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肺癌中的代谢重编程及其对治疗反应的潜在影响。

The Metabolic Remodelling in Lung Cancer and Its Putative Consequence in Therapy Response.

机构信息

CEDOC, Chronic Diseases Research Centre, NOVA Medical School | Faculdade de Ciências Médicas, Universidade NOVA de Lisboa, Lisbon, Portugal.

Instituto Português de Oncologia de Lisboa Francisco Gentil (IPOLFG), Lisbon, Portugal.

出版信息

Adv Exp Med Biol. 2020;1219:311-333. doi: 10.1007/978-3-030-34025-4_16.

DOI:10.1007/978-3-030-34025-4_16
PMID:32130706
Abstract

Lung cancer is the leading cause of cancer-related deaths worldwide in both men and women. Conventional chemotherapy has failed to provide long-term benefits for many patients and in the past decade, important advances were made to understand the underlying molecular/genetic mechanisms of lung cancer, allowing the unfolding of several other pathological entities. Considering these molecular subtypes, and the appearance of promising targeted therapies, an effective personalized control of the disease has emerged, nonetheless benefiting a small proportion of patients. Although immunotherapy has also appeared as a new hope, it is still not accessible to the majority of patients with lung cancer.The metabolism of energy and biomass is the basis of cellular survival. This is true for normal cells under physiological conditions and it is also true for pathophysiologically altered cells, such as cancer cells. Thus, knowledge of the metabolic remodelling that occurs in cancer cells in the sense of, on one hand, surviving in the microenvironment of the organ in which the tumour develops and, on the other hand, escaping from drugs conditioned microenvironment, is essential to understand the disease and to develop new therapeutic approaches.

摘要

肺癌是全世界男性和女性癌症相关死亡的主要原因。传统化疗未能为许多患者提供长期益处,在过去十年中,人们在理解肺癌的潜在分子/遗传机制方面取得了重要进展,从而揭示了其他几种病理实体。考虑到这些分子亚型以及有前途的靶向治疗方法的出现,疾病的有效个体化控制已经出现,但仅使一小部分患者受益。尽管免疫疗法也作为新的希望出现,但大多数肺癌患者仍无法获得该疗法。能量和生物量的代谢是细胞存活的基础。在生理条件下,正常细胞如此,病理生理改变的细胞(如癌细胞)也是如此。因此,了解癌细胞发生的代谢重编程对于理解疾病和开发新的治疗方法至关重要,这种代谢重编程一方面是为了在肿瘤发生的器官的微环境中存活,另一方面是为了逃避药物调节的微环境。

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本文引用的文献

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Prognostic role of tumour-infiltrating T lymphocytes in stage IIA (T3N0) colon cancer: A broad methodological study in a fairly homogeneous population.肿瘤浸润 T 淋巴细胞在 IIA 期(T3N0)结肠癌中的预后作用:在相当同质人群中的广泛方法学研究。
Ann Diagn Pathol. 2019 Aug;41:69-78. doi: 10.1016/j.anndiagpath.2019.05.007. Epub 2019 May 16.
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Current status of immune checkpoint inhibition in early-stage NSCLC.早期非小细胞肺癌的免疫检查点抑制现状。
Ann Oncol. 2019 Aug 1;30(8):1244-1253. doi: 10.1093/annonc/mdz175.
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IL-17A-stimulated endothelial fatty acid β-oxidation promotes tumor angiogenesis.
HS合成酶是肺癌个体化治疗中的潜在决定因素。
Antioxidants (Basel). 2023 Dec 28;13(1):51. doi: 10.3390/antiox13010051.
IL-17A 刺激内皮细胞脂肪酸 β-氧化促进肿瘤血管生成。
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Metabolic enzymes expressed by cancer cells impact the immune infiltrate.癌细胞表达的代谢酶会影响免疫浸润。
Oncoimmunology. 2019 Mar 30;8(6):e1571389. doi: 10.1080/2162402X.2019.1571389. eCollection 2019.
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Metabolic reprogramming toward oxidative phosphorylation identifies a therapeutic target for mantle cell lymphoma.向氧化磷酸化代谢重编程鉴定出治疗套细胞淋巴瘤的一个治疗靶点。
Sci Transl Med. 2019 May 8;11(491). doi: 10.1126/scitranslmed.aau1167.
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Asparaginase combined with discontinuous dexamethasone improves antileukemic efficacy without increasing osteonecrosis in preclinical models. asparaginase 联合间断地塞米松治疗可提高临床前模型的抗白血病疗效,而不增加骨坏死。
PLoS One. 2019 May 6;14(5):e0216328. doi: 10.1371/journal.pone.0216328. eCollection 2019.
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Mol Carcinog. 2019 Jul;58(7):1118-1133. doi: 10.1002/mc.22996. Epub 2019 Mar 4.
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GSK-3β regulates the endothelial-to-mesenchymal transition via reciprocal crosstalk between NSCLC cells and HUVECs in multicellular tumor spheroid models.GSK-3β 通过 NSCLC 细胞和 HUVECs 之间的相互串扰调节多细胞肿瘤球体模型中的血管内皮到间充质转化。
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