Main TSGs with dual functions reported in lung cancer.
\r\n\t
\r\n\tThe aim of this book project is to compile the updated research work on medicinal applications of noble metal complexes mainly focusing the structure activity relationship of metal complexes with targeting biological components.
This chapter treats a topic on probabilistic representations of solutions to a certain class of deterministic nonlinear integral equations. Indeed, this is a short review article to introduce the star-product functional and a probabilistic construction of solutions to nonlinear integral equations treated in [1]. The principal parts for the existence and uniqueness of solutions are taken from [1] with slight modification. Since the nonlinear integral equations which we handle are deterministic, they have nothing to do with random world. Hence, we assume that an integral formula may hold, which plays an essential role in connecting a deterministic world with a random one. Once this relationship has been established, we begin with constructing a branching model and we are able to construct a star-product functional based upon the model. At the end we prove that the function provided by the expectation of the functional with respect to the law of a branching process in question solves the original integral equations (see also [2, 3, 4]).
\nMore precisely, in this chapter we consider the deterministic nonlinear integral equation of the type:
One of the reasons why we are interested in this kind of integral equations consists in its importance in applicatory fields, especially in mathematical physics. For instance, in quantum physics or applied mathematics, a variety of differential equations have been dealt with by many researchers (e.g., [5, 6]), and in most cases, their integral forms have been discussed more than their differential forms on a practical basis. There can be found plenty of integral equations similar to Eq. (1) appearing in mathematical physics.
\nThe purpose of this article is to provide with a quite general method of giving a probabilistic interpretation to deterministic equations. Any deterministic representation of the solutions to Eq. (1) has not been known yet in analysis. The main contents of the study consist in derivation of the probabilistic representation of the solutions to Eq. (1). Our mathematical model is a kind of generalization of the integral equations that were treated in [7], and our kernel appearing in Eq. (1) is given in a more abstract setting. We are aiming at establishment of new probabilistic representations of the solutions.
\nThis paper is organized as follows: In Section 2 we introduce notations which are used in what follows. In Section 3 principal results are stated, where we refer the probabilistic representation of the solutions to a class of deterministic nonlinear integral equations in question. Section 4 deals with branching model and its treelike structure. Section 5 treats construction of star-product functional based upon those tree structures of branching model described in the previous section. The proof of the main theorem will be stated in Sections 6 and 7. Section 6 provides with the proof of existence of the probabilistic solutions to the integral equations. We also consider \n
We think that it would not be enough to derive simply explicit representations of probabilistic solutions to the equations, but it is extremely important to make use of the formulae practically in the problem of computations. We hope that our result shall be a trigger to further development on the study in this direction.
\nLet \n
Here, \n
Suppose that the integral kernel \n
Moreover, we assume that for every measurable functions \n
holds, where the measure \n
The equality (Eq. (4)) is not only a simple integral transform formula. In fact, in the analytical point of view, it merely says that the double integral with respect to \n
In this section we shall introduce our main results, which assert the existence and uniqueness of solutions to the nonlinear integral equation. That is to say, we derive a probabilistic representation of the solutions to Eq. (2) by employing the star-product functional. As a matter of fact, the solution \n
be a probabilistic representation in terms of tree-based star-product functional with weight \n
Theorem 1. Suppose that \n
holds. Then, there exists a \n
gives a unique solution to the integral equation (Eq. (2)). Here, \n
In this section we consider a continuous time binary critical branching process \n
by \n
is a set of all labels, namely, finite sequences of symbols with length \n
This section treats a tree-based star-product functional. First of all, we denote by the symbol \n
Notice that this product ★ is noncommutative. This property will be the key point in defining the star-product functional below, especially as far as the uniqueness of functional is concerned. We shall define \n
whereas for the product order in the star-product ★, when we write \n
especially when \n
Under these circumstances, we consider a random quantity which is obtained by executing the star-product ★ inductively at each node in \n
where \n
Example 2. Let us consider a typical realization \n
Similarly, for the pair of particles \n
For the pair of particles \n
Next, when we take a look at the groups of particles with nodes of the level \n
Therefore, it follows by a similar argument that the explicit representation of star-product functional for \n
In this section we first begin with constructing a \n
In what follows we shall give an outline of the existence in Theorem 1. We need the following lemma, which is essentially important for the proof.
\nLemma 3. For \n
Proof of Lemma 3. By making use of the conditional expectation, we may decompose \n
We are next going to take into consideration an equivalence between the events \n
the tree-based \n
As to the third term, we need to note the following matters. A particle generates two offsprings or descendants \n
Note that as for the second term, it goes almost similarly as the computation of the above-mentioned third one. Finally, summing up we obtain
On this account, if we multiply both sides of Eq. (18) by \n
By a glance at the expression Eq. (15) obtained in Lemma 3, it is quite obvious that, for each \n
holds for \n
Lemma 4. (\n
holds \n
This inequality enables us to govern the behavior of the star-product functional with a very complicated structure by that of the \n
Next, we are going to derive the space of solutions to Eq. (2). If we define
On this account, from Eq. (15) in Lemma 3, by finiteness of the expectation of tree-based \n
Hence, taking Eq. (22) into consideration, we define the space \n
By employing the Markov property [13] with respect to time \n
Furthermore, we may apply the integral equality Eq. (4) in the assumption on the Markov kernel for Eq. (24) to obtain
because in the above last equality we need to rewrite its double integral relative to the space parameters into a single integral. Finally, we attain that \n
First of all, note that we can choose a proper measurable subset \n
and
is convergent for a.e.-\n
satisfying \n
We are now in a position to introduce a new class \n
Lemma 5. (\n
holds \n
because of the domination property: \n
Let us now introduce a filtration \n
for each \n
Lemma 6. For each \n
holds \n
Proof. By its construction, we can conclude the equality of Eq. (30) from the strong Markov property [13] applied at times \n
Moreover, an application of Lemma 6 with the \n
Lemma 7. The \n
Proof. When we set \n
by virtue of the inclusion property of the \n
holds a.s. By employing the representation formula (Eq. (8)), an conditioning argument leads to Eq. (31), because the establishment is verified by the Markov property applied at \n
Finally, the uniqueness yields from the following assertion.
\nProposition 8. When \n
holds for every \n
Proof. Our proof is technically due to a martingale method. We need the following lemma.
\nLemma 9. Let \n
holds for every \n
Proof of Lemma 9. Recall that \n
Next, for the case \n
We resort to the mathematical induction with respect to \n
where we made use of the martingale property in the first equality and employed the hypothesis of induction in the last identity. This concludes the assertion. \n
To go back to the proof of Proposition 8. We define an \n
Hence, for every \n
where the symbol \n
Furthermore, we continue computing
Since \n
it follows by the bounded convergence theorem of Lebesgue that
Consequently, from Eq. (39) and Eq. (41), we readily obtain
holds for every \n
Concurrently, this completes the proof of the uniqueness.
\nThis work is supported in part by the Japan MEXT Grant-in-Aids SR(C) 17 K05358 and also by ISM Coop. Res. Program: 2011-CRP-5010.
\nCancer cells arise in non-malignant tissue due to the sequential acquisition of molecular alterations that drive proliferation, permit the evasion of growth suppression and apoptosis signals and promote angiogenesis, invasion and metastasis [1]. This process is stochastic, and over time the tumour continues to evolve in a dynamic manner, generating a group of cells harbouring different genetic and epigenetic features [2]. The resulting heterogeneity is the basis of tumour evolution and leads to the selection of tumour cells. These cells often present with rewired signalling networks and often oncogene addiction [3].
\nThe uncontrolled growth of cancer cells can in part be explained by their aberrant gene expression patterns. While most cancer genes are characterized as either oncogenes or tumour suppressors based on their typical behaviour in tumours, some genes display dual oncogenic and tumour suppressive functions [4, 5]. The majority of these genes encode multiple isoforms, which are further post-translationally modified and form a variety of protein complexes, generating a context-dependent cellular network [6]. In diploid organisms, gain-of-function (GOF) mutations in oncogenes are typically dominant (single events are sufficient to promote tumourigenesis), while loss-of-function alterations are recessive in TSGs (requires two inactivation events) [7]. For example, for a TSG with dual oncogenic roles, one gain-of-function mutation can potentially cease its tumour suppressive function and turn on oncogenic signalling [5].
\nRecently, genes with both oncogenic and tumour-suppressive functions were described across 12 main cancer types using The Cancer Genome Atlas (TCGA) database [5]. Using a text mining approach, the authors identified genes mainly represented by kinases (e.g. BCR, CHEK2, MAP2K4, NTRK3 and SYK) or transcription factors (e.g. BRCA1, EZH2, NOTCH1, NOTCH2, STAT3 and TP53) and evaluated them at the genomic and gene expression levels. Using an in silico analysis, it was shown that genes with dual functions interact with more partners and are more important hub-genes in protein-protein interaction networks.
\nIn this chapter, we discuss TSGs with both tumour suppressive and oncogenic functions in lung cancer.
\nLung cancer is one of the most common cancers and the leading cause of cancer-related deaths worldwide [8]. In the United States, lung cancer accounts for 13.5% of all new cancer cases and 25.3% of all cancer deaths. The five-year survival rate is dismal, with only 18.6% of patients surviving 5 years [9]. The majority of lung cancer cases (approximately 80%) are attributed to cigarette smoking [10]. About 10–25% of cases occur in people who have never smoked [11]. The aetiology behind these cases is most likely a combination of genetic factors, as well as the effects of exposure to environmental carcinogens such as asbestos, radon gas or other forms of pollution [12].
\nLung cancer is classified according to histological type. There are two major types: small cell lung cancer (SCLC), which accounts for 15–20% of lung cancer patients, and non-small cell lung cancer (NSCLC), comprising the remaining 80–85% (Figure 1) [13]. SCLC, primarily originating from the central airways, is thought to be derived from neuroendocrine cells [14]. NSCLC is composed of three major histological subtypes: adenocarcinoma (LUAD), squamous cell carcinoma (LUSC) and large cell carcinoma (LCC). LUAD is the most common, accounting for approximately 40% of all lung cases [15]. LUAD typically arises from glandular epithelium, from bronchioalveolar stem cells, club (Clara) cells or type II pneumocytes in the lung periphery [13]. LUAD is also the predominant subtype that arises in patients who have never smoked [15]. LUSC develops primarily in the central airways and segmental bronchi, strongly associates with a history of smoking and accounts for approximately 20% of all lung cancer cases. LCC may arise anywhere in the lung and are classified as tumours without general features associated with SCLC, LUAD or LUSC [13].
\nHistological classification of lung cancer. (A) Lung cancer histological types. (B) Location of the tumours and cell origins. SCLC, small cell lung cancer; NSCLC, non-small cell lung cancer; LUAD, lung adenocarcinoma; LUSC, lung squamous cell carcinoma; LCC, large cell carcinoma.
Beyond the histological heterogeneity of lung cancer, genomic studies of large cohorts have uncovered the complex molecular landscape of lung tumours. Indeed, it has been observed that a wide variety of oncogenes and TSGs can be altered in lung cancer, and these molecular events are vastly different between histological subtypes [16, 17].
\nClinical studies have shown that molecularly defined lung cancer subgroups can correlate with characteristics such as ethnicity [18], smoking history [19], treatment sensitivity [20] or prognosis [21]. Many of the commonly identified gain-of-function alterations in proto-oncogenes have been actively investigated for therapeutic purposes. For example, EGFR, ALK, ROS1, BRAF, MET, RET and HER2 are routinely assessed in the clinic to offer targeted therapy for eligible LUAD patients [22].
\nThree TSGs are frequently mutated in all three major lung cancer subtypes: TP53, LRP1B and CSMD3. Other TSGs of particular interest in lung cancer are as follows RB1 and CREBBP in SCLC, KEAP1 and STK11 in LUAD, CDKN2A in LUSC, NOTCH1 and PTEN in both SCLC and LUSC and NF1 in both LUAD and LUSC (Figure 2). Mutations in these TSGs are usually mutually exclusive, indicating that individual genes are capable of driving lung cancer progression.
\nMutational frequency of TSGs in small cell lung cancer (SCLC; n = 110) [16], lung adenocarcinoma (LUAD; n = 660) [23] and lung squamous cell carcinoma (LUSC; n = 484) [23]. TSGs were defined according to COSMIC Cancer Gene Census (https://cancer.sanger.ac.uk/census) and mutation frequency of the most commonly disrupted TSGs in these subtypes of lung cancer were retrieved using cBioPortal (http://www.cbioportal.org/).
Several TSGs in lung cancer have also been shown to behave as oncogenes, depending on the molecular context and/or the mechanism by which they are altered (Table 1). Among them are TP53, NFIB, members of the NOTCH family, NKX2-1, NFE2L2, as well as some non-coding RNAs (MALAT1, mir-125, and mir-378), which will be discussed in detail below.
\nGene | \nMain function | \nRole as TSG | \nRole as oncogene | \n
---|---|---|---|
TP53 | \nTF: regulates cell cycle, DNA repair, senescence and apoptosis | \nTSG in several tissues: frequently lost through mutations [24] | \nMissense mutations confer gain-of-function oncogenic properties [31] | \n
NFIB | \nTF: crucial in lung development | \nUnderexpressed in NSCLC and associated with poor survival in LUAD [32] | \nAmplified and OE in SCLC: inducing chromatin reprogramming during metastasis [33] | \n
NOTCH1/NOTCH2 | \nTransmembrane receptors: proliferation, differentiation and survival | \nInactivated by inhibitor ligands and through mutations, especially in SCLC [34] | \nMaintains stem cell features; promotes proliferation in LUAD [35] | \n
NFE2L2 | \nTF: cellular defense mechanism against oxidative stress | \nProtects lung tissue against exposure to oxidative stress [36] | \nMutational activation: aids cells to escape from endogenous tumour suppression [37] | \n
NKX2-1 | \nTF: essential for lung development | \nActs as a TSG in KRAS-driven p53-mutant LUAD [38] | \nEnhanced oncogenic signals in EGFR-driven LUAD [39] | \n
STK11 | \nSerine-threonine kinase: regulation of energetic metabolism and cell polarity | \nMutational inactivation promotes cancer development [40] | \nOE maintains metabolic homeostasis and attenuates oxidative stress [40] | \n
TGFB | \nCytokine: regulates development, differentiation and homeostasis | \nExpression loss leads to growth arrest in early-stage lung and other cancers [41] | \nOE promotes tumour growth in advanced cancer stages [42] | \n
TUSC3 | \nEndoplasmic reticulum protein in magnesium uptake, glycosylation and embryonic development | \nHypermethylation; expression loss in NSCLC; inhibits cell proliferation and promotes apoptosis [43] | \nOE in NSCLC accelerates cancer growth; induces EMT [44] | \n
WT1 | \nTF: role in urogenital system development | \nLoss of function enhances cell viability and proliferation in Wilms’ tumour [45] | \nOE promotes survival in KRAS-mutated NSCLC [46] | \n
MALAT1 | \nLong non-coding RNA | \nOE reduces invasiveness in PTEN expressing tumours [47] | \nOE associated with chemotherapy resistance in NSCLC [48] | \n
miR-125b | \nmicroRNA | \nOE induces apoptosis [49] | \nOE promotes metastasis [50] | \n
miR-378 | \nmicroRNA | \nOE reverses chemoresistance to cisplatin in LUAD [51] | \nOE is associated with invasion and brain metastasis [52] | \n
Main TSGs with dual functions reported in lung cancer.
TF, transcription factor; OE, overexpression; EMT, epithelial-mesenchymal transition. Numbers in brackets refer to the list of reference.
TP53 is a well-known TSG, representing the most common somatically mutated gene in human cancer, especially in lung tumours [24]. The classic functions of the encoded p53 protein are cell cycle regulation, DNA repair, senescence mediated by stress, apoptosis and angiogenesis. These functions mainly occur through the binding of a p53 tetramer to the promoter of target genes [25]. In many cancer types, TP53 mutation is associated with poor prognosis, including local and distant metastases events, resistance to treatment and decreased survival [26, 27].
\nDespite having a reputation as a ‘guardian of the genome’, recent work has shown that activating TP53 alterations can act to promote cancer development and progression [25, 28]. Depending on the location of the mutation within the TP53 gene, protein structure and subsequent DNA binding activity can be lost or altered, resulting in either loss or gain of function [25]. In contrast to the majority of TSGs, TP53 is not commonly inactivated by deletions or truncating mutations. Indeed, 74% of mutations within the TP53 locus are missense point mutations, which can be found in proteins in human tumours [25]. In fact, altered TP53 was initially considered as a cancer antigen with putative oncogenic properties [25]. Together, this highlights the dichotomous role of TP53 disruptions, in that both the loss of wild-type p53 and gain-of-function mutations can provide a growth advantage to tumours [28].
\nLung cancer is commonly associated with tobacco use, where the prolonged exposure to carcinogens damages the DNA of the exposed cells. These alterations are especially enriched in missense mutations in TP53, leading to GOF-p53 [29]. The oncogenic GOF mutation in p53 was previously shown to be related with the inactivation of AMP-activated protein kinase (AMPK) signalling in head and neck cancer and another tobacco-related cancer [30]. AMPK is a master regulator of metabolic homeostasis and GOF-mutated p53 is able to physically interact and inhibit AMPK, stimulating aerobic glycolysis under energetic stress conditions and leading to invasive growth.
\nIn lung cancer mouse models, prevention of tumour formation by inhibiting GOF p53 mutants has been demonstrated [53]. Although the highly aberrant genomes in p53-mutated tumours should lead to unfeasible mitosis, these mutations facilitate the survival and proliferation of these cells through stabilizing replication forks and promoting micronuclei arrangement [31].
\nGOF p53 mutants are most likely involved in multiple mechanisms that coordinate tumour progression. For example, GOF-p53 (R175H, R273H and D281G) was demonstrated to upregulate CXCL5, CXCL8 and CXCL12 through its transcription factor activity, promoting migration of lung cancer cell lines [54]. CXCL5 expression was shown to be elevated in human lung tumour samples harbouring GOF-p53, and its inhibition could reverse cell motility in lung cancer and melanoma cell lines [54]. In NSCLC, it was recently reported that GOF-p53 can physically interact with HIF-1 and binds to the SWI/SNF chromatin remodelling complex, inducing the expression of hypoxia-responsive genes [55]. Importantly, specific extracellular matrix components are upregulated by this process and mediate pro-tumourigenic features in NSCLC [55].
\nNuclear factor I (NFI) is a transcription factor family, comprising NFIA, NFIB, NFIC and NFIX, that plays important roles in normal development and in numerous diseases [56]. These proteins bind to specific DNA sequences leading to repression or activation of gene expression in a context-dependent manner, regulating cell differentiation and proliferation through their target genes [57]. NFIB, in particular, has been implicated in a wide range of malignancies, being described as both an oncogene and a potential TSG [58].
\nUsing an in vivo model, it was demonstrated that NFIB is a metastatic driver in SCLC, inducing global chromatin reprogramming during metastasis [33]. The authors isolated tumour cells from primary and metastatic sites of genetically engineered mice, and using genome-wide analysis, they showed a pronounced increase in chromatin accessibility during tumour progression, resulting from NFIB copy number amplifications. Interestingly, the distal regions that became accessible upon NFIB upregulation were similar to open regions found in neural tissue. Recently, the same group described two metastatic models in SCLC, one dependent and other independent of NFIB amplification [59]. NFIB was likewise reported as amplified and/or overexpressed in melanoma [60], breast [61], oesophagus [62] and salivary gland malignancies [63].
\nA gene fusion involving NFIB (MYB-NFIB) is frequently found in adenoid cystic carcinomas from salivary glands [64] and in adenoid cystic carcinoma from other topologies [65]. Despite the putative oncogenic function of NFIB, studies have focused on its fusion partner MYB as the main oncogenic driver in these cancers [66]. Given the fact that other fusion partners of NFIB have been reported in adenoid cystic carcinomas [67] and that MYB-NFIB fusions lead to NFIB truncation [68], NFIB may have a possible independent role as a TSG in these malignancies.
\nWhile the MYB-NFIB fusion is not observed in lung cancers, NFIB is frequently underexpressed in NSCLC tissues [32] and during epithelial-to-mesenchymal transition in NSCLC cell lines [69]. NFIB is an essential transcriptional factor in lung development [70] and was demonstrated to be targeted by many microRNAs that recapitulate their foetal lung expression patterns in NSCLC [32]. Lower expression of this gene was associated with shorter overall survival, less-differentiated tumour features and repressed expression of cell differentiation markers in LUAD patients [32]. Therefore, contrary to the established oncogenic role of NFIB in SCLC, these observations suggest a tumour suppressive role in NSCLC.
\nThe Notch signalling pathway is important in the regulation of cell fate during embryogenesis and maintenance of homeostasis in adult tissues [71]. It includes Notch receptors (NOTCH1, NOTCH2, NOTCH3 and NOTCH4) and ligands from the DSL family, which suppress or induce tumour-related mechanisms under specific cellular contexts [71].
\nIn SCLC, Notch signalling is frequently inactivated by either a mutation in Notch receptors or the overexpression of ligands that inhibit downstream signalling [34]. Despite this potential role as a TSG, Notch signalling in lung tumours is complex, as it has also been shown to be related to chemoresistance in SCLC [72]. In addition, the overactivation of this pathway through several mechanisms acts like an oncogene in LUAD by preserving stem cell features and promoting proliferation [35, 73]. Notch1 expression is required in Kras-driven LUAD carcinogenesis, suppressing apoptosis via the p53 pathway [35]. The inhibition of the Notch pathway is able to restrain lung cancer stem cell maintenance, which is characterized by subpopulations of cells expressing aldehyde dehydrogenase [74].
\nConversely, loss-of-function mutations of Notch receptors generating truncated receptors imply a TSG role in LUSC [75]. Although functional studies to further corroborate this hypothesis are still needed, reports in other squamous cell carcinomas substantiate the idea that the inactivation of this signalling pathway promotes tumourigenesis [76].
\nNkx2-1 is a homeobox-containing transcription factor that is essential for lung development and is expressed in type II pneumocytes and bronchiolar cells in adults [77]. It is expressed in 40–50% of lung cancers and is amplified and overexpressed in 6–11% of LUAD [78].
\nNkx2-1 acts as a lineage-specific oncogene in some LUAD cases [79], enhancing cell viability and proliferation in lung cancer cell lines [78]. This function relies on the activation of (i) the pro-survival PI3K-AKT pathway, through ROR1 kinase-dependent c-Src activation as well as maintaining the EGFR-ERBB3 association [80], and (ii) LMO3, a member of the LMO family of oncogenes that is translocated in T-ALL [81].
\nOn the other hand, Nkx2-1 expression has been associated with good patient outcome [82] and the loss of Nkx2-1 expression was associated with the aggressive behaviour of NSCLCs [83]. Mechanistically, tumour suppressive functions of Nkx2-1 in lung adenocarcinoma rely on the restriction of cell motility, invasion and metastatic ability, through the inhibition of the TGF-β [41] and IKK-B/NFk-B [39] pathways. The dual role of Nkx2-1 is dependent on EGFR, KRAS and TP53 status in LUAD: NKX2-1 acts as a TSG in KRAS-driven and TP53-mutant tumours, whereas it enhances EGFR-driven tumourigenesis [84, 85].
\nNFE2L2 encodes a transcription factor that regulates proteins involved in cellular defense mechanisms against metabolic, xenobiotic and oxidative stress [86]. NFE2L2 has been often considered a TSG due to its protective role against genome-damaging agents, the higher propensity to cancer development in NFE2L2-deficient mice and its protective effects in cancer chemoprevention [87].
\nDue to the constant exposure to oxidative stress in the lung, the NFE2L2 pathway is important to guarantee the genomic stability of these cells [88]. However, once transformation of normal to cancer cells occurs, NFE2L2 favours tumour development by acting to protect against oxidative stress resulting from the tumour microenvironment and exposure to genotoxic agents during patient treatment [86]. In fact, mutations in NFE2L2 and KEAP1, an important member of the NFE2L2 signalling, are very common and mutually exclusive in NSCLC [89]. Curiously, a recent study demonstrated that lung cancer patients presenting NFE2L2 or KEAP1 mutations are highly resistant to chemotherapy [89]. However, the relation between the NFE2L2 pathway and treatment response prediction needs further investigation.
\nWhile large-scale genomic sequencing efforts have uncovered an invaluable number of genetic alterations related to cancer biology, in the past, they were commonly focused on the 2% of the genome that encodes protein [90]. In the last decade, non-coding RNA transcripts have been shown to have important regulatory functions in normal and disease biology [91]. Indeed, many non-coding genes have been shown to play tumour-suppressive or oncogenic roles in numerous cancer types [92].
\nMetastasis-associated lung adenocarcinoma transcript 1 (MALAT1) was one of the first cancer-related long non-coding RNAs to be described [93]. MALAT1 is broadly expressed in normal cells, where it has been shown to regulate the alternative splicing of pre-mRNAs by changing the distribution of splicing regulators in nuclear speckles [94]. MALAT1 was primarily identified as an oncogenic transcript in lung cancer and has since been widely considered a marker of metastasis, poor patient survival [93] and chemotherapy resistance in NSCLC [48]. Mechanistically, MALAT1 has been shown to promote carcinogenesis through P53 deacetylation [95] and enhance cell migration through Akt/mTOR signalling [96] and TGF-β-induced endothelial-to-mesenchymal transition [97]. Conversely, MALAT1 has also been shown to reduce invasiveness by modulating the expression of EpCAM and ITGB4 in PTEN-expressing tumours [47] and by downregulation of MMP2 and inactivation of ERK/MAPK signalling [98]. MALAT1 also binds the nuclear p65/p50 heterodimer and thus inhibits NF-κB-dependent pathways [99] and is thought to be involved in the response to DNA damage [100]. Furthermore, MALAT1 reduces the invasiveness of cerebral metastases by sustaining the blood-brain barrier [101]. MALAT1 expression and subcellular location is finely tuned through various regulatory mechanisms [102], which may drive its pro- or anti-tumour effects [103]. Analysis of the dual role of MALAT1 highlights not only the complexity of non-coding RNA function but also their relevance to broad areas of cancer biology and management.
\nMicroRNAs (miRNAs) are short transcripts that typically regulate coding genes post-transcriptionally through direct interaction with mRNA transcripts. Many are deregulated in lung cancer [104], where they have documented tumour-suppressive and oncogenic roles [105]. For example, miRNA-125b has been shown to have a multifaceted function as a tumour suppressor and oncogene, being underexpressed in bladder [106] and ovarian cancer [107] and overexpressed in glioma [108] and prostate cancer [109]. It was shown that miRNA-125b induces apoptosis in cancer cell lines exposed to nutrient starvation and chemotherapy, including in lung cancer [49]. On the other hand, miRNA-125b may also function as an oncogene in NSCLC, as it is able to promote metastasis by targeting TP53INP1 [50]. In addition, inhibition of miR-125b can also decrease the invasive potential and leads to cell cycle arrest and apoptosis in NSCLC [110]. Similarly, miR-378 was reported to be overexpressed in lung cancer and other tumour types, inducing cell migration, invasion and tumour angiogenesis [111]. However, it was previously demonstrated that upregulation of this miRNA sensitizes lung cancer cell lines to cisplatin [51].
\nHere, we summarize the commonly disrupted genes in lung cancer with dual roles as both tumour suppressors and oncogenes. These conflicting roles are a result from the complexity of biological pathways and the heterogeneity of cancer cells.
\nMost of the current molecular therapies are based on hyperactivated oncogene inhibitors. In lung cancer, only a fraction of the cases exhibit alterations in targetable genes, such as EGFR, BRAF and MET mutations and ALK, RET and ROS1 fusions [112]. Therefore, there is an urgent need for the development of novel therapeutic strategies exploiting non-oncogene alterations of lung tumour cells.
\nConsidering that TSGs are found altered more frequently than oncogenes in human tumours [113], the existence of TSGs with dual oncogenic roles opens a new window of opportunities for the development of new targeted therapies. However, therapeutic action against TSGs remains challenging, as many are not amenable to current pharmacologic inactivation strategies. Most of the TSGs are not a kinase that can be pharmacologically blocked and are not located at the cell surface to be targeted by an antibody.
\nIn summary, there is an unmet need to clarify the ambiguity found within genes, both coding and non-coding, with both pro- and anti-tumour functions. Broadening our understanding of these features may enable the development of novel and specific therapeutic strategies that consider both molecular and tissue contexts.
\nThis work was supported by grants from the Canadian Institutes for Health Research (CIHR FDN-143345) and scholarships from CIHR, the BC Cancer Foundation, the Ligue nationale contre le cancer, the Fonds de Recherche en Santé Respiratoire (appel d’offres 2018 emis en commun avec la Fondation du Souffle), the Fondation Charles Nicolle and the São Paulo Research Foundation (FAPESP 2015/17707-5 and 2018/06138-8). D.D.B.S. and E.A.M. are Vanier Canada Scholars.
\nThe authors have no conflicts to declare.
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\\n\\nSubject to the license granted above, the Corresponding Author and any Co-Author retains patent, trademark and other intellectual property rights to the Chapter.
\\n\\n2.3 All rights granted to IntechOpen in this Article are assignable, sublicensable or otherwise transferrable to third parties without the Corresponding Author's or any Co-Author’s specific approval.
\\n\\n2.4 The Corresponding Author (on their own behalf and on behalf of each Co-Author) will not assert any rights under the Copyright, Designs and Patents Act 1988 to object to derogatory treatment of the Chapter as a consequence of IntechOpen's changes to the Chapter arising from translation of it, corrections and edits for house style, removal of problematic material and other reasonable edits.
\\n\\n3. CORRESPONDING AUTHOR'S DUTIES
\\n\\n3.1 When distributing or re-publishing the Chapter, the Corresponding Author agrees to credit the Book in which the Chapter has been published as the source of first publication, as well as IntechOpen. The Corresponding Author warrants that each Co-Author will also credit the Book in which the Chapter has been published as the source of first publication, as well as IntechOpen, when they are distributing or re-publishing the Chapter.
\\n\\n3.2 When submitting the Chapter, the Corresponding Author agrees to:
\\n\\nThe Corresponding Author will be held responsible for the payment of the Open Access Publishing Fees.
\\n\\nAll payments shall be due 30 days from the date of the issued invoice. The Corresponding Author or the payer on the Corresponding Author's and Co-Authors' behalf will bear all banking and similar charges incurred.
\\n\\n3.3 The Corresponding Author shall obtain in writing all consents necessary for the reproduction of any material in which a third-party right exists, including quotations, photographs and illustrations, in all editions of the Chapter worldwide for the full term of the above licenses, and shall provide to IntechOpen upon request the original copies of such consents for inspection (at IntechOpen's option) or photocopies of such consents.
\\n\\nThe Corresponding Author shall obtain written informed consent for publication from people who might recognize themselves or be identified by others (e.g. from case reports or photographs).
\\n\\n3.4 The Corresponding Author and any Co-Author shall respect confidentiality rights during and after the termination of this Agreement. The information contained in all correspondence and documents as part of the publishing activity between IntechOpen and the Corresponding Author and any Co-Author are confidential and are intended only for the recipient. The contents may not be disclosed publicly and are not intended for unauthorized use or distribution. Any use, disclosure, copying, or distribution is prohibited and may be unlawful.
\\n\\n4. CORRESPONDING AUTHOR'S WARRANTY
\\n\\n4.1 The Corresponding Author represents and warrants that the Chapter does not and will not breach any applicable law or the rights of any third party and, specifically, that the Chapter contains no matter that is defamatory or that infringes any literary or proprietary rights, intellectual property rights, or any rights of privacy. The Corresponding Author warrants and represents that: (i) the Chapter is the original work of themselves and any Co-Author and is not copied wholly or substantially from any other work or material or any other source; (ii) the Chapter has not been formally published in any other peer-reviewed journal or in a book or edited collection, and is not under consideration for any such publication; (iii) they themselves and any Co-Author are qualifying persons under section 154 of the Copyright, Designs and Patents Act 1988; (iv) they themselves and any Co-Author have not assigned and will not during the term of this Publication Agreement purport to assign any of the rights granted to IntechOpen under this Publication Agreement; and (v) the rights granted by this Publication Agreement are free from any security interest, option, mortgage, charge or lien.
\\n\\nThe Corresponding Author also warrants and represents that: (i) they have the full power to enter into this Publication Agreement on their own behalf and on behalf of each Co-Author; and (ii) they have the necessary rights and/or title in and to the Chapter to grant IntechOpen, on behalf of themselves and any Co-Author, the rights and licenses expressed to be granted in this Publication Agreement. If the Chapter was prepared jointly by the Corresponding Author and any Co-Author, the Corresponding Author warrants and represents that: (i) each Co-Author agrees to the submission, license and publication of the Chapter on the terms of this Publication Agreement; and (ii) they have the authority to enter into this Publication Agreement on behalf of and bind each Co-Author. The Corresponding Author shall: (i) ensure each Co-Author complies with all relevant provisions of this Publication Agreement, including those relating to confidentiality, performance and standards, as if a party to this Publication Agreement; and (ii) remain primarily liable for all acts and/or omissions of each such Co-Author.
\\n\\nThe Corresponding Author agrees to indemnify and hold IntechOpen harmless against all liabilities, costs, expenses, damages and losses and all reasonable legal costs and expenses suffered or incurred by IntechOpen arising out of or in connection with any breach of the aforementioned representations and warranties. This indemnity shall not cover IntechOpen to the extent that a claim under it results from IntechOpen's negligence or willful misconduct.
\\n\\n4.2 Nothing in this Publication Agreement shall have the effect of excluding or limiting any liability for death or personal injury caused by negligence or any other liability that cannot be excluded or limited by applicable law.
\\n\\n5. TERMINATION
\\n\\n5.1 IntechOpen has a right to terminate this Publication Agreement for quality, program, technical or other reasons with immediate effect, including without limitation (i) if the Corresponding Author or any Co-Author commits a material breach of this Publication Agreement; (ii) if the Corresponding Author or any Co-Author (being an individual) is the subject of a bankruptcy petition, application or order; or (iii) if the Corresponding Author or any Co-Author (being a company) commences negotiations with all or any class of its creditors with a view to rescheduling any of its debts, or makes a proposal for or enters into any compromise or arrangement with any of its creditors.
\\n\\nIn case of termination, IntechOpen will notify the Corresponding Author, in writing, of the decision.
\\n\\n6. INTECHOPEN’S DUTIES AND RIGHTS
\\n\\n6.1 Unless prevented from doing so by events outside its reasonable control, IntechOpen, in its discretion, agrees to publish the Chapter attributing it to the Corresponding Author and any Co-Author.
\\n\\n6.2 IntechOpen has the right to use the Corresponding Author’s and any Co-Author’s names and likeness in connection with scientific dissemination, retrieval, archiving, web hosting and promotion and marketing of the Chapter and has the right to contact the Corresponding Author and any Co-Author until the Chapter is publicly available on any platform owned and/or operated by IntechOpen.
\\n\\n6.3 IntechOpen is granted the authority to enforce the rights from this Publication Agreement, on behalf of the Corresponding Author and any Co-Author, against third parties (for example in cases of plagiarism or copyright infringements). In respect of any such infringement or suspected infringement of the copyright in the Chapter, IntechOpen shall have absolute discretion in addressing any such infringement which is likely to affect IntechOpen's rights under this Publication Agreement, including issuing and conducting proceedings against the suspected infringer.
\\n\\n7. MISCELLANEOUS
\\n\\n7.1 Further Assurance: The Corresponding Author shall and will ensure that any relevant third party (including any Co-Author) shall, execute and deliver whatever further documents or deeds and perform such acts as IntechOpen reasonably requires from time to time for the purpose of giving IntechOpen the full benefit of the provisions of this Publication Agreement.
\\n\\n7.2 Third Party Rights: A person who is not a party to this Publication Agreement may not enforce any of its provisions under the Contracts (Rights of Third Parties) Act 1999.
\\n\\n7.3 Entire Agreement: This Publication Agreement constitutes the entire agreement between the parties in relation to its subject matter. It replaces and extinguishes all prior agreements, draft agreements, arrangements, collateral warranties, collateral contracts, statements, assurances, representations and undertakings of any nature made by or on behalf of the parties, whether oral or written, in relation to that subject matter. Each party acknowledges that in entering into this Publication Agreement it has not relied upon any oral or written statements, collateral or other warranties, assurances, representations or undertakings which were made by or on behalf of the other party in relation to the subject matter of this Publication Agreement at any time before its signature (together "Pre-Contractual Statements"), other than those which are set out in this Publication Agreement. Each party hereby waives all rights and remedies which might otherwise be available to it in relation to such Pre-Contractual Statements. Nothing in this clause shall exclude or restrict the liability of either party arising out of its pre-contract fraudulent misrepresentation or fraudulent concealment.
\\n\\n7.4 Waiver: No failure or delay by a party to exercise any right or remedy provided under this Publication Agreement or by law shall constitute a waiver of that or any other right or remedy, nor shall it preclude or restrict the further exercise of that or any other right or remedy. No single or partial exercise of such right or remedy shall preclude or restrict the further exercise of that or any other right or remedy.
\\n\\n7.5 Variation: No variation of this Publication Agreement shall be effective unless it is in writing and signed by the parties (or their duly authorized representatives).
\\n\\n7.6 Severance: If any provision or part-provision of this Publication Agreement is or becomes invalid, illegal or unenforceable, it shall be deemed modified to the minimum extent necessary to make it valid, legal and enforceable. If such modification is not possible, the relevant provision or part-provision shall be deemed deleted.
\\n\\nAny modification to or deletion of a provision or part-provision under this clause shall not affect the validity and enforceability of the rest of this Publication Agreement.
\\n\\n7.7 No partnership: Nothing in this Publication Agreement is intended to, or shall be deemed to, establish or create any partnership or joint venture or the relationship of principal and agent or employer and employee between IntechOpen and the Corresponding Author or any Co-Author, nor authorize any party to make or enter into any commitments for or on behalf of any other party.
\\n\\n7.8 Governing law: This Publication Agreement and any dispute or claim (including non-contractual disputes or claims) arising out of or in connection with it or its subject matter or formation shall be governed by and construed in accordance with the law of England and Wales. The parties submit to the exclusive jurisdiction of the English courts to settle any dispute or claim arising out of or in connection with this Publication Agreement (including any non-contractual disputes or claims).
\\n\\nLast updated: 2020-11-27
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The Corresponding Author (acting on behalf of all Authors) and INTECHOPEN LIMITED, incorporated and registered in England and Wales with company number 11086078 and a registered office at 5 Princes Gate Court, London, United Kingdom, SW7 2QJ conclude the following Agreement regarding the publication of a Book Chapter:
\n\n1. DEFINITIONS
\n\nCorresponding Author: The Author of the Chapter who serves as a Signatory to this Agreement. The Corresponding Author acts on behalf of any other Co-Author.
\n\nCo-Author: All other Authors of the Chapter besides the Corresponding Author.
\n\nIntechOpen: IntechOpen Ltd., the Publisher of the Book.
\n\nBook: The publication as a collection of chapters compiled by IntechOpen including the Chapter. Chapter: The original literary work created by Corresponding Author and any Co-Author that is the subject of this Agreement.
\n\n2. CORRESPONDING AUTHOR'S GRANT OF RIGHTS
\n\n2.1 Subject to the following Article, the Corresponding Author grants and shall ensure that each Co-Author grants, to IntechOpen, during the full term of copyright and any extensions or renewals of that term the following:
\n\nThe aforementioned licenses shall survive the expiry or termination of this Agreement for any reason.
\n\n2.2 The Corresponding Author (on their own behalf and on behalf of any Co-Author) reserves the following rights to the Chapter but agrees not to exercise them in such a way as to adversely affect IntechOpen's ability to utilize the full benefit of this Publication Agreement: (i) reprographic rights worldwide, other than those which subsist in the typographical arrangement of the Chapter as published by IntechOpen; and (ii) public lending rights arising under the Public Lending Right Act 1979, as amended from time to time, and any similar rights arising in any part of the world.
\n\nThe Corresponding Author confirms that they (and any Co-Author) are and will remain a member of any applicable licensing and collecting society and any successor to that body responsible for administering royalties for the reprographic reproduction of copyright works.
\n\nSubject to the license granted above, copyright in the Chapter and all versions of it created during IntechOpen's editing process (including the published version) is retained by the Corresponding Author and any Co-Author.
\n\nSubject to the license granted above, the Corresponding Author and any Co-Author retains patent, trademark and other intellectual property rights to the Chapter.
\n\n2.3 All rights granted to IntechOpen in this Article are assignable, sublicensable or otherwise transferrable to third parties without the Corresponding Author's or any Co-Author’s specific approval.
\n\n2.4 The Corresponding Author (on their own behalf and on behalf of each Co-Author) will not assert any rights under the Copyright, Designs and Patents Act 1988 to object to derogatory treatment of the Chapter as a consequence of IntechOpen's changes to the Chapter arising from translation of it, corrections and edits for house style, removal of problematic material and other reasonable edits.
\n\n3. CORRESPONDING AUTHOR'S DUTIES
\n\n3.1 When distributing or re-publishing the Chapter, the Corresponding Author agrees to credit the Book in which the Chapter has been published as the source of first publication, as well as IntechOpen. The Corresponding Author warrants that each Co-Author will also credit the Book in which the Chapter has been published as the source of first publication, as well as IntechOpen, when they are distributing or re-publishing the Chapter.
\n\n3.2 When submitting the Chapter, the Corresponding Author agrees to:
\n\nThe Corresponding Author will be held responsible for the payment of the Open Access Publishing Fees.
\n\nAll payments shall be due 30 days from the date of the issued invoice. The Corresponding Author or the payer on the Corresponding Author's and Co-Authors' behalf will bear all banking and similar charges incurred.
\n\n3.3 The Corresponding Author shall obtain in writing all consents necessary for the reproduction of any material in which a third-party right exists, including quotations, photographs and illustrations, in all editions of the Chapter worldwide for the full term of the above licenses, and shall provide to IntechOpen upon request the original copies of such consents for inspection (at IntechOpen's option) or photocopies of such consents.
\n\nThe Corresponding Author shall obtain written informed consent for publication from people who might recognize themselves or be identified by others (e.g. from case reports or photographs).
\n\n3.4 The Corresponding Author and any Co-Author shall respect confidentiality rights during and after the termination of this Agreement. The information contained in all correspondence and documents as part of the publishing activity between IntechOpen and the Corresponding Author and any Co-Author are confidential and are intended only for the recipient. The contents may not be disclosed publicly and are not intended for unauthorized use or distribution. Any use, disclosure, copying, or distribution is prohibited and may be unlawful.
\n\n4. CORRESPONDING AUTHOR'S WARRANTY
\n\n4.1 The Corresponding Author represents and warrants that the Chapter does not and will not breach any applicable law or the rights of any third party and, specifically, that the Chapter contains no matter that is defamatory or that infringes any literary or proprietary rights, intellectual property rights, or any rights of privacy. The Corresponding Author warrants and represents that: (i) the Chapter is the original work of themselves and any Co-Author and is not copied wholly or substantially from any other work or material or any other source; (ii) the Chapter has not been formally published in any other peer-reviewed journal or in a book or edited collection, and is not under consideration for any such publication; (iii) they themselves and any Co-Author are qualifying persons under section 154 of the Copyright, Designs and Patents Act 1988; (iv) they themselves and any Co-Author have not assigned and will not during the term of this Publication Agreement purport to assign any of the rights granted to IntechOpen under this Publication Agreement; and (v) the rights granted by this Publication Agreement are free from any security interest, option, mortgage, charge or lien.
\n\nThe Corresponding Author also warrants and represents that: (i) they have the full power to enter into this Publication Agreement on their own behalf and on behalf of each Co-Author; and (ii) they have the necessary rights and/or title in and to the Chapter to grant IntechOpen, on behalf of themselves and any Co-Author, the rights and licenses expressed to be granted in this Publication Agreement. If the Chapter was prepared jointly by the Corresponding Author and any Co-Author, the Corresponding Author warrants and represents that: (i) each Co-Author agrees to the submission, license and publication of the Chapter on the terms of this Publication Agreement; and (ii) they have the authority to enter into this Publication Agreement on behalf of and bind each Co-Author. The Corresponding Author shall: (i) ensure each Co-Author complies with all relevant provisions of this Publication Agreement, including those relating to confidentiality, performance and standards, as if a party to this Publication Agreement; and (ii) remain primarily liable for all acts and/or omissions of each such Co-Author.
\n\nThe Corresponding Author agrees to indemnify and hold IntechOpen harmless against all liabilities, costs, expenses, damages and losses and all reasonable legal costs and expenses suffered or incurred by IntechOpen arising out of or in connection with any breach of the aforementioned representations and warranties. This indemnity shall not cover IntechOpen to the extent that a claim under it results from IntechOpen's negligence or willful misconduct.
\n\n4.2 Nothing in this Publication Agreement shall have the effect of excluding or limiting any liability for death or personal injury caused by negligence or any other liability that cannot be excluded or limited by applicable law.
\n\n5. TERMINATION
\n\n5.1 IntechOpen has a right to terminate this Publication Agreement for quality, program, technical or other reasons with immediate effect, including without limitation (i) if the Corresponding Author or any Co-Author commits a material breach of this Publication Agreement; (ii) if the Corresponding Author or any Co-Author (being an individual) is the subject of a bankruptcy petition, application or order; or (iii) if the Corresponding Author or any Co-Author (being a company) commences negotiations with all or any class of its creditors with a view to rescheduling any of its debts, or makes a proposal for or enters into any compromise or arrangement with any of its creditors.
\n\nIn case of termination, IntechOpen will notify the Corresponding Author, in writing, of the decision.
\n\n6. INTECHOPEN’S DUTIES AND RIGHTS
\n\n6.1 Unless prevented from doing so by events outside its reasonable control, IntechOpen, in its discretion, agrees to publish the Chapter attributing it to the Corresponding Author and any Co-Author.
\n\n6.2 IntechOpen has the right to use the Corresponding Author’s and any Co-Author’s names and likeness in connection with scientific dissemination, retrieval, archiving, web hosting and promotion and marketing of the Chapter and has the right to contact the Corresponding Author and any Co-Author until the Chapter is publicly available on any platform owned and/or operated by IntechOpen.
\n\n6.3 IntechOpen is granted the authority to enforce the rights from this Publication Agreement, on behalf of the Corresponding Author and any Co-Author, against third parties (for example in cases of plagiarism or copyright infringements). In respect of any such infringement or suspected infringement of the copyright in the Chapter, IntechOpen shall have absolute discretion in addressing any such infringement which is likely to affect IntechOpen's rights under this Publication Agreement, including issuing and conducting proceedings against the suspected infringer.
\n\n7. MISCELLANEOUS
\n\n7.1 Further Assurance: The Corresponding Author shall and will ensure that any relevant third party (including any Co-Author) shall, execute and deliver whatever further documents or deeds and perform such acts as IntechOpen reasonably requires from time to time for the purpose of giving IntechOpen the full benefit of the provisions of this Publication Agreement.
\n\n7.2 Third Party Rights: A person who is not a party to this Publication Agreement may not enforce any of its provisions under the Contracts (Rights of Third Parties) Act 1999.
\n\n7.3 Entire Agreement: This Publication Agreement constitutes the entire agreement between the parties in relation to its subject matter. It replaces and extinguishes all prior agreements, draft agreements, arrangements, collateral warranties, collateral contracts, statements, assurances, representations and undertakings of any nature made by or on behalf of the parties, whether oral or written, in relation to that subject matter. Each party acknowledges that in entering into this Publication Agreement it has not relied upon any oral or written statements, collateral or other warranties, assurances, representations or undertakings which were made by or on behalf of the other party in relation to the subject matter of this Publication Agreement at any time before its signature (together "Pre-Contractual Statements"), other than those which are set out in this Publication Agreement. Each party hereby waives all rights and remedies which might otherwise be available to it in relation to such Pre-Contractual Statements. Nothing in this clause shall exclude or restrict the liability of either party arising out of its pre-contract fraudulent misrepresentation or fraudulent concealment.
\n\n7.4 Waiver: No failure or delay by a party to exercise any right or remedy provided under this Publication Agreement or by law shall constitute a waiver of that or any other right or remedy, nor shall it preclude or restrict the further exercise of that or any other right or remedy. No single or partial exercise of such right or remedy shall preclude or restrict the further exercise of that or any other right or remedy.
\n\n7.5 Variation: No variation of this Publication Agreement shall be effective unless it is in writing and signed by the parties (or their duly authorized representatives).
\n\n7.6 Severance: If any provision or part-provision of this Publication Agreement is or becomes invalid, illegal or unenforceable, it shall be deemed modified to the minimum extent necessary to make it valid, legal and enforceable. If such modification is not possible, the relevant provision or part-provision shall be deemed deleted.
\n\nAny modification to or deletion of a provision or part-provision under this clause shall not affect the validity and enforceability of the rest of this Publication Agreement.
\n\n7.7 No partnership: Nothing in this Publication Agreement is intended to, or shall be deemed to, establish or create any partnership or joint venture or the relationship of principal and agent or employer and employee between IntechOpen and the Corresponding Author or any Co-Author, nor authorize any party to make or enter into any commitments for or on behalf of any other party.
\n\n7.8 Governing law: This Publication Agreement and any dispute or claim (including non-contractual disputes or claims) arising out of or in connection with it or its subject matter or formation shall be governed by and construed in accordance with the law of England and Wales. The parties submit to the exclusive jurisdiction of the English courts to settle any dispute or claim arising out of or in connection with this Publication Agreement (including any non-contractual disputes or claims).
\n\nLast updated: 2020-11-27
\n\n\n\n
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I am also a member of the team in charge for the supervision of Ph.D. students in the fields of development of silicon based planar waveguide sensor devices, study of inelastic electron tunnelling in planar tunnelling nanostructures for sensing applications and development of organotellurium(IV) compounds for semiconductor applications. I am a specialist in data analysis techniques and nanosurface structure. I have served as the editor for many books, been a member of the editorial board in science journals, have published many papers and hold many patents.",institutionString:null,institution:{name:"Sheffield Hallam University",country:{name:"United Kingdom"}}},{id:"54525",title:"Prof.",name:"Abdul Latif",middleName:null,surname:"Ahmad",slug:"abdul-latif-ahmad",fullName:"Abdul Latif Ahmad",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"20567",title:"Prof.",name:"Ado",middleName:null,surname:"Jorio",slug:"ado-jorio",fullName:"Ado Jorio",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Universidade Federal de Minas Gerais",country:{name:"Brazil"}}},{id:"47940",title:"Dr.",name:"Alberto",middleName:null,surname:"Mantovani",slug:"alberto-mantovani",fullName:"Alberto Mantovani",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"12392",title:"Mr.",name:"Alex",middleName:null,surname:"Lazinica",slug:"alex-lazinica",fullName:"Alex Lazinica",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/12392/images/7282_n.png",biography:"Alex Lazinica is the founder and CEO of IntechOpen. After obtaining a Master's degree in Mechanical Engineering, he continued his PhD studies in Robotics at the Vienna University of Technology. Here he worked as a robotic researcher with the university's Intelligent Manufacturing Systems Group as well as a guest researcher at various European universities, including the Swiss Federal Institute of Technology Lausanne (EPFL). During this time he published more than 20 scientific papers, gave presentations, served as a reviewer for major robotic journals and conferences and most importantly he co-founded and built the International Journal of Advanced Robotic Systems- world's first Open Access journal in the field of robotics. Starting this journal was a pivotal point in his career, since it was a pathway to founding IntechOpen - Open Access publisher focused on addressing academic researchers needs. Alex is a personification of IntechOpen key values being trusted, open and entrepreneurial. Today his focus is on defining the growth and development strategy for the company.",institutionString:null,institution:{name:"TU Wien",country:{name:"Austria"}}},{id:"19816",title:"Prof.",name:"Alexander",middleName:null,surname:"Kokorin",slug:"alexander-kokorin",fullName:"Alexander Kokorin",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/19816/images/1607_n.jpg",biography:"Alexander I. Kokorin: born: 1947, Moscow; DSc., PhD; Principal Research Fellow (Research Professor) of Department of Kinetics and Catalysis, N. Semenov Institute of Chemical Physics, Russian Academy of Sciences, Moscow.\r\nArea of research interests: physical chemistry of complex-organized molecular and nanosized systems, including polymer-metal complexes; the surface of doped oxide semiconductors. He is an expert in structural, absorptive, catalytic and photocatalytic properties, in structural organization and dynamic features of ionic liquids, in magnetic interactions between paramagnetic centers. The author or co-author of 3 books, over 200 articles and reviews in scientific journals and books. He is an actual member of the International EPR/ESR Society, European Society on Quantum Solar Energy Conversion, Moscow House of Scientists, of the Board of Moscow Physical Society.",institutionString:null,institution:{name:"Semenov Institute of Chemical Physics",country:{name:"Russia"}}},{id:"62389",title:"PhD.",name:"Ali Demir",middleName:null,surname:"Sezer",slug:"ali-demir-sezer",fullName:"Ali Demir Sezer",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/62389/images/3413_n.jpg",biography:"Dr. Ali Demir Sezer has a Ph.D. from Pharmaceutical Biotechnology at the Faculty of Pharmacy, University of Marmara (Turkey). He is the member of many Pharmaceutical Associations and acts as a reviewer of scientific journals and European projects under different research areas such as: drug delivery systems, nanotechnology and pharmaceutical biotechnology. Dr. Sezer is the author of many scientific publications in peer-reviewed journals and poster communications. Focus of his research activity is drug delivery, physico-chemical characterization and biological evaluation of biopolymers micro and nanoparticles as modified drug delivery system, and colloidal drug carriers (liposomes, nanoparticles etc.).",institutionString:null,institution:{name:"Marmara University",country:{name:"Turkey"}}},{id:"61051",title:"Prof.",name:"Andrea",middleName:null,surname:"Natale",slug:"andrea-natale",fullName:"Andrea Natale",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"100762",title:"Prof.",name:"Andrea",middleName:null,surname:"Natale",slug:"andrea-natale",fullName:"Andrea Natale",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"St David's Medical Center",country:{name:"United States of America"}}},{id:"107416",title:"Dr.",name:"Andrea",middleName:null,surname:"Natale",slug:"andrea-natale",fullName:"Andrea Natale",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Texas Cardiac Arrhythmia",country:{name:"United States of America"}}},{id:"64434",title:"Dr.",name:"Angkoon",middleName:null,surname:"Phinyomark",slug:"angkoon-phinyomark",fullName:"Angkoon Phinyomark",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/64434/images/2619_n.jpg",biography:"My name is Angkoon Phinyomark. I received a B.Eng. degree in Computer Engineering with First Class Honors in 2008 from Prince of Songkla University, Songkhla, Thailand, where I received a Ph.D. degree in Electrical Engineering. My research interests are primarily in the area of biomedical signal processing and classification notably EMG (electromyography signal), EOG (electrooculography signal), and EEG (electroencephalography signal), image analysis notably breast cancer analysis and optical coherence tomography, and rehabilitation engineering. I became a student member of IEEE in 2008. During October 2011-March 2012, I had worked at School of Computer Science and Electronic Engineering, University of Essex, Colchester, Essex, United Kingdom. In addition, during a B.Eng. I had been a visiting research student at Faculty of Computer Science, University of Murcia, Murcia, Spain for three months.\n\nI have published over 40 papers during 5 years in refereed journals, books, and conference proceedings in the areas of electro-physiological signals processing and classification, notably EMG and EOG signals, fractal analysis, wavelet analysis, texture analysis, feature extraction and machine learning algorithms, and assistive and rehabilitative devices. I have several computer programming language certificates, i.e. Sun Certified Programmer for the Java 2 Platform 1.4 (SCJP), Microsoft Certified Professional Developer, Web Developer (MCPD), Microsoft Certified Technology Specialist, .NET Framework 2.0 Web (MCTS). 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