Relevant bibliographies by topics / TAM, miR-155, tumor microenvironment

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  1. Journal articles
  2. Dissertations / Theses

Academic literature on the topic 'TAM, miR-155, tumor microenvironment'

Author: Grafiati
Published: 9 March 2023
Last updated: 31 July 2025

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Journal articles on the topic "TAM, miR-155, tumor microenvironment"

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Szebeni, Gabor J., Csaba Vizler, Klara Kitajka, and Laszlo G. Puskas. "Inflammation and Cancer: Extra- and Intracellular Determinants of Tumor-Associated Macrophages as Tumor Promoters." Mediators of Inflammation 2017 (2017): 1–13. http://dx.doi.org/10.1155/2017/9294018.

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One of the hallmarks of cancer-related inflammation is the recruitment of monocyte-macrophage lineage cells to the tumor microenvironment. These tumor infiltrating myeloid cells are educated by the tumor milieu, rich in cancer cells and stroma components, to exert functions such as promotion of tumor growth, immunosuppression, angiogenesis, and cancer cell dissemination. Our review highlights the ontogenetic diversity of tumor-associated macrophages (TAMs) and describes their main phenotypic markers. We cover fundamental molecular players in the tumor microenvironment including extra- (CCL2, C
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Husain, Kazim, Krystal Villalobos-Ayala, Valentina Laverde, et al. "Apigenin Targets MicroRNA-155, Enhances SHIP-1 Expression, and Augments Anti-Tumor Responses in Pancreatic Cancer." Cancers 14, no. 15 (2022): 3613. http://dx.doi.org/10.3390/cancers14153613.

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Pancreatic cancer (PC) is a deadly disease with a grim prognosis. Pancreatic tumor derived factors (TDF) contribute to the induction of an immunosuppressive tumor microenvironment (TME) that impedes the effectiveness of immunotherapy. PC-induced microRNA-155 (miRNA-155) represses expression of Src homology 2 (SH2) domain-containing Inositol 5′-phosphatase-1 (SHIP-1), a regulator of myeloid cell development and function, thus impacting anti-tumor immunity. We recently reported that the bioflavonoid apigenin (API) increased SHIP-1 expression which correlated with the expansion of tumoricidal mac
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Gerloff, Dennis, Jana Lützkendorf, Rose K. C. Moritz, et al. "Melanoma-Derived Exosomal miR-125b-5p Educates Tumor Associated Macrophages (TAMs) by Targeting Lysosomal Acid Lipase A (LIPA)." Cancers 12, no. 2 (2020): 464. http://dx.doi.org/10.3390/cancers12020464.

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Tumor-associated macrophages (TAMs) are the most abundant immune cells in the tumor microenvironment, promoting tumor initiation, growth, progression, metastasis, and immune evasion. Recently it was shown that cancer cell-derived exosomes induce a tumor-promoting phenotype in TAMs. Exosome-loaded proteins, DNA, and RNAs may contribute to the macrophage reprogramming. However, the exact mediators and mechanisms, particularly in melanoma, are not known. In this study we examined the effects of cutaneous melanoma-derived exosomes on macrophage function and the underlying mechanisms. First, we sho
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Gajeton, Jasmine, Irene Krukovets, Santoshi Muppala, Dmitriy Verbovetskiy, Jessica Zhang, and Olga Stenina-Adognravi. "Hyperglycemia-Induced miR-467 Drives Tumor Inflammation and Growth in Breast Cancer." Cancers 13, no. 6 (2021): 1346. http://dx.doi.org/10.3390/cancers13061346.

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The tumor microenvironment contains the parenchyma, blood vessels, and infiltrating immune cells, including tumor-associated macrophages (TAMs). TAMs affect the developing tumor and drive cancer inflammation. We used mouse models of hyperglycemia and cancer and specimens from hyperglycemic breast cancer (BC) patients to demonstrate that miR-467 mediates the effects of high blood glucose on cancer inflammation and growth. Hyperglycemic patients have a higher risk of developing breast cancer. We have identified a novel miRNA-dependent pathway activated by hyperglycemia that promotes BC angiogene
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Murugan, Poongkavithai Vadevoo Sri, Gunassekaran Gowri Rangaswamy, and Byungheon Lee. "Abstract 2870: Inhibition of DNA methylation and histone deacetylation synergistically reprograms M2-polarized macrophages and inhibits tumor growth by upregulating miR-7083-5p." Cancer Research 83, no. 7_Supplement (2023): 2870. http://dx.doi.org/10.1158/1538-7445.am2023-2870.

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Abstract Reactivation of epigenetically suppressed miRs, in tumors, have become increasingly relevant in clinical practice. But less epigenetic studies have been performed on tumor associated M2 macrophages that plays a key role in the functional regulation of epithelial cancer development. In this study, we used 5-Aza-2’5’Aza-deoxycytidine (Aza) or decitabine (5-Aza) plus Trichostatin A (TSA) as epigenetic drugs to study the M2 macrophage modulation in the tumor microenvironment. Epigenetic therapy, not only modulated the M2 macrophages to a tumoricidal phenotype, but also strengthened the tu
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Arora, Shweta, Prithvi Singh, Shaniya Ahmad, et al. "Comprehensive Integrative Analysis Reveals the Association of KLF4 with Macrophage Infiltration and Polarization in Lung Cancer Microenvironment." Cells 10, no. 8 (2021): 2091. http://dx.doi.org/10.3390/cells10082091.

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Macrophage polarization and infiltration to the tumor microenvironment (TME) is a critical determining factor for tumor progression. Macrophages are polarized into two states—M1 (pro-inflammatory, anti-tumorigenic and stimulated by LPS or IFN-γ) and M2 (anti-inflammatory pro-tumorigenic and stimulated by IL-4) phenotypes. Specifically, M2 macrophages enhance tumor cell growth and survival. Recent evidences suggest the pivotal role of microRNAs in macrophage polarization during the development of Non-small cell lung cancer (NSCLC), thus proposing a new therapeutic option to target lung cancer.
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Banerjee, Hirendra, Christopher Krauss, Myla Worthington, et al. "Differential expression of efferocytosis and phagocytosis associated genes in tumor associated macrophages exposed to African American patient derived prostate cancer microenvironment." Journal of Solid Tumors 9, no. 2 (2019): 22. http://dx.doi.org/10.5430/jst.v9n2p22.

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Macrophages are the first line of defense in the cellular environment in response to any antigenic or foreign invasion. Since cancer cells express antigenic molecules and create a tumor microenvironment quite different from the normal cellular environment, macrophages will attack this cancer cells as foreign Invaders. However, the cancer cells adept their ability to suppress macrophage activity by secreting compounds/proteins through unknown mechanisms and train these macrophages to aid in tumorigenesis. These macrophages are commonly known as tumor associated macrophages (TAM). In this study,
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8

Chen, Hao, Chao Tang, Chun Tan, et al. "IL-2 Modulates TAMs Derived Exosomal MiRNAs to Ameliorate Hepatocellular Carcinoma Development and Progression." Journal of Oncology 2022 (February 21, 2022): 1–11. http://dx.doi.org/10.1155/2022/3445350.

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Background. Interleukin-2 (IL-2) is proved to play an irreplaceable role in antitumor regulation in numerous experimental and clinical trials. Tumor-associated macrophages (TAMs) are able to release exosomes to promote the development and progression of hepatocellular carcinoma (HCC) as essential component of microenvironment. In this study, our intention is to explore the effects of the exosomes from TAMs with IL-2 treatment on HCC development. TAMs were collected and cultured from HCC tissues. The exosomes from the TAMs treated with IL-2 (ExoIL2-TAM) or not (ExoTAM) were identified and used
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Yu, Haiyang, Jing Pan, Siyue Zheng, et al. "Hepatocellular Carcinoma Cell-Derived Exosomal miR-21-5p Induces Macrophage M2 Polarization by Targeting RhoB." International Journal of Molecular Sciences 24, no. 5 (2023): 4593. http://dx.doi.org/10.3390/ijms24054593.

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M2-like polarized tumor-associated macrophages (TAMs) are the major component of infiltrating immune cells in hepatocellular carcinoma (HCC), which have been proved to exhibit significant immunosuppressive and pro-tumoral effects. However, the underlying mechanism of the tumor microenvironment (TME) educating TAMs to express M2-like phenotypes is still not fully understood. Here, we report that HCC-derived exosomes are involved in intercellular communications and exhibit a greater capacity to mediate TAMs’ phenotypic differentiation. In our study, HCC cell-derived exosomes were collected and u
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Zelli, Veronica, Alessandra Corrente, Chiara Compagnoni, et al. "Ultrasound as a New Method for the Release and Identification of Novel microRNAs and Proteins as Candidate Biomarkers in Pancreatic Cancer." Cancers 17, no. 12 (2025): 1979. https://doi.org/10.3390/cancers17121979.

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Background/Objectives: Pancreatic cancer (PC) is among the most aggressive malignancies, often diagnosed at late stages. MicroRNAs (miRNAs) and proteins released from the tumor microenvironment into body fluids represent promising non-invasive biomarkers for early cancer detection. In this study, we took advantage of an innovative ultrasound (US)-based instrument (SonoWell®, Inno-Sol srl, Rome, Italy) to treat PC cells in order to promote and amplify the release of molecules, with the aim of identifying novel putative diagnostic PC biomarkers. Methods: Three human pancreatic adenocarcinoma cel
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Dissertations / Theses on the topic "TAM, miR-155, tumor microenvironment"

1

ZONARI, ERIKA. "Tumor infiltrating myeloid cells: modulators of tumor microenvironment and novel therapeutic targets." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2012. http://hdl.handle.net/10281/29814.

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Activation of a productive immune response requires transient upregulation of miR155 in the hematopoietic compartment. In order to investigate miR-155 in the context of tumor-associated immune responses, we stably knocked down (KD) miR-155 in the myeloid compartment of MMTV-PyMT mice (PyMT), a mouse model of spontaneous breast carcinogenesis that closely mimics tumor-host interactions seen in humans. Notably, myeloid cell specific miR-155 KD significantly accelerated tumor growth, as reflected by increased tumor mass and more pronounced secondary hematopoietic changes, i.e. leukocytosis and an
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