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Barriers in the Tumor Microenvironment to Nanoparticle Activity
Published in Dan Peer, Handbook of Harnessing Biomaterials in Nanomedicine, 2021
Hanan Abumanhal-Masarweh, Lilach Koren, Omer Adir, Maya Kaduri, Maria Poley, Gal Chen, Aviram Avital, Noga Sharf Pauker, Yelena Mumblat, Jeny Shklover, Janna Shainsky-Roitman, Avi Schroeder
Cancer-associated fibroblasts (CAFs) are a main component in the heterogeneous cells’ complex network within the tumor microenvironment [100]. CAFs are often the dominant cell type within a solid tumor cell population and act as tumor promoters by expressing and secreting various growth factors, metabolites, cytokines and enzymes that induce cancer cells proliferation [101, 102]. In advanced stages of cancer, these cells produce matrix metalloproteinases (MMPs) leading to ECM degradation, thus enabling cancer cell’ motility and invasion [103, 104]. On the other hand, CAFs overexpressing ECM components such as fibronectin and collagen increase ECM rigidity due to cross-linking [105, 106]. As a result of ECM stiffness along with tumor solid stress, drug molecules and nanoparticles effective uptake and penetration into cancer cells is hindered [107].
Biomaterials in Cancer Research
Published in Heather N. Hayenga, Helim Aranda-Espinoza, Biomaterial Mechanics, 2017
Cancer arises from the uncontrolled proliferation of cells leading to the formation of clinically detectable solid tumors. While benign tumors stay in their original locations, high mortality in cancers is attributed to metastasis, that is, the spreading of cancer cells to distant tissues eventually leading to their destruction. Behavior of cancer cells is dictated by factors in the tumor microenvironment; these include the extracellular matrix (ECM), blood vessels, and noncancerous cells including immune cells and fibroblasts. The ECM exhibits dynamic remodeling in response to pathological condition. Tumor development is accompanied with the stiffening of the surrounding matrix (Egeblad et al. 2010; Provenzano et al. 2006), which results in alterations of nearly 1500 genes as reported in human mammary epithelial cells (Alcaraz et al. 2008). Proliferation of cancer cells in a confined environment results in a microenvironment that is oxygen deprived (i.e., hypoxic); upregulation of hypoxia-inducible factor (HIF-1) in turn activates the vascular endothelial growth factor (VEGF) (Liao and Johnson 2007) leading to sprouting of new blood vessels (angiogenesis) (Ferrara 2002). Additionally, the tumor microenvironment consists of normal fibroblasts that are activated to form cancer-associated fibroblasts (CAFs) (Kalluri and Zeisberg 2006). These CAFs play a crucial role in the development of tumor, angiogenesis as well as metastasis (Elenbaas and Weinberg 2001; Orimo et al. 2005; Vered et al. 2010). The cancer cells slowly breach the basement membrane, invade the blood vessels, and relocate to distant locations in the body (Figure 4.1). In recent years, in addition to the enormous research carried out to understand the genetic and molecular basis of cancer, given the role of ECM alterations in driving cancer progression (Lu et al. 2012), and the close cross talk between cancer cells and stromal cells (Pollard 2004), targeting the tumor microenvironment has been the focus of many evolving therapies (Engels et al. 2012).
Introduction to Cancer, Conventional Therapies, and Bionano-Based Advanced Anticancer Strategies
Published in D. Sakthi Kumar, Aswathy Ravindran Girija, Bionanotechnology in Cancer, 2023
Cancer associated fibroblasts (CAFs) have been shown to either promote the growth, spread, and survival of tumors through improvement in functionality or to retard tumorigenesis via unknown mechanisms [83]. At an early stage of tumor development, CAFs can mediate a tumor-enhancing inflammation derived by interleukin-1β [84].
Understanding the complex microenvironment in oral cancer: the contribution of the Faculty of Dentistry, University of Otago over the last 100 years
Published in Journal of the Royal Society of New Zealand, 2020
Alison Mary Rich, Haizal Mohd Hussaini, Benedict Seo, Rosnah Bt Zain
Research in OSCC tumour microenvironment (TME) began to intensify at the University of Otago with the establishment of the Oral Molecular and Immunopathology Research Group (OMIRG) in 2007 under the umbrella of Sir John Walsh Research Institute. The OMIRG is based in the Oral Pathology Centre, which also operates New Zealand’s only official Oral Pathology Tissue Bank. Initially, our focus was on the interactions of immune cells and cytokines with OSCC tumour cells. However, this research genre has expanded into various focus areas including angiogenesis, endoplasmic reticulum stress, DNA methylation, cancer-associated fibroblasts and exosomes. The aim of this paper is to showcase recent projects and developments relating to the OSCC TME undertaken in the OMIPRG and to highlight the historical journey that the Faculty has taken in an attempt to become the premier OSCC research centre in New Zealand. This paper also seeks to highlight our contribution to the conceptualisation of the development novel cancer therapies that have the flexibility to cope within the complex dynamics of tumour cells in the TME.