Standard

Intratumor heterogeneity: models of malignancy emergence and evolution. / Ivanov, R A; Lashin, S A.

в: Vavilovskii Zhurnal Genetiki i Selektsii, Том 27, № 7, 12.2023, стр. 815-819.

Результаты исследований: Научные публикации в периодических изданияхстатьяРецензирование

Harvard

Ivanov, RA & Lashin, SA 2023, 'Intratumor heterogeneity: models of malignancy emergence and evolution', Vavilovskii Zhurnal Genetiki i Selektsii, Том. 27, № 7, стр. 815-819. https://doi.org/10.18699/VJGB-23-94

APA

Ivanov, R. A., & Lashin, S. A. (2023). Intratumor heterogeneity: models of malignancy emergence and evolution. Vavilovskii Zhurnal Genetiki i Selektsii, 27(7), 815-819. https://doi.org/10.18699/VJGB-23-94

Vancouver

Ivanov RA, Lashin SA. Intratumor heterogeneity: models of malignancy emergence and evolution. Vavilovskii Zhurnal Genetiki i Selektsii. 2023 дек.;27(7):815-819. doi: 10.18699/VJGB-23-94

Author

Ivanov, R A ; Lashin, S A. / Intratumor heterogeneity: models of malignancy emergence and evolution. в: Vavilovskii Zhurnal Genetiki i Selektsii. 2023 ; Том 27, № 7. стр. 815-819.

BibTeX

@article{9746e4359a1042229bfeb05e0467066a,
title = "Intratumor heterogeneity: models of malignancy emergence and evolution",
abstract = "Cancer is a complex and heterogeneous disease characterized by the accumulation of genetic alterations that drive uncontrolled cell growth and proliferation. Evolutionary dynamics plays a crucial role in the emergence and development of tumors, shaping the heterogeneity and adaptability of cancer cells. From the perspective of evolutionary theory, tumors are complex ecosystems that evolve through a process of microevolution influenced by genetic mutations, epigenetic changes, tumor microenvironment factors, and therapy-induced changes. This dynamic nature of tumors poses significant challenges for effective cancer treatment, and understanding it is essential for developing effective and personalized therapies. By uncovering the mechanisms that determine tumor heterogeneity, researchers can identify key genetic and epigenetic changes that contribute to tumor progression and resistance to treatment. This knowledge enables the development of innovative strategies for targeting specific tumor clones, minimizing the risk of recurrence and improving patient outcomes. To investigate the evolutionary dynamics of cancer, researchers employ a wide range of experimental and computational approaches. Traditional experimental methods involve genomic profiling techniques such as next-generation sequencing and fluorescence in situ hybridization. These techniques enable the identification of somatic mutations, copy number alterations, and structural rearrangements within cancer genomes. Furthermore, single-cell sequencing methods have emerged as powerful tools for dissecting intratumoral heterogeneity and tracing clonal evolution. In parallel, computational models and algorithms have been developed to simulate and analyze cancer evolution. These models integrate data from multiple sources to predict tumor growth patterns, identify driver mutations, and infer evolutionary trajectories. In this paper, we set out to describe the current approaches to address this evolutionary complexity and theories of its occurrence.",
author = "Ivanov, {R A} and Lashin, {S A}",
note = "The work was supported by Budget Project No. FWNR 2022 0020. Copyright {\textcopyright} AUTHORS. Публикация для корректировки.",
year = "2023",
month = dec,
doi = "10.18699/VJGB-23-94",
language = "English",
volume = "27",
pages = "815--819",
journal = "Вавиловский журнал генетики и селекции",
issn = "2500-0462",
publisher = "Institute of Cytology and Genetics of Siberian Branch of the Russian Academy of Sciences",
number = "7",

}

RIS

TY - JOUR

T1 - Intratumor heterogeneity: models of malignancy emergence and evolution

AU - Ivanov, R A

AU - Lashin, S A

N1 - The work was supported by Budget Project No. FWNR 2022 0020. Copyright © AUTHORS. Публикация для корректировки.

PY - 2023/12

Y1 - 2023/12

N2 - Cancer is a complex and heterogeneous disease characterized by the accumulation of genetic alterations that drive uncontrolled cell growth and proliferation. Evolutionary dynamics plays a crucial role in the emergence and development of tumors, shaping the heterogeneity and adaptability of cancer cells. From the perspective of evolutionary theory, tumors are complex ecosystems that evolve through a process of microevolution influenced by genetic mutations, epigenetic changes, tumor microenvironment factors, and therapy-induced changes. This dynamic nature of tumors poses significant challenges for effective cancer treatment, and understanding it is essential for developing effective and personalized therapies. By uncovering the mechanisms that determine tumor heterogeneity, researchers can identify key genetic and epigenetic changes that contribute to tumor progression and resistance to treatment. This knowledge enables the development of innovative strategies for targeting specific tumor clones, minimizing the risk of recurrence and improving patient outcomes. To investigate the evolutionary dynamics of cancer, researchers employ a wide range of experimental and computational approaches. Traditional experimental methods involve genomic profiling techniques such as next-generation sequencing and fluorescence in situ hybridization. These techniques enable the identification of somatic mutations, copy number alterations, and structural rearrangements within cancer genomes. Furthermore, single-cell sequencing methods have emerged as powerful tools for dissecting intratumoral heterogeneity and tracing clonal evolution. In parallel, computational models and algorithms have been developed to simulate and analyze cancer evolution. These models integrate data from multiple sources to predict tumor growth patterns, identify driver mutations, and infer evolutionary trajectories. In this paper, we set out to describe the current approaches to address this evolutionary complexity and theories of its occurrence.

AB - Cancer is a complex and heterogeneous disease characterized by the accumulation of genetic alterations that drive uncontrolled cell growth and proliferation. Evolutionary dynamics plays a crucial role in the emergence and development of tumors, shaping the heterogeneity and adaptability of cancer cells. From the perspective of evolutionary theory, tumors are complex ecosystems that evolve through a process of microevolution influenced by genetic mutations, epigenetic changes, tumor microenvironment factors, and therapy-induced changes. This dynamic nature of tumors poses significant challenges for effective cancer treatment, and understanding it is essential for developing effective and personalized therapies. By uncovering the mechanisms that determine tumor heterogeneity, researchers can identify key genetic and epigenetic changes that contribute to tumor progression and resistance to treatment. This knowledge enables the development of innovative strategies for targeting specific tumor clones, minimizing the risk of recurrence and improving patient outcomes. To investigate the evolutionary dynamics of cancer, researchers employ a wide range of experimental and computational approaches. Traditional experimental methods involve genomic profiling techniques such as next-generation sequencing and fluorescence in situ hybridization. These techniques enable the identification of somatic mutations, copy number alterations, and structural rearrangements within cancer genomes. Furthermore, single-cell sequencing methods have emerged as powerful tools for dissecting intratumoral heterogeneity and tracing clonal evolution. In parallel, computational models and algorithms have been developed to simulate and analyze cancer evolution. These models integrate data from multiple sources to predict tumor growth patterns, identify driver mutations, and infer evolutionary trajectories. In this paper, we set out to describe the current approaches to address this evolutionary complexity and theories of its occurrence.

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UR - https://elibrary.ru/item.asp?id=56697296

U2 - 10.18699/VJGB-23-94

DO - 10.18699/VJGB-23-94

M3 - Article

C2 - 38213707

VL - 27

SP - 815

EP - 819

JO - Вавиловский журнал генетики и селекции

JF - Вавиловский журнал генетики и селекции

SN - 2500-0462

IS - 7

ER -

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