatellite instability, aneuploidy, hypoxia, low pH, and low nutrient conditions. In order to survive and reproduce in these stressful environments, BC cells rapidly undergo adaptive mutations, rearrange their chromosomes, and repress tumor suppressor genes while inducing oncogene activities that cause the natural selection of cancer cells and result in heterogeneous cancer cells in the tumor environment. Unfortunately, these genetic alterations result in aggressive BC cells that can not only proliferate aggressively but also migrate and invade the other tissues in the body to form secondary tumors. In this review, molecular mechanisms of metastasis of BC subtypes are discussed.
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Wilding, Jennifer, and Walter Bodmer. "Genetic instability." In Oxford Textbook of Oncology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199656103.003.0008.

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Most cancers are thought to exhibit some form of genetic instability, which can either be at the nucleotide or chromosome level. It is tempting to speculate that because genetic instability accelerates the rate of accumulation of mutations, it would act as a necessary driving force for the development and progression of cancer, and there has been much debate as to whether there is an absolute requirement for genetic instability during tumorigenesis. Although the mechanism of the acquired genetic instability is clear in many germline cancer-predisposing syndromes, the molecular basis for genetic instability in sporadic cancers remains unclear. This chapter will give a very brief summary of the main features of the major DNA damage response and repair pathways, the germline mutations in genes within these pathways which predispose to cancers, and an overview of some of the possible mechanisms through which sporadic cancers may become genetically unstable.
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Kumar, Umesh, Garima Rathi, Lakshit Sharma, et al. "Epigenetic Regulation of Breast Cancer." In Research Anthology on Advancements in Women's Health and Reproductive Rights. IGI Global, 2022. http://dx.doi.org/10.4018/978-1-6684-6299-7.ch013.

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Breast cancer is a carcinoma of mammary glands, which starts off as abnormal proliferation of ductal cells. This could, then, become either benign tumours or metastatic carcinomas. It is one of the most common causes of deaths because of cancer, and is one of the most common types of cancer in women in the whole world. India along with the US and China accounts for one-third of the breast cancer burden. The breast cancer carcinogenesis is attributed to epigenetics, which is the study of the reversible changes in the phenotype without any change in the DNA sequence. Genes, which are concerned with proliferation, anti-apoptosis, invasion, and metastasis, have been seen undergoing epigenetic changes in breast cancer. Cancer can be caused either by global hypomethylation (causing activation of oncogenes and leading to chromosomal instability) or by locus-specific hypermethylation (causing repression of gene expression and genetic instability due to inactivation of DNA repair genes). Other epigenetic mechanisms involved in carcinogenesis are histone modification and nucleosomal remodeling.
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Kumar, Umesh, Garima Rathi, Lakshit Sharma, et al. "Epigenetic Regulation of Breast Cancer." In Handbook of Research on Advancements in Cancer Therapeutics. IGI Global, 2021. http://dx.doi.org/10.4018/978-1-7998-6530-8.ch006.

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Breast cancer is a carcinoma of mammary glands, which starts off as abnormal proliferation of ductal cells. This could, then, become either benign tumours or metastatic carcinomas. It is one of the most common causes of deaths because of cancer, and is one of the most common types of cancer in women in the whole world. India along with the US and China accounts for one-third of the breast cancer burden. The breast cancer carcinogenesis is attributed to epigenetics, which is the study of the reversible changes in the phenotype without any change in the DNA sequence. Genes, which are concerned with proliferation, anti-apoptosis, invasion, and metastasis, have been seen undergoing epigenetic changes in breast cancer. Cancer can be caused either by global hypomethylation (causing activation of oncogenes and leading to chromosomal instability) or by locus-specific hypermethylation (causing repression of gene expression and genetic instability due to inactivation of DNA repair genes). Other epigenetic mechanisms involved in carcinogenesis are histone modification and nucleosomal remodeling.
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Conference papers on the topic "Chromosomal Instability (CIN)"

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Weiler, Sofia, Thomas Wolf, Federico Pinna, et al. "Abstract 4269: A gene signature defines chromosomal instability (CIN) and poor survival in liver cancer patients." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4269.

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Rodriguez, Angel, Jerry Lee, Ramsay Sutton, et al. "Abstract A061: Tumor mutation burden (TMB), microsatellite instability (MSI), and chromosomal instability (CIN) analysis using low pass whole genome sequencing of single circulating tumor cell (CTC)." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; October 26-30, 2017; Philadelphia, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1535-7163.targ-17-a061.

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Yamada, Hiroshi Y., Yuting Zhang, Wei Dai, and Chinthalapally V. Rao. "Abstract 1752: Consequences of high Chromosome Instability (CIN) in SGO1(Shugoshin1) CIN model mice." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1752.

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Haomin, Huang, and Timothy J. Yen. "Abstract 3892: Chromosome instability mediated by impaired AuroraB kinase activity on kinetochores in CIN cancer cells." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3892.

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Rao, Chinthalapally V., Saira Sanghera, Yuting Zhang, et al. "Abstract 2881: Systemic Chromosome Instability (CIN) resulted in transcriptomic changes in metabolic and proliferation regulators in colonic mucosal tissue of Sgo1-/+ mice." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2881.

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Rao, Chinthalapally V., Saira Sanghera, Yuting Zhang, et al. "Abstract 93: Antagonizing pathways leading to differential dynamics in colonic carcinogenesis in azoxymethane (AOM)-treated Sgo1 (Shugoshin1)-haploinsufficient chromosome instability (CIN) model mice." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-93.

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Reports on the topic "Chromosomal Instability (CIN)"

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Yen, Timothy J. Suppression of Chromosome Instability (CIN) to Enhance Chemosensitivity of Ovarian Tumor Cells by Modulating the Aurora B Pathway at Kinetochores. Defense Technical Information Center, 2013. http://dx.doi.org/10.21236/ada585095.

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