Details of optimized design parameters and results of the proposed SPR biosensors [86].
\\n\\n
Released this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\\n\\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'IntechOpen is proud to announce that 179 of our authors have made the Clarivate™ Highly Cited Researchers List for 2020, ranking them among the top 1% most-cited.
\n\nThroughout the years, the list has named a total of 252 IntechOpen authors as Highly Cited. Of those researchers, 69 have been featured on the list multiple times.
\n\n\n\nReleased this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\n\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
\n'}],latestNews:[{slug:"stanford-university-identifies-top-2-scientists-over-1-000-are-intechopen-authors-and-editors-20210122",title:"Stanford University Identifies Top 2% Scientists, Over 1,000 are IntechOpen Authors and Editors"},{slug:"intechopen-authors-included-in-the-highly-cited-researchers-list-for-2020-20210121",title:"IntechOpen Authors Included in the Highly Cited Researchers List for 2020"},{slug:"intechopen-maintains-position-as-the-world-s-largest-oa-book-publisher-20201218",title:"IntechOpen Maintains Position as the World’s Largest OA Book Publisher"},{slug:"all-intechopen-books-available-on-perlego-20201215",title:"All IntechOpen Books Available on Perlego"},{slug:"oiv-awards-recognizes-intechopen-s-editors-20201127",title:"OIV Awards Recognizes IntechOpen's Editors"},{slug:"intechopen-joins-crossref-s-initiative-for-open-abstracts-i4oa-to-boost-the-discovery-of-research-20201005",title:"IntechOpen joins Crossref's Initiative for Open Abstracts (I4OA) to Boost the Discovery of Research"},{slug:"intechopen-hits-milestone-5-000-open-access-books-published-20200908",title:"IntechOpen hits milestone: 5,000 Open Access books published!"},{slug:"intechopen-books-hosted-on-the-mathworks-book-program-20200819",title:"IntechOpen Books Hosted on the MathWorks Book Program"}]},book:{item:{type:"book",id:"1723",leadTitle:null,fullTitle:"DNA Methylation - From Genomics to Technology",title:"DNA Methylation",subtitle:"From Genomics to Technology",reviewType:"peer-reviewed",abstract:"Epigenetics is one of the most exciting and rapidly developing areas of modern genetics with applications in many disciplines from medicine to agriculture. 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Besides the upgrade of LHC to higher luminosity and center of mass energy, a large number of novel international high energy physics facilities is currently in consideration, including, among others, the International Linear Collider (ILC), the Compact Linear Collider (CLIC), the Circular Electron Positron Collider (CEPC), the Super Proton Proton Collider (SPPC), and the Future Circular Collider (FCC). The first aim of this book is to provide an overview of the physics case of such novel facilities, with particular focus on the discovery potential beyond the Physics beyond the Standard Model. The second aim of the book is to outline novel detection technologies under development in order to fulfill the demanding experimental conditions of future facilities, with particular focus on sensors, calorimetry, and tracking detectors. Cross-disciplinary applications of novel theoretical findings and technologies play an important role in modern research. Therefore, the book also aims to show how novel theories and technologies developed for future facilities can be applied to develop the new generation of nuclear medical equipment.
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This requires extensive analysis of developing trends in scientific research in order to offer our readers relevant content. Creating the book catalogue is also based on keeping track of the most read, downloaded and highly cited chapters and books and relaunching similar topics. I am also responsible for consulting with our Scientific Advisors on which book topics to add to our catalogue and sending possible book proposal topics to them for evaluation. Once the catalogue is complete, I contact leading researchers in their respective fields and ask them to become possible Academic Editors for each book project. Once an editor is appointed, I prepare all necessary information required for them to begin their work, as well as guide them through the editorship process. I also assist editors in inviting suitable authors to contribute to a specific book project and each year, I identify and invite exceptional editors to join IntechOpen as Scientific Advisors. 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Venkateswarlu",coverURL:"https://cdn.intechopen.com/books/images_new/371.jpg",editedByType:"Edited by",editors:[{id:"58592",title:"Dr.",name:"Arun",surname:"Shanker",slug:"arun-shanker",fullName:"Arun Shanker"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"878",title:"Phytochemicals",subtitle:"A Global Perspective of Their Role in Nutrition and Health",isOpenForSubmission:!1,hash:"ec77671f63975ef2d16192897deb6835",slug:"phytochemicals-a-global-perspective-of-their-role-in-nutrition-and-health",bookSignature:"Venketeshwer Rao",coverURL:"https://cdn.intechopen.com/books/images_new/878.jpg",editedByType:"Edited by",editors:[{id:"82663",title:"Dr.",name:"Venketeshwer",surname:"Rao",slug:"venketeshwer-rao",fullName:"Venketeshwer Rao"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"4816",title:"Face Recognition",subtitle:null,isOpenForSubmission:!1,hash:"146063b5359146b7718ea86bad47c8eb",slug:"face_recognition",bookSignature:"Kresimir Delac and Mislav Grgic",coverURL:"https://cdn.intechopen.com/books/images_new/4816.jpg",editedByType:"Edited by",editors:[{id:"528",title:"Dr.",name:"Kresimir",surname:"Delac",slug:"kresimir-delac",fullName:"Kresimir Delac"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"51782",title:"Is Extracellular Matrix a Castle Against to Invasion of Cancer Cells?",doi:"10.5772/64495",slug:"is-extracellular-matrix-a-castle-against-to-invasion-of-cancer-cells-",body:'\nExtracellular matrix (ECM) was synthesized and secreted by embryonic cells starting from the early stages of its development. Our knowledge on the composition, structure, and function of ECM increased significantly in recent years. The most prominent among these is that extracellular microenvironment holds a critical importance in cellular growth, survival, differentiation, and morphogenesis [1].
\nThe major role played by the local microenvironment or niches in the arrangement of cellular behavior is gradually accepted more and more in cancer biology [2–5]. The fact that extracellular matrix is a dynamic source in the progression of cancer became the center of attention for researchers [1, 5–7].
\nECM affects negatively multiple proteases in remodeling, but it should be debated whether proteolysis constitutes a mandatory step in tissue invasion [8]. Many groups reported that the crossed structural barriers of cancer cells may be transferred to ECM only via the proteolytic pathway. Yet, others suggested that the neoplastic cells progressed toward the matrix by pushing or suppressing without proteases [9–12]. No matter what the route is, neoplastic cells invade the two major subtypes of ECM, namely basal membrane and interstitium [13–17].
\nAbnormal ECM promotes cancer progression. (A) ECM remodeling is tightly controlled to ensure organ homeostasis and functions. Normal ECM dynamics are essential for maintaining tissue integrity and keep rare tumor‐prone cells, together with resident fibroblasts, eosinophils, macrophages, and other stromal cells, in check by maintaining an overall healthy microenvironment. (B) With age or under pathological conditions, tissues can enter a series of tumorigenic events. One of the earlier events is the generation of activated fibroblasts or CAFs (stage 1), which contributes to abnormal ECM buildup and deregulated expression of ECM remodeling enzymes (stage 2). Abnormal ECM has profound impacts on surrounding cells, including epithelial, endothelial, and immune cells and other stromal cell types. Deregulated ECM promotes epithelial cellular transformation and hyperplasia (stage 3). (C) In late‐stage tumors, immune cells are often recruited to the tumor site to promote cancer progression (stage 4). In addition, deregulated ECM affects various aspects of vascular biology and promotes tumor‐associated angiogenesis (stage 5). Creation of a leaky tumor vasculature in turn facilitates tumor cell invasion and metastasis to distant sites (stage 6). (D) At distant sites, cancer cells leave the circulation and take hold of the local tissue. Together with local stromal cells, cancer cells express ECM remodeling enzymes and create a local metastatic niche. Abnormal niche ECM promotes extravasation, survival, and proliferation of cancer cells (stage 7). At later stages when cancer cells awake from dormancy, abnormal ECM turns on the angiogenic switch (stage 8), presumably using a mechanism similar to that used at the primary site (stage 5), and promotes the rapid growth of cancer cells and an expansion of micrometastasis to macrometastasis (see ref. [5]).
The dissemination of tumors is a complex process occurring in a sequential series which can be named as a sequence of invasive‐metastatic events (Figure 1). These phases are composed of local invasion, entry into blood and lymphatic vessels (intravasation), intravenous journey, exit from the veins (extravasation), development of micrometastases, and finally the growth of the micrometastases into macroscopic tumors [18, 19]. As it might be expected, any one of these phases may be interrupted by factors associated with the tumor or host. The series of metastatic events may also be divided into two phases, namely (1) ECM invasion and (2) intravenous dissemination of tumor cells and their homing in distant tissues/organs [20].
\nSummary of ECM functions in development. The ECM is multi‐functional and can influence multiple biochemical and mechanical processes simultaneously. This figure illustrates different functional states of the ECM and their biological contexts. The five categories are not mutually exclusive. When interpreting ECM loss‐of‐function phenotypes, one should consider that multiple processes may be compromised thus specific roles of individual ECM components are difficult to glean. A couple of important properties of ECM are not illustrated in this cartoon. First, ECMs are highly dynamic and can be modified by the cells that come into contact with them creating a bi‐directional mode of cell‐matrix communication. Second, ECM‐ECM interactions vary the chemical and mechanical composition of the extracellular microenvironment. In this review, we incorporate several examples of how the functions of ECM are utilized during embryonic development (see ref. [1]).
As known, human tissues are composed of a series of compartments separated from each other by two types of ECMs, namely basal membranes and interstitial connective tissues. Although organized in different manners, each ECM type is composed of collagens, glycoproteins, and proteoglycans [21].
\nIn addition to the ECM molecules, the general critical functions are important also for developmental events (Figure 2). Extracellular compartment comprises various ECM components and this organization and composition modifies the development with the initiation of fertilization. The most prominent characteristic of cell‐ECM interaction is that it is mutual. On one hand, cells are continuously formed, destroyed, or rearranged. ECM components modify one or multiple characteristics of ECM. On the other hand, as ECM arranges different cellular behaviors, this will impact adjacent cells as a result of any different cellular activity and modify its behaviors [22]. This feedback regulating mechanism between the cells and ECM enables rapid adaptation to the surrounding of cells and tissues [23].
\nThe extracellular matrix (ECM) structure is dynamic and may be destroyed by the enzyme family known as the matrix metalloproteinases (MMPs). These enzymes are actually secreted by stromal cells or heparinase (this is an endoglycosidase enzyme which separates heparin sulfate chains expressed and secreted particularly by tumor cells). Thus, the microenvironment may contribute to tumor dormancy or metastatic growth with the impact of MMPs. The expression and secretion of MMPs by leukocytes and macrophages may lead to the release of angiostatic factors inhibiting angiogenesis and metastatic growth from ECM. These anti‐angiogenesis factors comprise endostatin, restin, arrestin, three chains of collagen IV, and macrophage elastase [24]. Similarly, stromal MMPs may release cytokines and angiogenic factors affiliated with ECM such as fibroblast growth factor (FGF) and vascular endothelial growth factor (VEGF) and may initiate the angiogenic switch required for the transition from micrometastatic dormancy to metastatic growth. MMPs may also contribute to the formation of a suitable place for the transition from dormancy to metastatic growth. For instance, modifications in ECM components, such as the arrangement and production of type I collagen and fibronectin, were detected in gene expression signals associated with metastasis and poor prognosis in breast cancer [25]. Furthermore, the leukocyte secretion of MMP2 and MMP9 may activate latent transforming growth factor (TGF)‐beta localized in ECM. The activation of TGF‐beta may enhance the Type I collagen and lysyl oxidase expression synthesis and thus provide a suitable setting for metastatic growth [26]. On the other hand, the heparinase synthesis of tumor cells regulates the re‐arrangement and destruction of ECM in association with angiogenic factors promoting angiogenesis and tumor cell migration [27]. In summary, the crosstalk between dormant tumor cells and ECM regulated by stromal and tumor cells may control the initiation or termination of the dormant status of the cell.
\nTumor dormancy may be defined as the long‐term asymptomatic, non‐detectable and latent state of disseminated tumor cells (DTCs). This period is a stage where the residual disease exists, but is not clinically visible. The cells in dormant state avail of the capacity to grow slowly, escape treatment and the immune system of the host and to renew themselves. Tumor dormancy may contribute to the progression and relapse of the tumor metastatically both in local and distant sites. Cancer cells go into a dormant stage at the beginning of the disease or following the first treatment and may remain dormant even for years or for decades after the first treatment. The mechanisms and the sleep markers regulating the transition between the dormancy and proliferation phases have not been fully designated [28]. A part of the latent period in all patients may take place as the slow accumulation of the genetic modifications leading to immortality (TP53, RB1, P16 loss, and/or telomerase gain, etc.) and the transformations during and/or following carcinogenesis (Ras‐activating mutations, ERBB2 amplification, BRAF‐activating mutations, etc.). Breast and prostate tumors, melanoma, B‐cell lymphoma, and leukemia are malignancies displaying dormant cancer cells [29, 30].
\nThe metastatic growth of disseminated tumor cells (DTCs) from the primary tumor constitutes the main reason of cancer‐associated deaths. DTCs should survive around the circulation when they mix with blood and avoid physical damage and immune system attacks. Thus, DTCs adapt themselves to the new microenvironment of the secondary site and the reprogramming periods to the micrometastasis or quiescent state begin according to the characteristics of the microenvironment [31].
\nVarious metastasis suppressant genes responding to microenvironmental stress may regulate the dormancy. Metastasis suppressant genes have the capacity to encourage apoptosis or the dormancy of cells and prevent the development of metastasis. KISS‐1 is a tumor suppressor gene contained inside kisspeptins, and it has been demonstrated that the cells expressing kisspeptins remain dormant in many organs. Kangai 1 (Kai1/CD82) is a cell surface transmembrane protein which joins the inhibition of invasion and cancer cell migration by forming complexes with integrins. Furthermore, Kai 1 reduces the formation of distant metastasis upon binding to duffy antigen‐chemokine receptor on the surface of vascular endothelial cells [32]. It was demonstrated that in melanoma, colon, breast, and lung cancer models that the metastasis is suppressed via the Nm23–1H (NME1) protein [33, 34]. Mitogen‐activated protein kinase 4 (MKK4) is a specific kinase which plays a role in dormancy in the micrometastatic stage. MKK7 and MKK6 are other kinases with less metastasis suppressor effects. BRMS1, SMAD7, SSeCKS, RhoGD12, and CTGF are metastasis suppressor genes which play a potential role in dormancy. In case of more activated P38 in the cell, tumor cells may be encouraged to enter dormancy [35].
\nIt is necessary for a carcinoma first to pass through the basal membrane beneath and then through the interstitial tissue and consequently reach the circulation upon penetrating into the basal membrane in the veins. The referred cycle is repeated also when the tumor cells embolisms extravasate from a different site. Due to these reasons, a tumor cell may metastasize only when they pass through different and high number of basal membranes and at least two interstitial matrices [36, 37]. The ECM invasion is achieved in four steps.
\nThe first step of the series of metastatic events is the relaxation of tumor cells. E‐cadherins act as intercellular adhesives and their parts within the cytoplasm bind to β‐catenin. Neighboring E‐cadherin molecules hold together cells, and as also explained earlier, they may send anti‐proliferative signals over the β‐catenin sequestration [38]. The E‐cadherin function in almost all epithelial‐derived cancers is lost due to the mutations achieved via the β‐catenin gene activation of the E‐cadherin genes or the inadequate expression of the SNAIL and TWIST transcription factors suppressing the E‐cadherin expression [39, 40].
\nThe second step in the invasion is composed of the local disintegration of the basal membrane and the interstitial connective tissue. The tumor cells themselves secrete proteolytic enzymes or stimulate stroma cells such as fibroblasts and inflammatory cells so that they secrete proteases. It was expressed indirectly that many different protease families, such as matrix metalloproteinases (MMPs), cathepsin D and urokinase plasminogen activators, play a role in the achievement of the invasive characteristic in the tumor cell. Matrix metalloproteinases regulate the tumor invasion not only by reshaping the insoluble components of the basal membrane and interstitial matrix but also by releasing the growth factors at ECM [41]. Actually, the cleavage collagens and proteoglycans also have effects which promote chemotactic, angiogenic, and growth. For instance, MMP‐9 is a gelatinase which may release type IV collagen in the basal membrane of the epithelial and the veins; furthermore, it also stimulates the VEGF secretion of ECM from sequestered pools. Type IV collagenous activity, which is very rare in the benign tumors of the breast, large intestine, and stomach is at an abundant amount in the malignant tumors of the same organs. Meanwhile, indeed, an overexpression of metalloproteases and other proteases was reported for many tumors [42–44].
\nThe third step of tumor invasion involves changes in the adhesion of tumor cells to ECM proteins. There are receptors in the normal epithelial cells, such as integrin, which belong to the basal membrane laminin polarized on the basal surfaces and to collagens, and these help the cell to maintain its undifferentiated status at rest. While the loss of adhesion initiates apoptosis in normal cells, tumor cells are resistant to the death of cells to take place via this path [36]. Furthermore, the matrix itself is changed in a manner so as to promote invasion and the occurrence of metastasis. For instance, the cleavage of basal membrane proteins (collagen IV and laminin) by MMP‐2 or MMP‐9 creates new sites to which the receptors in the tumor cells may bind and stimulate the migration [42, 44].
\nThe final step of the tumor invasion is the locomotion of malignant cells. During the locomotion process, the tumor cells pass through fragmented basal membranes and proteolyzed matrix regions and translocate. The migration of cancerous cells is a multi‐phased process, which impacts the cytoskeleton in the actin structure at the end and where many receptor families and the signalization protein family play a role (Figure 3). This last step appears to be a process which is promoted and directed by cytokines deriving from the tumor cell such as the autocrine motility factor. Furthermore, the cleavage products of the matrix proteins (such as collagen and laminin) and some growth factors (such as insulin‐like growth factor I and II) have a chemotaxis effect on these cells.
\nMoreover, the stroma cells also produce paracrine effector factors such as HGF/SCF (hepatocyte growth factor/diffusion factor) which bind to the receptors on the tumor cells. HGF inhibition is as effective as standard chemotherapy in inhibiting local tumor growth [45]. The fact that the concentration of these factors is high in the peripheral region of glioblastoma multiform, which is a strong brain tumor with advanced invasion skills, supports the view that they play a role in motility [46].
\nSchematic model of enzymatic disruption of extracellular matrix at the tumor invasion zone: (A) The tumor‐surrounding extracellular matrix consists of a meshwork of collagen fibers (1) and interdispersed glycosaminoglycan‐containing proteoglycans (2) that provide swelling pressure to maintain tissue volume; (B) collagen molecules (3) are aligned in staggered fashion overlapping by one quarter of their length to form a cross‐striated collagen fiber (1). Covalent cross links (4) between neighboring collagen molecules are responsible for tensile strength and insolubility of the fiber meshwork. The interdispersed proteoglycans shows limited aggregation with hyaluronate (5). It is restricted from swelling by an intact collagen network; (C) collagen fibers are degraded by two enzymatic pathways: (a) proteinases (i.e., cathepsins, elastase, plasmin, thrombin) act as “cross‐linkases” (4) to liberate collagen monomers from fibers (6). Collagen monomers then denature (7), solubilize, and become susceptible to many proteinases. (b) Vertebrate collagenases specifically cleave the collagen triple helix at the ¾-¼ point between the NH2‐ and COOH‐termini (8). The resulting TCA and TCS fragments denature (9) and are further cleaved by neutral proteinases: (D) Collagen and concomitant proteoglycan degradation (10) transforms the matrix from an insoluble (solid) to a liquified (fluid) state. The remaining proteoglycans swell (11) due to breakdown of the restricting collagen network. These physical changes may allow locomotion and tumor cell penetration (see ref. [6]).
The structure of tumor‐associated ECM is basically different than that of the normal tissue stroma. Relaxed, non‐oriented fibrils and collagen I are significantly oriented with epithelia which are significantly linearized and attached in the breast tissue or are designed vertically to the tissue [41].
\nAbnormal ECM dynamics have been well documented in clinical studies as a sign of many diseases and cancer. For instance, excessive ECM production or decreased ECM destruction is evident in many organ fibroses [47]. The storage of various collagens containing collagen I, II, III, V, and IX increases during tumor formation [48]. These abnormal changes in the composition and rate of ECM may significantly modify the biochemical characteristics of ECM and potentialize the oncogenic effects of various growth factor signal pathways [49]. Increased collagen deposition or ECM stiffness may support cell survival and proliferation alone or with the upregulation of the integrin signal [50, 51].
\nIncreased collagen cross links and ECM stiffness stimulate ERK and PI3 kinase signal as a result of LOX overproduction and facilitate oncogenic transformation [47].
\nStudies have demonstrated that ECM is essential in the protection and achievement of tissue polarity and structure. Abnormal ECM dynamics may cause basal membranes to compromise as a physical barrier and facilitate tissue invasion of cancer cells by supporting epithelial mesenchymal transition [52, 53].
\nThe changes in ECM topography may facilitate the migration of cancer cells. Thickening and linearization are observed in collagen fibers in cancer cases, and these are mostly seen in tissue invasion and vascular tumor sites, which demonstrates that they may play an active role in this cancer cell invasion [41, 54].
\nTumor microenvironment plays a critical role in the progression of cancer and is the main factor determining the growth and survival of DTCs in prioritized metastatic sites [43, 55]. It was recently revealed that the stroma cells surrounding tumor cells constitute a variable environment which promotes or prevents tumor formation of mutual signalizations between the tumor and stroma cells and not as a static barrier that prevents the motility of tumor cells [56]. The congenital and adaptive immunity cells as well as fibroblasts are among stroma cells which interact with tumors. It was revealed in various studies that tumor‐accompanying cells contain ECM molecules, proteases, protease inhibitors, and genes encoding various growth factors in modified forms [57]. Dormant tumor cells are in close contact via the extracellular matrix via the integrin signalization pathway regulating tumor cell growth, migration, differentiation, and survival. Metastasis‐associated urokinase receptor (uPAR) causes tumor growth via fibronectin receptor alfa5beta1‐integrin activation and interaction. This complex enables the functioning of EFGR which promotes focal adhesion kinase (FAK) and adhesion to fibronectin and transfers mitogenic signals via Ras extracellular signal‐regulated kinase (ERK), respectively. In an in vitro study, the downregulation of uPAR and the loss of function of integrin reduced the proliferative signals from a fibronectin‐rich microenvironment which led to the transition from a tumorigenic status to a dormant status in human carcinoma cells. Furthermore, the blockade of uPAR, beta1‐integrinler, FAK or EGFR alone or in combination results in in vivo tumor suppression which is demonstrated to be associated with the induction of tumor cell dormancy [58, 59].
\nIn vivo ERK1/2 signalization revealed that dormancy derives from an almost complete full inhibition of the Raf‐MEK‐ERK pathway and triggers the stopping of cell cycle in the G0‐G1 phase as in the dormant cells. It was demonstrated that the mitogen‐activated protein kinase (MAPK) signalization cascade activated with (P38/c‐Jun N‐terminal kinase (JNK) has an impact as a tumor suppressor via various tumor suppressor (TP53 and Rb‐mediated) pathways and by the decrease of various oncogenic signals and become responsible for the stopping of the growth. The disruption of the UPAR complex activates the p38 MAPK signalization pathway. Proliferation in primary and secondary tumors requires a high ERK1/2/p38 MAPK, pathway activation—contrary to tumor dormancy. Thus, the molecular mechanisms of growth inhibition have become comprehensible during dormancy, which is observed both I the p38 MAPK pathway activation and ERK1/2 pathway inhibition [60].
\nThus, tumor cells maintain their existence within a complex and constantly changing environment in which ECM, fibroblasts, and the immunity system cells communicate with one another. The cells which cooperate with the referred environment in order to fulfill their bad intentions and may adapt themselves to this environment can be the most successful tumor cells.
\nWhen cells are transformed and the solid tumor mass formation is initiated, they lead to a modification in the phenotypes of the cells surrounding them. A transformation occurs in the extracellular matrix in addition to the modification in the cellular phenotype, and this tumor formation occurs simultaneously [57, 61]. It was recently discovered that increased matrix stiffness may also lead to the increase in the oncogenic YAP/TAZ complex increased in association with signal regulators comprising the Hippo signal pathway, enhanced cellular proliferation, decreased contact inhibition, increased cancer stem cell phenotype, and increased metastasis [62]. However, it was demonstrated in the recent publication by the authors that YAP/TAZ was not activate only at CAFs: Cancer associated fibroblasts, but that YAP/TAZ was necessary also for CAF development [63]. The authors demonstrated that CAF activation led to a matrix remodeling developing to increased stiffness with the myosin light‐chain 2 (MYL9/MLC) expression which plays a vital role in the formation of ECM. Another point pinpointed by these authors was that the YAP/TAZ activation was not specific only to CAFs, but that it was also revealed in the normal tissue fibroblasts surrounding the cancerous tissue.
\nThe growth of a tumor size requires an increase in the need for nutrients, oxygen, and waste exchange. Tumor vascularization constitutes the main path in metastases of cancer cells [36, 64].
\nWhen tumor cells reach the circulatory system, the host is likely to be destroyed by immune cells. Some tumor cells in the blood circulation aggregate and adhere on leukocytes in the circulation, particularly on thrombocytes, and cause embolism; thus, part of tumor cells in the circulation achieves a certain degree of protection against the antitumor effects of the effector cells of the host. However, the majority of tumor cells circulate alone in the circulation. During the extravasation of free tumor cells or the development of tumor embolism, the referred cells first adhere on the vascular endothelium and then enter the organ parenchyma upon passing through the basal membrane via mechanisms similar to those in the invasion process [64].
\nIt is possible to estimate the site of extravasation of tumor cells and the distribution of the metastases in the organs by looking at the site of the primary tumor and the vascular or lymphatic drainage (Figure 4). Most tumors metastasize in the first organ they encounter in the capillary bed upon entering the circulation. However, natural drainage paths may not easily explain the distribution of metastases in many cases. Some tumors such as lung cancers frequently metastasize in the adrenals, while they almost never spread to the skeletal muscle [65]. This organ tropism may be associated with the following described mechanisms:
\nECM role in tumor angiogenesis, lymphangiogenesis. Angiogenesis and lymphangiogenesis depend on the ECM. Tumor cells produce various components, including VEGF and angiogenic and antiangiogenic ECM fragments, to regulate blood vessel formation (stage 1). During branch initiation, endothelial cells secrete proteases to break down the basement membrane to grow out (stage 2). The outgrowth process of endothelial branching is propelled by at least two groups of cells: tip cells, which lead the migration toward the angiogenic chemoattractant source, and stalk cells, which depend on the ECM and its derivatives to survive and proliferate to provide building blocks for vessel formation (stage 3). Additionally, ECM components participate in cell migration and other aspects of tubulogenesis of blood vessels. Although details remain unclear, lymphangiogenesis depends on the ECM and, together with angiogenesis, provides routes for cancer cell metastasis and immune cell infiltration (see ref. [5]).
1. The expression of the ligands in the tumor cells and preferably of the adhesion molecules present in the endothelium of the target organs. 2. The expression of chemokines and their receptors. Chemokines contribute to the guided movements of leukocytes (chemotaxis), and cancer cells appear as cells which utilize similar tricks in order to settle in special tissues. Chemokine receptors named CXCR4 and CCR7 have a high expression in human breast cancer. The ligands of these receptors (CXCK12 and CCL21) are present in high amounts only in the organs where breast cancer cells have metastasized. Based on this observation, it was claimed that the blockage of chemokine receptors may limit metastases [44, 66].
\nWhen tumor cells reach their target, they may be colonized in that target. The factors regulating the referred colonization have not yet been fully understood. However, in order for tumor cells to proliferate after extravasation, they need a stroma that will accept them. In some cases, the target tissue may not carry a suitable environment identity for metastasis and is not the suitable soil, so to say, for the development of the tumor seeds. For instance, although the skeletal muscle is not rich in terms of vessels, it rarely becomes a stage for metastases [44].
\nBecause, the biochemical characteristics of ECM, which play an important role in tubulogenesis during tumor angiogenesis [67, 68] in the vein lumen formation blood vessel lumen formation [69], are different in terms of displaying different branching patterns and various elasticities in these fields [70].
\nWillis et al. drew attention to the astuteness in the invasion of the devilish hidden cancer cells in the review they published [7]. Many groups reached the conclusion that cancer cells acquire an amoeboid phenotype characterized by insensitivity to proteinous inhibitors and surpass type I collagen barriers [12]. Now we know that a wide spectrum of types of cancer cells are definitely dependent on MT1‐MMP when they are faced with cross‐linked Type I collagen barriers [12, 71].
\nStill, when cancer cells encounter structural barriers, they hold the potential to adapt themselves to a protease‐dependent position. Although there is limited information on the size of ECM pores, it is estimated via confocal reflection microscope that micropores range between of 40–10 μm2 and macropores of 40–1000 μm2 inside in vivo tissues [72–74]. These results increase the probability indicating that the collagen structure combined in an in vitro setting may not be repeated in a complex in vivo setting.
\nHowever, it should be noted that the defects in the migration of vascular smooth muscle cells, adipocytes differentiation, and stem cell origin displayed an in vitro setting duplication with the use of dense acid extracted type I collagen hydrogels in MT1‐MMP‐targeted mice [75–77]. Interestingly, the diameter of collagen fibers at in vivo neoplastic fields matched with the self‐polymerized collagen hydrogels prepared in acid extractor type I collagen under standard conditions [78].
\nThese results led to the thought that cancer cells may rapidly migrate to precleared tunnels via the proteolytic pathway through proteinaceous‐independent processes similar to those in the in vitro setting [11, 79–81].
\nAs cancer cells accumulate mutations or other molecular signals during the metastatic process, they are predisposed to become more easily malignant and lose contact with the surrounding cells and ECM in the primary tumor. These surrounding cells provide the opportunity for invasion. Thus, ECM and ECM‐associated adhesion proteins play a critical role in the metastatic process [82]. Therefore, Zacharia et al. [83] published a review describing roles of the new molecules named migfilin, mitogen‐inducible gene‐2 (Mig‐2), and Ras suppressor‐1 (RSU‐1) in the cell‐ECM adhesion fields. The authors reached the conclusion that cell‐ECM adhesion proteins are predisposed to function such as adaptor proteins in the form of multiple protein‐protein interaction in the cell‐ECM adhesion fields.
\nEven though the different effects in various types of cancer cells were discussed, they added that cell adhesion, which is crucial in terms of cell metastasis in many cases, supported cell invasion and apoptosis.
\nDespite the “skill” they display in moving away from the site in which they were first formed, tumor cells are rather ineffective in terms of forming colonies in distant organs. Millions of cells drop off even from small tumors every single day; even though macroscopic metastases have not developed, it is possible to identify these cells in the blood circulation and in small foci in the bone marrow. The dormant state of micrometastases, which is defined as the capacity to preserve their existence for a long period without any progression, was observed in breast and prostate cancer [29, 30, 44].
\nIn the studies demonstrating that ECM undertook a dynamic niche role in the progression of cancer in recent years [5–7], investigators indicated that the microenvironment or niche played a major role in the development of cancer. Abnormal ECM directly promotes cellular transformation and metastasis and impacted the progression of cancer [84].
\nA successful metastasis does not require local niche supporting only cancer cell development in the primary focus, but also necessitates the survival, colonization of the cancer cells invading the metastatic niches and their achievement of macrometastasis [85–87].
\nThe molecular mechanisms of colonization have just begun to be enlightened in mice models, but the view claiming that tumor cells impact normal stroma cells and secrete cytokines, growth factors and proteases, which transform the site of metastasis into an environment where cancer cells may live, appears to be suitable [88, 89].
\nAs metastatic mechanisms are better understood at a molecular level, it will be significantly easier for physicians to use these mechanisms as a treatment goal [90]. The identification of tissue‐specific signals involved in metastatic progression will open the way to new therapeutic strategies. For this purpose, the authors [91] reviewed recent progress in the field, with particular emphasis on the mechanisms of organ‐specific dissemination and colonization of breast cancer (Figure 5). Despite what has been described so far, it may not be possible to estimate exactly which cancer type may metastasize. But a noteworthy area of forthcoming cancer research will be to determine whether abnormal ECM could be an effective cancer therapeutic target. So we should understand how ECM composition and organization are normally maintained and how they may be deregulated in cancer. Then, we may protect the ECM as a castle against to invasion of cancer.
\nGene mediating organ‐specific breast cancer metastasis. Breast cancer genes promoting organ‐specific metastasis to bone, lung, and brain have been identified. They include proinflammatory molecules and chemokines/receptors (e.g., COX‐, CXCL12/CXCR4), matrix‐degrading and modifying enzymes (e.g., MMP1/2, LOX), adhesion and extracellular matrix molecules (e.g., VCAM‐1, TNC, OPN), transcription factors (e.g., ID1, KLF17), intracellular signaling proteins (e.g., SRC, NF‐_B), and cell communication proteins (JAGGED1, CTGF). Some genes promote seeding (e.g., ST6GALNAC5, AGPTL4), whereas others promote colonization (e.g., OPN, CXCR4) (see ref. [91]).
Surface plasmon resonance (SPR) biosensors have become one of the most promising, standard, and affordable technology due to prompt research and expansion of SPR phenomenon in the last two decades. Nowadays, SPR sensors are broadly implemented for numerous biological and biochemical analytes identification and characterization due to its high sensitivity, real-time monitoring, level free detection assay, small sample size, and reusable sensor chip [1, 2, 3, 4, 5]. To be detailed, the SPR biosensors are adopted to agriculture and food quality monitoring [6], security and safely analysis [7], in need of medical diagnostics, environmental monitoring, bio-imaging [8, 9, 10], cancer detection [11, 12], DNA hybridization [13, 14], enzyme detection [15], protein-protein, protein-DNA, and protein-virus hybridization [16, 17], microorganisms identifying [18], industrial appliance’s condition monitoring, temperature monitoring [19], gas sensing [20, 21], chemical and biochemical analysis [22, 23], pharmaceutical and biological molecule analysis [24, 25], oil condition monitoring [26], and so on. In the year 1902, Wood [27] first observed unexpected optical power attenuation characteristic at the time of measuring the reflection of light from metallic gratings. This phenomenon occurs due to absorbance and conversion of photon energy to surface plasma wave (SPW) which is the result of combined oscillation of excited electrons called surface plasmon polaritons (SPPs). This oscillating electron consumes maximum energy at a certain wavelength for a specific angle of incidence of light which is called resonance condition. That is why this phenomenon is named surface plasmon resonance (SPR). In 1968, Otto [28] and Kretschmann [29] introduced attenuated total internal reflection (ATR), which encouraged scientists and researchers to concentrate on the implementation of SPR sensing technology practically. In 1982, the SPR sensing technique was first demonstrated by Nylander and Liedberg [4, 30] for the practical application of gas sensing. After that, SPR sensing technology has been getting ceaselessly developing consideration from the scientific and academic network. In 1990, the SPR sensing instrument was first commercially produced and introduced to the market by Biacore AB. Since then a considerable number of manufacturers e.g. IBIS Technologies B.V., Graffinity pharmaceuticals, GWC Technologies, Bio-Red, AutoLab, Farfield Sensors, Genoptics Bio Interactions, Microvaccum, Biosensing Instrument, and SPR Navi have launched their SPR instruments to the market [17, 31].
\nDifferent optical techniques are currently proposed for sensing purposes, including Ramman scattering based sensors [32, 33], grating coupled sensors [34, 35], prism coupled sensors [36, 37], optical fiber-based sensors [38, 39], planner waveguide-based sensors [40, 41] etc. The optical biosensors basically work with the measurement of change in input incident light and detected light at the output terminal. To be specific, the change in phase, amplitude, wavelength, frequency, or polarization of light is measured at the output terminal of the sensors and the changes in these parameters are observed. Among them, the commonly used technique is observing the reflected light angle where maximum light is attenuated. This method is called angular interrogation approach with attenuated total internal reflection (ATR) that is applied usually in prism coupled devices. The performance of an optical sensor is basically measured in terms of its sensitivity, detection accuracy or detection limit, the figure of merits (FOM) and quality factor (QF), etc. The researchers and scientists are continuously working for the improvement of the performances of the SPR sensors [31, 42, 43, 44].
\nIn SPR biosensors, the most crucial parameters determining the characteristics of the sensors are plasmonic materials. Materials with adequate free electrons at their valance bands can be used as plasmonic materials. To be specific, metals e.g. gold (Au), aluminum (Al), silver (Ag), copper (Cu), etc. are a good candidate to be used as a plasmonic material [45, 46]. Al and Cu have not gained much interest to be used because of their high damping nature, prone to oxidation, corrosion, and interband transition characteristics. But Silver (Ag) can be nominated as a potential candidate for SPR sensors as it attributes outstanding optical properties, such as no interband transfer at the visible light frequency, small optical damping, and sharper resonance peak [46, 47, 48], etc. Using Ag in SPR sensors, better sensitivity can be captured, but it shows poor chemical stability as it creates brittle oxide layers with liquid analyte [49]. Some researchers have reported that applying bimetallic layer on the Ag surface can resolve this problem [50, 51]. On the other hand, Au is more chemically stable compared to Ag and free of corrosion and oxidation problems. But, gold offers a slightly higher damping loss and widen SPR curve that restricts the detection accuracy and figure of merits (FOM) of the sensors [52]. The sensitivity of Au-based sensors is also slightly lower because of the low biomolecular adsorption characteristics of the gold surface. In order to improve the sensitivity of the sensors, researchers recommended various approaches in which the application of hybrid structures (multilayer structures) are widely used [53, 54, 55, 56]. Various 2D materials are used in the hybrid configuration of SPR based sensors. A single atom thick carbon nanostructure (graphene) is often applied on the top of the plasmonic materials to avoid oxidation problems and increase the performance of the sensors because of its chemical inertness and high adsorption characteristics [57, 58]. There are also some other nanomaterials e.g. graphene oxides, graphene carbon nitrite (g-C3N4), transition metal dichalcogenides (TMDCs: MoS2, MoSe2, WS2, WSe2, PtSe2, SnSe2, etc.), transition metal chalcogenides (NbSe3, TaSe3), transition metal oxides (TMOs: LaVO3, LaMnO3), Black phosphorene (BP), hexagonal boron nitride (hBN), group IV elements [59, 60] and so on which are summarized in the Figure 1.
\n2D materials library where blue shaded materials are stable at ambient condition, green-shaded are probably stable, pink shaded are unstable at ambient condition but stable at inert condition. The gray shaded mistrials are 3D but can be exfoliated down to monolayers [60, 61].
This chapter mainly focuses on the recent trends applied for enhancing the performance of the Kretschmann configuration based prism coupled SPR sensors and their potential applications. The fundamental theory of SPR phenomena is presented first. Then, the method of angular interrogation utilizing attenuated total internal reflection and the performance measuring parameters of the SPR sensors are narrated. Finally, with their compressive architectures, recent developments of the prism coupled SPR sensors are discussed.
\nMetals are composed of positively charged nuclei with a lot of free electrons in their conduction band (surface of the metal). If an external electric field is applied close to the metal surface, free electrons are dislocated, resulting in an electric dipole [61]. A longitudinal oscillation has resulted from such electron transportation in a metal surface known as surface plasmons (SPs) [49]. To support the generated SPs a metal and dielectric interface is needed [46] whereas excitation of these SPs leads to an enhanced electromagnetic field resulting in a collective oscillation of free electrons or electron plasma [46, 61, 62]. The basic principle of the construction of SPR based sensors lies in the generation and propagation of electromagnetic waves called surface plasmon wave (SPW) due to the interaction of irradiating electric fields and the generated fields for dislocation of the electrons between the metal-dielectric interface [4]. The SPWs can only be produced by the incidence of a transverse magnetic (TM-) or plane (p-) polarized field as Maxwell’s equations supports no solution for transverse electric (TE-) polarized case [46]. Furthermore, the fact that electron oscillation means resistive losses. Thus, when an optical field appears at the metal-dielectric boundary, the SPW produces due to optical absorption of exponentially decaying evanescent waves. Mathematically, when the wave vector of the SPW is equal to the propagation constant of the irradiating lightwave, maximum absorption of evanescent field is observed leading to a strong SPW generation [63, 64]. This condition is called resonance condition. The propagating evanescent wave can be characterized by propagation constant βev\n as follows [10, 65]:
\nWhere λ, n, θ indicate the incident light wavelength, refractive index of the medium, and angle of incident of light at the metal surface, respectively. The equation as follows characterizes the SPW [66]:
\nWhere \n
Where the RI of plasmonic material (\n
Due to its outstanding performance characteristics, commercial standardization, and ease of manufacturing technology, the angular interrogation method using ATR has become more popular today among various SPR based sensors. When light is directly coupled to the metal-dielectric interface, due to a mismatch of momentum, the SPs are not sufficiently excited to generate SPWs [70]. Researchers have suggested several special arrangements called Otto configuration [71], Kretschmann configuration [72, 73] as visualized in Figure 2 to alter the momentum of the photon to couple with the SPPs leading to propagation of SPW. In prism based Otto configuration, there is a distance where a dielectric layer with a smaller RI is used between the prism and metal sheet on which the light is employed. On contrary, Kretschmann configuration the metallic layer is in direct contact with the prism. Among them, the Kretschmann configuration is the most popular solution to ensure the coupling of the strongest evanescent wave passing through the metal and generate SPW [53, 74, 75, 76]. In the Kretschmann configuration, the light is incident at the metal-dielectric interface through a high index prism [77].
\nSpecial Arrangements [74] e.g. (a) Kretschmann configuration, and (b) Otto configuration to match the momentum of incident photon and SPW.
Usually, the incident light bounces back from the interface while the evanescent field is induced by a portion of light penetrating through the metal. For a particular sensor configuration and light frequency, the momentum of the evanescent field is aligned with the wave vector of SPW at a specific angle called resonance angle [76]. Maximum light is coupled to the oscillating electrons at this resonance condition, leading to minimum reflection. If the reflected light is plotted concerning the incident angle, then a resonance dip of reflection spectrum is observed called SPR point which is highly responsive to the RI of the sensing medium. By interrogating this SPR point the analyte can be detected easily. The performance measuring parameters e.g. sensitivity, detection accuracy, FOM, and QF should be as high as possible to eliminate false positive detection. The sensitivity of the sensor operating on the angular interrogation approach depends on the change in the SPR point or resonance angle with a change in RI of the sensing medium. Figure 3 illustrates the SPR curve variation due to change in sensing medium RI where the resonance point is found at \n
Illustration of the SPR curve variation due to change in sensing medium RI.
A sensor’s detection accuracy, which depends on the width of the SPR curve, determines how quickly and accurately the SPR point can be measured by the sensor. It is inversely proportional to the width of SPR. If \n
Nowadays, the prime concern of scientists, researchers, and academicians are to enhance the performance of the SPR based sensor. To date, several attempts have been reported to attain highly sensitive sensors where the use of bimetallic coating and hybridization of numerous 2D materials along with plasmonic materials are the most popular approach to accommodate the angular interrogation approach. Benaziez S. et al. [81] reported a sensor where Ag is considered as an SPR active material. They showed that the addition of mostly used 2D material graphene on Ag surface enables to reduce the oxidation problem as well as increase the sensitivity up to 9.3%. Yet, the detection accuracy of the sensor is slightly reduced. Also, Rouf H. K. and Haque A. [82] proposed a hybrid structure using InP and Ti with the Ag-Au bimetallic configuration. Their sensor shows maximum sensitivity of 70.90 deg/RIU. Similarly, Mishra S. K. and their team [83] have demonstrated a configuration with excellent sensor sensitivity of 229 deg/RIU. They used a rarely used material Rhodium (Rh) with Ag to realize bimetallic configuration. Also, they used a silicon layer on the bimetallic layer to lessen the limitations of Ag. Likewise, N. Mudgal et al. [3] proposed a four-layer hybrid structure that consists of Au, molybdenum disulfide (MoS2), h-BN (hexagonal boron nitride), and graphene to detect urine glucose. The structure can enhance the sensor sensitivity up to 194.12 deg/RIU with the detection accuracy of 16.04/RIU. In the same way, Hailin Xu et al. [84] proposed an optical sensor with the graphene-Al-graphene sandwich structure where graphene prevents the oxidation issue of Al as well as enhances the sensor sensitivity 3.4 times more than only Al-based sensor. Besides, Wang M. et al. [85] suggested a sensor consisting of graphene, Tungsten disulfide (WS2), and Au-Ag bimetallic film. They observed that hybridization of single layer graphene and WS2 with Au-Ag bimetallic nanostructure leads to sensitivity up to 182.5 deg/RIU which is superior to Au-only based sensor. Incorporating the advantages of hybrid structure and bimetallic configuration, very recently Rahman M. et al. [86] also proposed a new configuration of SPR biosensors utilizing the newly emerged TMDC (PtSe2) embedded 2D materials as illustrated in Figure 4.
\nSchematic Illustration of SPR biosensor employing hybridization of 2D materials with Ag/Au [86].
In this configuration, a heterostructure of PtSe2/2D material (e.g., graphene, MoS2, WS2) has been employed to realize the hybrid configuration whereas BK7 prism is used as a coupler that increases the momentum of the evanescent wave to match with the wave vector of the SPW. The sensor comprises a thin layer (50 nm) of Au or Ag as an SPR active material between the prism coupler and PtSe2/2D material heterostructure. A monochromatic He-Ne laser source having a wavelength of 633 nm have been incorporated to excite the SPPs. The sensor parameters are altered and optimized varying the thickness of PtSe2 and number 2D material’s layer to get better performance where the results are revealed in Figure 5.
\nSensitivity variation due to change in the thickness of PtSe2, and number of (a) Graphene layer (b) MoS2 layer, (c) WS2 layer for BK7/Ag (50 nm)/PtSe2/2D materials (Graphene/MoS2/WS2) hybrid structure; and number of (d) Graphene layer, (e) MoS2 layer, and (f) WS2 layer for BK7/Au (50 nm)/PtSe2/2D materials (Graphene/MoS2/WS2) hybrid structure [86].
The effects of alteration of different parameters of PtSe2, and 2D materials have been analyzed comprehensively and two new sensors have been introduced with excellent performance characteristics. The details of optimized design parameters and performances are listed in Table 1. As well, Table 2 shows the performance comparison of different SPR biosensors based on Kretschmann configuration with a hybrid structure.
\nSl. no. | \nProposed SPR sensors with optimized structural parameters | \nOperating range of sensing medium RI | \nFOM [RIU–1] | \nQF [deg/RIU] | \nSensitivity [deg/RIU] | \n||
---|---|---|---|---|---|---|---|
01. | \nAg/PtSe2/WS2\n | \nThickness of Ag (nm) | \n50 | \n1.33-1.38 | \n17.64 | \n34.22 | \n194 | \n
Thickness of PtSe2 (nm) | \n02 | \n||||||
Number of WS2 Layers | \n04 | \n||||||
02. | \nAu/PtSe2/WS2\n | \nThickness of Au (nm) | \n50 | \n1.33-1.38 | \n15.72 | \n29.39 | \n187 | \n
Thickness of PtSe2 (nm) | \n02 | \n||||||
Number of WS2 Layers | \n02 | \n
Details of optimized design parameters and results of the proposed SPR biosensors [86].
Ref. | \nConfiguration of the sensors | \nSensitivity (deg/RIU) | \n
---|---|---|
[83] | \nPrism/Air/Titanium (Ti)/Ag/Au/InP | \n70.90 | \n
[84] | \nPrism/Rh/Ag/Si | \n229 | \n
[3] | \nPrism/MoS2/h-BN/graphene | \n194.12 | \n
[85] | \nPrism/Ag/Au/WS2/graphene | \n182.5 | \n
[86] | \nPrism/Ag/PtSe2/WS2\n | \n194 | \n
[86] | \nPrism/Au/PtSe2/WS2\n | \n187 | \n
[87] | \nPrism/Au/Black Phosphorous (BP) | \n180 | \n
[2] | \nPrism/Au/Graphene/MoS2\n | \n89.29 | \n
[1] | \nPrism/Au/MoS2\n | \n75.34 | \n
[88] | \nPrism/ZnO/Ag/Au/graphene | \n66 | \n
[89] | \nPrism/Au/MoS2/WS2/WSe2\n | \n142 | \n
[90] | \nPrism/Au/MoS2/Au film/graphene | \n182 | \n
[55] | \nPrism/MoS2/aluminum (Al) film/MoS2/graphene | \n190.83 | \n
[91] | \nPrism/Ag/PtSe2\n | \n162 | \n
[91] | \nPrism/Au/PtSe2\n | \n165 | \n
Sensitivity comparison of Kretschmann configuration based SPR biosensors comprising hybrid structures.
This chapter provides a detailed description of the surface plasmon resonance phenomenon with the recent trends that are being applied in the advancement of SPR based sensors where the application of hybrid structures as well as bimetallic configurations are found to be potential techniques to enhance the sensor performances. Besides, it demonstrates different 2D materials applied for sensing capability enhancement of the hybrid SPR biosensors. Also, two 5 layer prism based hybrid heterostructures (Prism-Au-PtSe2-WS2 and Prism-Ag-PtSe2-WS2) have been comprehensively discussed here to show the effectiveness of hybrid technology.
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