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Introduction to Cancer, Conventional Therapies, and Bionano-Based Advanced Anticancer Strategies
Published in D. Sakthi Kumar, Aswathy Ravindran Girija, Bionanotechnology in Cancer, 2023
Cancer is not just a mass of malignant cells, but a complex system to which various cells are recruited to the environment and can be transformed by cancer cells. The interplay between malignant cells and non-malignant cells create the microenvironment of cancer/tumor [62]. This microenvironment is created by cancer itself and influenced by cancer-induced interactions. Cells found in the cancer microenvironment generally include proliferating cancer cells, tumor stroma, inflammatory cells, and other associated tissue cells and blood vessels. The tumor microenvironment is a unique environment in which it emerges during the progression of the tumor because of the interaction of cancer with the host. In addition, its cellular events are orchestrated and dominated by the tumor itself [63].
Cancer and exercise
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Tormod S. Nilsen, Pernille Hojman, Henning Wackerhage
Lastly, infiltrates of immune cells play an important role in the tumour environment. Cytotoxic immune cells, i.e. NK and CD8 T cells acts to control tumour growth through eradication of cancer cells, and high levels of these immune cells within a tumour is associated with a better prognosis. In contrast, other immune cell subtypes may add to the pro-inflammatory profile of the intratumoral microenvironment. If left uncontrolled, this pro-inflammatory milieu might promote tumour growth through the release of various growth factors. This process mimics wound healing, and tumours have been described as “wounds that do not heal” (22).
Myeloid Growth Factors in the Lung
Published in Jason Kelley, Cytokines of the Lung, 2022
Jack Gauldie, Manel Jordana, Gerald Cox
Respiratory structural cells in inflamed or involved tissue are likely to be sources of locally produced CSFs. In addition, inflammatory cells present in the tissue may add to the cytokine makeup of the microenvironment. In turn, the microenvironment dictates the response of further inflammatory cell accumulation, and this cascade of events contributes to continual activation, leading to the type of abnormalities seen in chronic inflammatory diseases such as IPF, nasal polyposis, and asthma. The roles played by respiratory cell-derived CSFs are more consistent with the propagation and enhancement of cellular inflammation than a reparative or anti-inflammatory role. Regardless, the broad spectrum of activities supported by these cytokines, and the multiple cells that are capable of producing them in the lungs and airways, indicate that the presence of CSFs in respiratory tissue is a significant event in lung defense, and that further direct examination of tissue is likely to lead to a clearer understanding of the function of colony-stimulating factors in the host response of the lung.
Bone morphogenetic protein (BMP)9 in cancer development: mechanistic, diagnostic, and therapeutic approaches?
Published in Journal of Drug Targeting, 2023
Ali G. Alkhathami, Mustafa Ryadh Abdullah, Muhjaha Ahmed, Hanan Hassan Ahmed, Sarab W. Alwash, Zahra Muhammed Mahdi, Fahad Alsaikhan, Ayed A. Dera
Other than tumour cells, the tumour microenvironment is composed of several different components, including fibroblasts, immune cells, mesenchymal stem cells, myeloid cells, cytokines and growth factors, and extracellular matrix. Meanwhile, mesenchymal stem cells (MSCs), which produce a variety of factors, play a pivotal role in tumour progression and tumour stemness. MSC-produced IL-6 and IL-8 are two important cytokines that are involved in tumour cell growth and metastasis [65]. These two factors, by inducing ERK/MAPK and NF-κB signalling pathways, contribute to the invasion of lung adenocarcinoma into the bone. Wang et al. have shown that BMP9 regulates cross-talk between MSCs and A549 lung adenocarcinoma cells through decreasing IL-6 and IL-8 production from MSCs and thereby reversed MSC-induced growth and metastasis of A549 cells in vitro [45]. In a co-culturing system composed of MDA-MB231 breast cancer cells and HS-5 bone marrow-derived mesenchymal cells, it was also demonstrated that BMP9 inhibited MSC-induced tumour cell migration and invasion (by blocking AKT signalling) and promoted osteogenic differentiation (by inhibiting RANKL and IL-6) and proliferation of MSCs through inducing Wnt/β-catenin pathway [28]. These two studies indicated that BMP9 could regulate cross-talk between tumour cells and tumour stroma in favour of tumour regression.
The role of immunotherapy in fusion-driven lung cancer
Published in Expert Review of Anticancer Therapy, 2021
Aaron C. Tan, Johan Chan, Mustafa Khasraw
The fundamental underlying biology of fusion-driven cancers may ultimately be responsible for this poor response. Fusion-driven cancers are known to generally exhibit lower tumor mutation burden (TMB) [11,12]. This is of heightened relevance given the increasing evidence for TMB as a biomarker for immunotherapy in NSCLC [13]. Moreover, the immune microenvironment and infiltrating immune cell populations likely play a significant role. Targetable gene fusions are more frequently identified in never smokers and younger patients, potentially influencing both the immune microenvironment and TMB. Although there have been limited studies on PD-L1 expression, ALK rearrangements may be associated with PD-L1 overexpression [14–16]. However, this may be accompanied by low rates of concurrent PD-L1 expression and CD8+ tumor-infiltrating lymphocytes (TILs) [17]. These issues are further compounded by challenges in testing and interpretation of both TMB and PD-L1 status [18]. Even so, results from the IMpower150 study discussed in further details below, demonstrated that anti-angiogenic therapy with bevacizumab in combination with chemotherapy and anti-PD-1 inhibition may potentially exert immunomodulatory effects on the tumor immune microenvironment to enhance the efficacy of immunotherapy [19]. Therefore, this suggests strategies for immunotherapy in fusion-driven NSCLC may need to harness rational combination therapies to overcome biological limitations.
Human Amniotic Epithelial Cells Promote the Proliferation of Human Corneal Endothelial Cells by Regulating Telomerase Activity via the Wnt/β-catenin Pathway
Published in Current Eye Research, 2021
Jiayan Liu, Ye Wen, Wei Luo, Yingying Liu, Xiangyin Sha
The cellular microenvironment plays an important regulatory role in the proliferation, apoptosis and immunity of adult cells.20 Studies have found that the cellular microenvironment can enable adult cells to obtain a stronger proliferative capacity, which not only helps people to obtain a large number of cells for clinical application but also facilitates further research on anti-aging and prevention and treatment of ageing degenerative diseases.21,22 Among microenvironments, the ability of the embryonic stem cell (ESs) microenvironment to regulate differentiation and proliferative capacity has been verified.23,24 In this study, we isolated and cultured HAECs and collected the HAEC culture supernatants and found that these supernatants can promote the proliferation of HCEnCs, increase telomerase activity and activate the Wnt/β-catenin pathway. Combined with our previous research,12,13 we infer that the human amniotic epithelial cell microenvironment can promote the proliferation of human corneal endothelial cells by regulating telomerase activity via the Wnt/β-catenin pathway.