Cancer microenvironment and genomics: evolution in process
Cancer heterogeneity is a result of genetic mutations within the cancer cells. Their proliferation is not only driven by autocrine functions but also under the influence of cancer microenvironment, which consists of normal stromal cells such as infiltrating immune cells, cancer-associated fibroblast...
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| Veröffentlicht in: | Clinical & experimental metastasis 2022-02, Vol.39 (1), p.85-99 |
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| container_title | Clinical & experimental metastasis |
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| creator | Leong, Stanley P. Witz, Isaac P. Sagi-Assif, Orit Izraely, Sivan Sleeman, Jonathan Piening, Brian Fox, Bernard A. Bifulco, Carlo B. Martini, Rachel Newman, Lisa Davis, Melissa Sanders, Lauren M. Haussler, David Vaske, Olena M. Witte, Marlys |
| description | Cancer heterogeneity is a result of genetic mutations within the cancer cells. Their proliferation is not only driven by autocrine functions but also under the influence of cancer microenvironment, which consists of normal stromal cells such as infiltrating immune cells, cancer-associated fibroblasts, endothelial cells, pericytes, vascular and lymphatic channels. The relationship between cancer cells and cancer microenvironment is a critical one and we are just on the verge to understand it on a molecular level. Cancer microenvironment may serve as a selective force to modulate cancer cells to allow them to evolve into more aggressive clones with ability to invade the lymphatic or vascular channels to spread to regional lymph nodes and distant sites. It is important to understand these steps of cancer evolution within the cancer microenvironment towards invasion so that therapeutic strategies can be developed to control or stop these processes. |
| doi_str_mv | 10.1007/s10585-021-10097-9 |
| format | Article |
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Their proliferation is not only driven by autocrine functions but also under the influence of cancer microenvironment, which consists of normal stromal cells such as infiltrating immune cells, cancer-associated fibroblasts, endothelial cells, pericytes, vascular and lymphatic channels. The relationship between cancer cells and cancer microenvironment is a critical one and we are just on the verge to understand it on a molecular level. Cancer microenvironment may serve as a selective force to modulate cancer cells to allow them to evolve into more aggressive clones with ability to invade the lymphatic or vascular channels to spread to regional lymph nodes and distant sites. It is important to understand these steps of cancer evolution within the cancer microenvironment towards invasion so that therapeutic strategies can be developed to control or stop these processes.</description><identifier>ISSN: 0262-0898</identifier><identifier>EISSN: 1573-7276</identifier><identifier>DOI: 10.1007/s10585-021-10097-9</identifier><identifier>PMID: 33970362</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Autocrine signalling ; Biomedical and Life Sciences ; Biomedicine ; Cancer ; Cancer Research ; Cell proliferation ; Channels ; Endothelial Cells ; Evolution ; Fibroblasts ; Genomics ; Hematology ; Heterogeneity ; Humans ; Immune system ; Lymph nodes ; Lymph Nodes - pathology ; Microenvironments ; Mutation ; Neoplasms - blood supply ; Oncology ; Pericytes ; Review ; Stromal cells ; Surgical Oncology ; Tumor Microenvironment - genetics</subject><ispartof>Clinical & experimental metastasis, 2022-02, Vol.39 (1), p.85-99</ispartof><rights>The Author(s), under exclusive licence to Springer Nature B.V. 2021</rights><rights>2021. 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Their proliferation is not only driven by autocrine functions but also under the influence of cancer microenvironment, which consists of normal stromal cells such as infiltrating immune cells, cancer-associated fibroblasts, endothelial cells, pericytes, vascular and lymphatic channels. The relationship between cancer cells and cancer microenvironment is a critical one and we are just on the verge to understand it on a molecular level. Cancer microenvironment may serve as a selective force to modulate cancer cells to allow them to evolve into more aggressive clones with ability to invade the lymphatic or vascular channels to spread to regional lymph nodes and distant sites. 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| fulltext | fulltext |
| identifier | ISSN: 0262-0898 |
| ispartof | Clinical & experimental metastasis, 2022-02, Vol.39 (1), p.85-99 |
| issn | 0262-0898 1573-7276 |
| language | eng |
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| source | MEDLINE; SpringerLink Journals |
| subjects | Autocrine signalling Biomedical and Life Sciences Biomedicine Cancer Cancer Research Cell proliferation Channels Endothelial Cells Evolution Fibroblasts Genomics Hematology Heterogeneity Humans Immune system Lymph nodes Lymph Nodes - pathology Microenvironments Mutation Neoplasms - blood supply Oncology Pericytes Review Stromal cells Surgical Oncology Tumor Microenvironment - genetics |
| title | Cancer microenvironment and genomics: evolution in process |
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