Relevant bibliographies by topics / NSCLP

Academic literature on the topic 'NSCLP'

Author: Grafiati
Published: 11 March 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'NSCLP.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "NSCLP"

1

Machado, Renato Assis, Lilianny Querino Rocha de Oliveira, Ana Lúcia Carrinho Ayroza Rangel, Silvia Regina de Almeida Reis, Rafaela Scariot, Daniella Reis Barbosa Martelli, Hercílio Martelli-Júnior, and Ricardo D. Coletta. "Brazilian Multiethnic Association Study of Genetic Variant Interactions among FOS, CASP8, MMP2 and CRISPLD2 in the Risk of Nonsyndromic Cleft Lip with or without Cleft Palate." Dentistry Journal 11, no. 1 (December 26, 2022): 7. http://dx.doi.org/10.3390/dj11010007.

Full text
Abstract:
Associations of CRISPLD2 (cysteine-rich secretory protein LCCL domain containing 2) and genes belonging to its activation pathway, including FOS (Fos proto-oncogene), CASP8 (caspase 8) and MMP2 (matrix metalloproteinase 2), with nonsyndromic orofacial cleft risk, have been reported, but the results are yet unclear. The aim of this study was to evaluate single nucleotide polymorphisms (SNPs) in FOS, CASP8 and MMP2 and to determine their SNP-SNP interactions with CRISPLD2 variants in the risk of nonsyndromic cleft lip with or without cleft palate (NSCL±P) in the Brazilian population. The SNPs rs1046117 (FOS), rs3769825 (CASP8) and rs243836 (MMP2) were genotyped using TaqMan allelic discrimination assays in a case-control sample containing 801 NSCL±P patients (233 nonsyndromic cleft lip only (NSCLO) and 568 nonsyndromic cleft lip and palate (NSCLP)) and 881 healthy controls via logistic regression analysis adjusted for the effects of sex and genomic ancestry proportions with a multiple comparison p value set at ≤0.01. SNP-SNP interactions with rs1546124, rs8061351, rs2326398 and rs4783099 in CRISPLD2 were performed with the model-based multifactor dimensionality reduction test complemented with a 1000 permutation-based strategy. Although the association between FOS rs1046117 and risk of NSCL±P reached only nominal p values, NSCLO risk was significantly higher in carriers of the FOS rs1046117 C allele (OR: 1.28, 95% CI: 1.10–1.64, p = 0.004), TC heterozygous genotype (OR: 1.59, 95% CI: 1.16–2.18, p = 0.003), and in the dominant model (OR: 1.50, 95% CI: 1.10–2.02, p = 0.007). Individually, no significant associations between cleft risk and the SNPs in CASP8 and MMP2 were observed. SNP-SNP interactions involving CRISPLD2 variants and rs1046117 (FOS), rs3769825 (CASP8) and rs243836 (MMP2) yielded several significant p values, mostly driven by FOS rs1046117 and CASP8 rs3769825 in NSCL±P, FOS rs1046117 in NSCLO and CRISPLD2 rs8061351 in NSCLP. Our study is the first in the Brazilian population to reveal the association of FOS rs1046117 with NSCLO risk, and to support that CRISPLD2, CASP8, FOS and MMP2 interactions may be related to the pathogenesis of this common craniofacial malformation.
APA, Harvard, Vancouver, ISO, and other styles
2

Savitha, Sathyaprasad, S. M. Sharma, Shetty Veena, and R. Rekha. "Single nucleotide polymorphism of bone morphogenetic protein 4 gene: A risk factor of non-syndromic cleft lip with or without palate." Indian Journal of Plastic Surgery 48, no. 02 (May 2015): 159–64. http://dx.doi.org/10.4103/0970-0358.163053.

Full text
Abstract:
ABSTRACT Background: The bone morphogenetic protein (BMP) signalling pathway is crucial in a number of developmental processes and is critical in the formation of variety of craniofacial elements including cranial neural crest, facial primordium, tooth, lip and palate. It is an important mediator in regulation of lip and palate fusion, cartilage and bone formation. Aim: To study the role of mutation of BMP4 genes in the aetiology of non-syndromic cleft lip with or without palate (NSCL ± P) and identify it directly from human analyses. Materials and Methods: A case-control study was done to evaluate whether BMP4T538C polymorphism, resulting in an amino acid change of Val=Ala (V152A) in the polypeptide, is associated with NSCL ± P in an Indian paediatric population. Genotypes of 100 patients with NSCL ± P and 100 controls (in whom absence of CL ± P was confirmed in three generations) were detected using a polymerase chain reaction-restriction fragment length polymorphism strategy. Logistic regression was performed to evaluate allele and genotype association with NSCLP. Results: Results showed significant association between homozygous CC genotype with CL ± P (odds ratio [OR]-5.59 and 95% confidence interval [CI] = 2.85-10.99). The 538C allele carriers showed an increased risk of NSCL ± P as compared with 538 T allele (OR - 4.2% CI = 2.75-6.41). Conclusion: This study suggests an association between SNP of BMP4 gene among carriers of the C allele and increased risk for NSCLP in an Indian Population. Further studies on this aspect can scale large heights in preventive strategies for NSCLP that may soon become a reality.
APA, Harvard, Vancouver, ISO, and other styles
3

Goldsberry, Grant, Dan O'Leary, Rich Hichwa, and Peg Nopoulos. "Functional Abnormalities in the Neural Circuitry of Reading in Men with Nonsyndromic Clefts of the Lip or Palate." Cleft Palate-Craniofacial Journal 43, no. 6 (November 2006): 683–90. http://dx.doi.org/10.1597/05-043.

Full text
Abstract:
Objective: The current study was designed to evaluate the neurobiology of reading in a group of men with nonsyndromic clefts of the lip or palate (NSCLP) compared with healthy controls by positron emission tomography. Design: Subjects included eight men with NSCLP compared with six healthy control men. By using radioactively labeled water (O15), regional brain blood flow was obtained during the performance of three simple reading tasks: reading unrelated words, reading unrelated sentences, and reading a story. Results: During each of the reading conditions, NSCLP subjects compared with healthy controls showed increased blood flow in areas previously reported to be involved in language processing and reading (inferior frontal lobe, cerebellum, and occipital lobe). The increased blood flow suggests a possible neural inefficiency. In contrast, when analyzing the brain regions involved in more complex language functioning (reading stories compared with reading only words), control subjects showed an increase in blood flow in a distributed neural circuit, whereas the NSCLP subjects showed a decrease in flow in these regions. Additionally, the NSCLP subjects had activation of several regions not activated in the healthy controls, suggesting a compensatory circuit used for this more complex reading task. Conclusions: These results indicate that subjects with NSCLP show abnormalities in the function of the distributed neural circuitry used for oral reading.
APA, Harvard, Vancouver, ISO, and other styles
4

Xavier, D. L., Y. A. Arif, R. V. Murali, S. Kishore Kumar, S. Vipin Kumar, R. Tamang, K. Thangaraj, and L. V. K. Bhaskar. "Analysis of Microsatellite Polymorphisms in South Indian Patients with Non Syndromic Cleft Lip and Palate." Balkan Journal of Medical Genetics 16, no. 1 (June 1, 2013): 49–54. http://dx.doi.org/10.2478/bjmg-2013-0017.

Full text
Abstract:
Abstract Non syndromic cleft lip and/or palate (NSCLP) is a complex congenital anomaly with varying incidence among patients of different geographical origins. Multiple contributing factors are known to trigger the cleft formation. There are several genes involved in the aetiology of NSCLP and they are different in different populations. The genetic components of clefts that underlie the susceptibility to respond to the environment still remain unclear. In this study, five microsatellite polymorphisms from five candidate genes were employed to analyze the association between these genes and NSCLP in 83 patients and 90 controls. Genotyping was performed by separating and visualizing the fluorescently-labeled polymerase chain reaction (PCR) products. The association of the five microsatellite polymorphisms with NSCLP was tested by using the CLUMP v1.9 program that uses the Monte Carlo method. The genotypic distribution is in Hardy-Weinberg equilibrium in the control group for only the MSX1 and DLX3 genes. The RARA microsatellite was significantly associated with NSCLP. Our results suggest that the RARA gene is involved in pathogenesis of cleft lip and palate in South Indians.
APA, Harvard, Vancouver, ISO, and other styles
5

Andrews-Casal, Melanie, Dennis Johnston, Jack Fletcher, John B. Mulliken, Samuel Stal, and Jacqueline T. Hecht. "Cleft Lip with or without Cleft Palate: Effect of Family History on Reproductive Planning, Surgical Timing, and Parental Stress." Cleft Palate-Craniofacial Journal 35, no. 1 (January 1998): 52–57. http://dx.doi.org/10.1597/1545-1569_1998_035_0052_clwowc_2.3.co_2.

Full text
Abstract:
Objective This study tested whether the presence of a family history of non-syndromic cleft lip with or without cleft palate (NSCLP) lessens the negative impact on reproductive planning, decreases treatment anxiety, and relieves parental stress when there is a recurrent cleft. Design Sixty-one participating families, retrospectively ascertained through their children with NSCLP, were divided into two groups: those with a family history of clefting and those in which only the proband was affected. Setting Each family completed a questionnaire either at their home or during a clinic visit. Participants Questionnaires were distributed to 117 families with an NSCLP child. Of these 117, 49 (42%) had another family member with NSCLP and 68 (58%) had no prior history of clefting. Sixty-one (52%) families returned the questionnaire and were categorized by family history. Main outcome Measures The Parenting Stess Index and the Hollingshead Index of Social Position were included with family and medical history questions in the 137-item questionnaire. Results The reproductive plans of the two groups were quite similar and were not dependent on the families' actual or perceived recurrence risks of NSCLP. The majority (85%) of the children with NSCLP underwent surgical closure at the recommended age. The two groups did not significantly differ on any score on the Parenting Stress Index, indicating a similar parental stress level between the groups. Conclusions These findings suggest that family history does not significantly influence reproductive plans, timing of cleft repair, or stress of parents of a child with NSCLP. Further, these results indicate a need for additional psychosocial study of this population.
APA, Harvard, Vancouver, ISO, and other styles
6

Otero, Liliana, Luis Bermudez, Karina Lizarraga, Irene Tangco, Rocelyn Gannaban, and Daniel Meles. "A Comparative Study of Facial Asymmetry in Philippine, Colombian, and Ethiopian Families with Nonsyndromic Cleft Lip Palate." Plastic Surgery International 2012 (October 24, 2012): 1–6. http://dx.doi.org/10.1155/2012/580769.

Full text
Abstract:
Objective. To compare the asymmetry displayed by Philippine, Colombian, and Ethiopian unaffected parents of patients with nonsyndromic cleft palate (NSCLP) and a control population. Methods. Facial measurements were compared between unaffected parents of NSCLP patients and those in the control group for three populations from South America, Asia, and Africa by anthropometric and photographic measurements. Fluctuating and directional asymmetries, height and width proportions, were analyzed and compared. Results. Fluctuating asymmetries (ear length, middle line to Zigion perpendicular for left and right sides) and variations in the facial thirds demonstrated statistical significance in the study group of unaffected parents from Colombia and Philippines, while increased interorbital distance was evident in the unaffected Ethiopian parents of NSCLP patients. Conclusions. The facial differences in unaffected parents could indicate an underlying genetic liability. Identification of these differences has relevance in the understanding of the etiology of NSCLP.
APA, Harvard, Vancouver, ISO, and other styles
7

Khan, Mahamad Irfanulla, Prashanth CS, and Narasimhamurty Srinath. "Role of PAX7 Gene rs766325 and rs4920520 Polymorphisms in the Etiology of Non-syndromic Cleft Lip and Palate: A Genetic Study." Global Medical Genetics 09, no. 03 (July 15, 2022): 208–11. http://dx.doi.org/10.1055/s-0042-1748531.

Full text
Abstract:
AbstractNon-syndromic cleft lip and palate (NSCLP) is one of the most common birth defects in humans with an overall prevalence of ∼1 in 700 live births around the world. The etiology of NSCLP is complex involving multiple genes, environmental factors, and gene-to-gene interactions. Several genome-wide associations (GWA) studies have shown the association of the paired box 7 (PAX7) gene in the etiology of cleft lip and palate in different populations worldwide. However, there are no reported studies on the association between the rs766325 and rs4920520 polymorphisms and the risk of developing NSCLP in the Indian population. Hence, the present study aimed to test for the probable association between rs766325 and rs4920520 polymorphisms among NSCLP Indian population using a case-parent trio design. Forty case-parent trios were selected from the cleft lip and palate center based on the inclusion and exclusion criteria. Genomic DNA was isolated from the cases and their parents. The rs766325 and rs4920520 polymorphisms of the PAX7 gene were analyzed for their association using the MassARRAY analysis. The statistical analysis was done using the PLINK software. The rs766325 and rs4920520 polymorphisms were tested for the Hardy–Weinberg equilibrium. None of the polymorphisms showed any statistical significance. Hence, the rs766325 and rs4920520 polymorphisms of the PAX7 gene were found to be not associated with NSCLP in the Indian case-parent trios.
APA, Harvard, Vancouver, ISO, and other styles
8

Alam, Mohammad Khursheed, Ahmed Ali Alfawzan, Fatema Akhter, Haytham Jamil Alswairki, and Prabhat Kumar Chaudhari. "Evaluation of Lip Morphology and Nasolabial Angle in Non-Syndromic Cleft Lip and/Palate and Non-Cleft Individuals." Applied Sciences 12, no. 1 (December 30, 2021): 357. http://dx.doi.org/10.3390/app12010357.

Full text
Abstract:
Objective: To investigate the variation between the non-syndromic cleft lip and/or palate (NSCLP) and non-cleft (NC) subjects in relation to the lip morphology (LM) and nasolabial angle (NLA). Materials and Methods: Lateral cephalogram (Late. Ceph.) of 123 individuals (92 NSCLP [29 = bilateral cleft lip and palate (BCLP), 41 = unilateral cleft lip and palate (UCLP), 9 = unilateral cleft lip and alveolus (UCLA), 13 = unilateral cleft lip (UCL)], and 31 NC) who did not undergo any orthodontic treatment were investigated. By WebCeph, an artificial intelligence- (A.I.) driven software, 2 (two) parameters of LM, namely upper lip to E line (LM-1) and lower lip to E line (LM-2), and NLA analysis was carried out for each individual. Multiple tests were carried out for statistical analysis. Results: The mean ± SD observed for LM-1, LM-2, and NLA for NC individuals were 1.56 ± 2.98, 0.49 ± 3.51, and 97.20 ± 16.10, respectively. On the other hand, the mean ± SD of LM-1, LM-2, and NLA for NSCLP individuals were 4.55 ± 4.23, 1.68 ± 2.82, and 82.02 ± 14.66, respectively. No significant variation was observed with respect to gender and side. NSCLP (different types) and NC individuals showed significant disparities in LM-1 and NLA. Conclusion: It can be concluded that parameters of lip morphology such as LM-1, LM-2, and NLA vary among NSCLP and NC individuals.
APA, Harvard, Vancouver, ISO, and other styles
9

Liberton, Denise K., Payal Verma, Konstantinia Almpani, Peter W. Fung, Rashmi Mishra, Snehlata Oberoi, Figen Ç. Şenel, et al. "Craniofacial Analysis May Indicate Co-Occurrence of Skeletal Malocclusions and Associated Risks in Development of Cleft Lip and Palate." Journal of Developmental Biology 8, no. 1 (January 28, 2020): 2. http://dx.doi.org/10.3390/jdb8010002.

Full text
Abstract:
Non-syndromic orofacial clefts encompass a range of morphological changes affecting the oral cavity and the craniofacial skeleton, of which the genetic and epigenetic etiologic factors remain largely unknown. The objective of this study is to explore the contribution of underlying dentofacial deformities (also known as skeletal malocclusions) in the craniofacial morphology of non-syndromic cleft lip and palate patients (nsCLP). For that purpose, geometric morphometric analysis was performed using full skull cone beam computed tomography (CBCT) images of patients with nsCLP (n = 30), normocephalic controls (n = 60), as well as to sex- and ethnicity- matched patients with an equivalent dentofacial deformity (n = 30). Our outcome measures were shape differences among the groups quantified via principal component analysis and associated principal component loadings, as well as mean shape differences quantified via a Procrustes distance among groups. According to our results, despite the shape differences among all three groups, the nsCLP group shares many morphological similarities in the maxilla and mandible with the dentofacial deformity group. Therefore, the dentoskeletal phenotype in nsCLP could be the result of the cleft and the coexisting dentofacial deformity and not simply the impact of the cleft.
APA, Harvard, Vancouver, ISO, and other styles
10

Neela, Praveen Kumar, Gosla Srinivas Reddy, Akhter Husain, Vasavi Mohan, Sravya Thumoju, and Rajeshwari BV. "Association of Single Nucleotide Polymorphisms on Locus 18q21.1 in the Etiology of Nonsyndromic Cleft Lip Palate (NSCLP) in Indian Multiplex Families." Global Medical Genetics 08, no. 01 (February 19, 2021): 024–31. http://dx.doi.org/10.1055/s-0041-1723087.

Full text
Abstract:
Abstract Background Cleft lip palate (CLP) is a common congenital anomaly with multifactorial etiology. Many polymorphisms at different loci on multiple chromosomes were reported to be involved in its etiology. Genetic research on a single multigenerational American family reported 18q21.1 locus as a high-risk locus for nonsyndromic CLP (NSCLP). However, its association in multiple multiplex families and Indian population is not analyzed for its association in NSCLP. Aim This study was aimed to evaluate whether high-risk single nucleotide polymorphisms (SNPs) on chromosome 18q21.1 are involved in the etiology of NSCLP in multiplex Indian families. Materials and Methods Twenty multigenerational families affected by NSCLP were selected for the study after following inclusion and exclusion criteria. Genomic DNA was isolated from the affected and unaffected members of these 20 multiplex families and sent for genetic analysis. High-risk polymorphisms, such as rs6507872 and rs8091995 of CTIF, rs17715416, rs17713847 and rs183559995 of MYO5B, rs78950893 of SMAD7, rs1450425 of LOXHD1, and rs6507992 of SKA1 candidate genes on the 18q21.1 locus, were analyzed. SNP genotyping was done using the MassARRAY method. Statistical analysis of the genomic data was done by PLINK. Results Polymorphisms followed the Hardy–Weinberg equilibrium. In the allelic association, all the polymorphisms had a p-value more than 0.05. The odds ratio was not more than 1.6 for all the SNPs. Conclusion High-risk polymorphisms, such as rs6507872 and rs8091995 of CTIF, rs17715416, rs17713847 and rs183559995 of MYO5B, rs78950893 of SMAD7, rs1450425 of LOXHD1, and rs6507992 of SKA1 in the locus 18q21.1, are not associated with NSCLP in Indian multiplex families.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "NSCLP"

1

Bianco, Anna Monica Rosaria. "Characterization of novel genes insolved in non syndromic cleft lip with or with out cleft palate (NSCLP)." Doctoral thesis, Università degli studi di Trieste, 2010. http://hdl.handle.net/10077/3735.

Full text
Abstract:
2008/2009
Non-syndromic cleft lip with or without cleft palate (NSCLP) is one of the most common birth defect. Genetic studies on human populations have identified numerous predisposing factors, as MYH9 and JARID2, whose role during palatogenesis remains obscure. In order to improve our knowledge on pathogenetic mechanisms, we carried out expression studies during mouse palate development using RNA in situ hybridization. As reference genes (Tgfb3, Irf6, Pvrl1, Foxe1 and Tp63) known to be required for correct palate formation, Jarid2 and Myh9 are expressed in the epithelial cells of the palatine processes before and at the time of contact. Then, this signal decreases and eventually disappears concomitantly with the degradation of the medial epithelial cells. Consistent with these observations, RT-PCR carried out on dissected palatal shelves detected products of Myh9 and Jarid2 from embryonic day E14.0 to E15.0 with a pick at E14.5, the stage when shelves appose in the midline. Taken together, these expression studies strongly support the association studies that designate these genes as predisposing factors for NSCLP. In multifactorial diseases as NSCLP once genetic studies demonstrate association, a major challenge is to identify mutations. In this regard, we started analyzing two in linkage disequilibrium SNPs (rs3752462 of MYH9 and rs2076056 of JARID2) that could be involved in defective splicing mechanisms, as hypothesized on the basis of their localization within splice sites. Using a hybrid minigene assay, however, we demonstrated that none of the allelic variants lead to any aberrant products at least in HeLa cells, the model used for this study. Moreover, we investigated whether alternative splicing events of the Myh9 gene detected in cochlea and brain (Li et al., 2008) could also be found in other tissues and palate. A small insertion of 12 bp between exon 4 and 5 (loop1) due to an alternative splicing was detected in all adult tissues analyzed. The same insertion was not detected in embryonic tissues, such as palatal samples at different stages of development, and brain. These results suggest that the genomic region of loop1 should be investigated in all risk haplotypes to search for pathogenetic variants. In conclusion, further investigations should be planned to explore the role of MYH9 and JARID2 in orofacial development in order to dissect signaling pathways during palate formation and identify the causative variants contributing to NSCLP.
XXII Ciclo
1973
APA, Harvard, Vancouver, ISO, and other styles
2

Krüger, Marcus. "Molekulare und funktionale Charakterisierung der neuronalen bHLH Transkritptionsfaktoren NSCL-1 und NSCL-2." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=969337183.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Pegoraro, Ilan Emanuel Moreira. "NSCL in the ETSI M2M platform." Master's thesis, Universidade de Aveiro, 2014. http://hdl.handle.net/10773/14704.

Full text
Abstract:
Mestrado em Engenharia de Computadores e Telemática
The evolution of every day gadgets into smart-devices able to react to their surrounding environment is enabling the development of novel applications aiming revolutionize the industry related to this technology. Currently much attention has been given to standardizing IoT and M2M in order to build an interoperable foundation that will enable the growth of the future Internet, where devices will communicate without, or at least minimizing, human intervention. In this dissertation is presented in first place issues such as: heterogeneity, scalability, addressing and the first approach taken by the ETSI M2M standard. Subsequently, is presented the ETSI M2M vision and high-level architecture together with current work in this area. Finally an implementation of the network middleware is going to be presented along with further testing.
A evolução dos dispositivos do dia a dia em dispositivos inteligentes capazes de reagir ao ambiente que os rodeia está a permitir a criação de novas aplicações que visam revolucionar a industria. Atualmente tem-se dado muita atenção a estandardização da Internet das Coisas e comunicações máquinaa- máquina, com o objetivo de construir uma fundação interoperável que permitirá o crescimento futuro da Internet, onde os dispositivos irão comunicar sem, ou com mínima, intervenção humana. Nesta dissertação é apresentado em primeiro lugar requisitos como heterogeneidade, escalabilidade, endereçamento e a primeira abordagem feita pelo standard M2M do ETSI. Consequentemente, é a apresentada a visão e a arquitetura e o trabalho realizado nesta área. Por fim é apresentada a implementação da componente de rede realizada nesta dissertação juntamente com os respetivos testes.
APA, Harvard, Vancouver, ISO, and other styles
4

Chater, Emily. "Novel therapeutic targets in NSCLC resistance to Erlotinib." Thesis, Imperial College London, 2017. http://hdl.handle.net/10044/1/50699.

Full text
Abstract:
Approximately 10% of non-small cell lung cancers (NSCLCs) have an activating mutation within the kinase domain of epidermal growth factor receptor (EGFR). Competitive tyrosine kinase inhibitors (TKIs), such as Erlotinib and Gefitinib, have been developed to therapeutically exploit this. These compounds have shown excellent clinical responses in approximately 77% of patients with EGFR-mutant driven lung cancer. However, despite positive initial response, patients develop resistance, and this is often attributed (50% of cases) to the T790M secondary mutation in the ATP binding pocket of EGFR. This mutation increases the receptors affinity for ATP which competes out reversible first-generation inhibitors such as erlotinib and gefitinib. This thesis aims to better understand the underlying mechanisms involved in the resistance to this compound. Changes in metabolism have frequently been associated with tumour progression and drug resistance in many cancer types. Here, to identify novel resistance mechanisms, 1H-NMR metabolic profiling was performed on EGFR-driven NSCLC cells with and without, the additional T790M-EGFR resistance mutation. This study identified both glutathione (GSH) and phosphatidylcholine metabolism as two key pathways perturbed in erlotinib-resistant cells. Interestingly, 1H-NMR revealed lower levels of both oxidised and reduced forms of GSH in erlotinib-resistant cell lines and this was verified by colorimetric assays. This change correlated with reduced mRNA expression of GSH synthesizing enzymes in resistant cell lines. Increasing cellular GSH levels by siRNA-mediated targeting of GSH degrading enzymes sensitised erlotinib-resistant cells to erlotinib treatment. In addition, the use of GSH synthesizing enzyme inhibitors such as Buthionine Sulfoximine (BSO), which targets the gamma-glutamylcysteine synthetase (GCS, GSH synthesising enzyme) and degrading enzyme inhibitors such as Ethacrynic acid (EA) (inhibits glutathione S-transferase) increased and decreased resistance to erlotinib, respectively. EA also showed promising results in vivo as BALB/c nude mice, injected subcutaneously with PC9ER cells, showed increased sensitivity to erlotinib treatment when co-administered with EA. Furthermore, we demonstrated that mutant EGFR signalling can modulate the transcription of GSH enzymes likely via changes in the regulation of the transcription factor, Nuclear Factor (Erythroid-Derived 2)-Like 2 (NRF2). Targeting NRF2 using siRNAs decreased GSH abundance and increased erlotinib resistance. However, at present we do not understand how raised GSH levels might cause resistance to erlotinib in lung cancer cells expressing activated T790M-EGFR. To discover other differences between erlotinib-resistant and sensitive cells, we employed reverse phase protein array (RPPA) and, following DAVID bio-informatics analysis, 4 identified changes in both beta-oxidation and ataxia telangiectasia mutated kinase (ATM)/Ataxia Telangiectasia and Rad3-related kinase (ATR) cell cycle checkpoint proteins. Changes in these signalling molecules were confirmed by Western blotting. Yet, only targeting the ATR pathway affected the resistance to erlotinib in PC9ER cell lines. Indeed, inhibition of WEE1 with the compound MK1775 may hold promise as a treatment for patients with erlotinib-resistant NSCLC. In short, this work has identified GSH degrading enzymes and WEE1 as novel targets for reversing erlotinib resistance in EGFR-driven NSCLC. However, further investigation is needed to understand the mechanisms involved.
APA, Harvard, Vancouver, ISO, and other styles
5

Holgersson, Georg. "Prognostic Factors in Non-Small Cell Lung Cancer (NSCLC)." Doctoral thesis, Uppsala universitet, Experimentell och klinisk onkologi, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-327925.

Full text
Abstract:
Background: Non-small cell lung cancer (NSCLC) is the cancer disease with the highest mortality globally. About 75% of NSCLC patients are diagnosed in an advanced stage where surgical treatment is not possible. For patients with locally advanced disease without distant metastases, the treatment of choice is curatively intended radiotherapy. However, this treatment has considerable side effects and many patients relapse. To individualize the treatment strategy for these patients, it is essential to have as much prognostic information as possible. The aim of this thesis was to investigate the prognostic significance of histology and pre-treatment hematopoietic blood parameters. Material and Methods: Data were collected retrospectively for NSCLC patients treated between 1990 and 2000 with curatively intended radiotherapy. The data were obtained by manually searching patient records from all radiation oncology departments in Sweden. The prognostic significance of histology, and pre-treatment levels of hemoglobin (Hgb), white blood cells (WBC) and platelets (Plt) were analyzed in relation to overall survival using univariate and multivariate statistical methods. These prognostic factors were further analyzed in a chemoradiation patient cohort and in a cohort of patients with recurrent NSCLC treated with palliative docetaxel, or the insulin-like growth factor 1 receptor (IGF-1R) modulator AXL1717. Results: In the cohort of NSCLC patients treated between 1990 and 2000, squamous cell carcinoma (SCC) histology and pre-treatment anemia (Hgb <110 g/L), leukocytosis (WBC > 9.0 x109/L), and thrombocytosis (Plt >350 x109/L) were independent prognostic factors for shorter overall survival. However, in the chemoradiation cohort only thrombocytosis retained independent prognostic significance in a multivariate analysis. In the cohort of patients with recurrent disease treated with palliative systemic therapy, only leukocytosis was significantly associated with worse survival. Conclusions: Routine pre-treatment hematopoietic blood parameters—together with other prognostic factors such as disease stage and performance status—can provide decision-making support when individualizing treatment of NSCLC. The prognostic role of histology is unclear and further research is warranted to determine its significance.
APA, Harvard, Vancouver, ISO, and other styles
6

Stamatkin, Christopher W. "PHOSPHATIDYLINOSITOL 3-KINASE (PI3K) AS A THERAPEUTIC TARGET IN NSCLC." UKnowledge, 2014. http://uknowledge.uky.edu/pharmacy_etds/58.

Full text
Abstract:
Deregulated activation of phosphatidylinositol 3-kinase (PI3K) pathway is central to many human malignancies. The functions of this pathway are critical for normal cell metabolism, proliferation, and survival. In lung cancers, the PI3K pathway activity is often aberrantly driven by multiple mutations, including EGFR, KRAS, and PIK3CA. Molecules targeting the PI3K pathway are intensely investigated as potential anti-cancer agents. Although inhibitors of the pathway are currently in clinical trials, rational and targeted use of these compounds, alone or in combination, requires an understanding of isoform-specific activity in context. We sought to identify class IA PI3K enzyme (p110a/PIK3CA, p110b/PIK3CB, p110d/PIK3CD) activities using isoform-specific inhibitors in a lung cancer model system. Treatment of non-small cell lung cancer (NSCLC) cell lines with PIK3CA, PIK3CB, PIK3CD or PIK3CB/D inhibitors resulted in pharmacokinetic and pharmacodynamic responses that frequently tracked with a specific mutation status. Activation of PIK3CA dictated response to the PIK3CA-specific inhibitor while deletion of PTEN phosphatase indicated response to the PIK3CB inhibitor. The PIK3CD isoform-specific inhibitors lacked efficacy in all NSCLC cell lines tested, however treatment at increased concentrations likely provide concurrent inhibition of both PIK3CB/D isoforms improving activity of either agent alone but did not track with a single biomarker. The observed pharmacodynamic and proliferation responses to isoform-specific inhibitors suggested that PI3K isoforms may functionally compensate for loss of another in certain genetic backgrounds. These studies demonstrate unanticipated cellular responses to PI3K isoform inhibition in NSCLC, suggesting that patient populations with specific mutations can benefit from certain isoform-selective inhibitors, or combinations, allowing for rational and targeted clinical use of these agents.
APA, Harvard, Vancouver, ISO, and other styles
7

Chatterjee, Saradiya. "Role of TLR7 in non-small cell lung carcinona (NSCLC)." Paris 6, 2013. http://www.theses.fr/2013PA066063.

Full text
Abstract:
Le cancer du poumon cause de plus d’un million de décès par an, et le progonstique est très somber, avec un taux de survie à 5 ans de l’ordre de 8 à 12%. La stimulation des TLRs par des ligands agonistes naturels comme les PAMPs et les DAMPs résulte en l’activation d’une cascade de signalisation conduisant à l’expression de molecules proinflammatoires. Nous avons montré que la stimulation de lignées cellulaires de tumeur pulmonaire par des agonistes de TLR7 induit une survie cellulaire et une résistance à la mort induite par chimiothérapie in vitro. Nous avons étudié in vivo les effets d’injections d’agonistes de TLR7 sur la croissance tumorale et la résistance à la chimiothérapie dans des souris NOD/SCID et C57BL/6. L’injection de loxoribine, ou de CL264 a un effet pro-tumoral sur la croissance des cellules A549 et CL264, respectivement, et induit une chimioresistance dans des souris NOD/SCID. Le blocage de TLR7 réverse l’effet pro-tumoral de l’agoniste. Par ailleurs, l’injection de faible dose de CL264 a un effet anti-tumoral sur les cellules LL/2, alors que l’injection d’une forte concentration de l’agonsite a un effet pro-tumoral. Nous avons également démontré qu’une forte expression de TLR7 par les cellules tumorales de patients NSCLC est de mauvais pronostique sur la survie globale des patients. Ces résultats démontrent le rôle pro- tumoral de TLR7 et son implication potentielle dans le phénomène de chimiorésistance. Ainsi l’utilisation d’agonistes de TLR7 comme adjuvant de vaccination antitumorale devrait prendre en compte le niveau d’expression de TLR7 sur les cellules tumorales des patients
Lung cancer accounts for over 1 million deaths per year with a 5-year survival of 8-12%. Stimulation of TLRs by the natural ligands like the PAMPs and DAMPs results in a proinflammatory signaling cascade. We have shown that stimulation of lung cancer cell lines with TLR7 agonist lead to tumor cell survival and chemoresistance in vitro. We studied the effect of TLR7 agonists on A549 and LL/2 cells injected in NOD/SCID and C57BL/6 mice either treated or not with cisplatin. Loxoribine has a pro-tumoral effect on A549 cells and induces chemoresistance in NOD/SCID mice. Blockade of TLR7 with IRS661 reversed the pro-tumoral effect of TLR7 agonist on A549 cells. CL264 was also found to have a pro-tumoral effect on LL/2 cells and induced chemoresistance in NOD/SCID mice. On the other hand CL264 at lower concentration induces an anti-tumoral effect on LL/2 cells while at a higher concentration demonstrated a pro-tumoral effect in C57BL/6 mice. We also demonstrated an overall bad prognostic value for higher expression of TLR7 by tumoral cells among NSCLC patients treated and not treated with neoadjuvant chemotherapy. These results suggest a pro- tumoral role and induction of chemoresistance by TLR7 in NSCLC patients. Use of TLR7 agonist as therapeutic option is recommended based on the TLR7 expression level for individual NSCLC patients. TLR7 antagonist holds promise for treatment of NSCLC in future
APA, Harvard, Vancouver, ISO, and other styles
8

Recondo, Gonzalo. "Resistance Mechanisms to ALK Tyrosine Kinase Inhibitors (TKIs) in NSCLC." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS248/document.

Full text
Abstract:
Les analyses moléculaires et la classification des adénocarcinomes bronchiques ont conduit au développement de thérapies ciblées sélectives visant à améliorer le contrôle de la maladie et la survie des patients. ALK (anaplastic lymphoma kinase) est un récepteur tyrosine kinase de la famille des récepteurs de l'insuline. Des réarrangements chromosomiques impliquant le domaine kinase d’ALK sont présents dans environ 3 à 6% des patients atteints d'un adénocarcinome bronchique. La protéine de fusion provoque une activation du domaine kinase de manière constitutive et indépendante du ligand. Lorlatinib est un inhibiteur d’ALK de troisième génération avec une efficacité et une sélectivité optimale, ainsi qu’une pénétration élevée vers le système nerveux central. Lorlatinib peut vaincre la résistance induite par plus de 16 mutations secondaires dans le domaine kinase d’ALK acquises lors de la progression aux ALK TKI de première et deuxième générations. Le traitement par lorlatinib est donc efficace chez les patients préalablement traités par un ALK TKI de première ou deuxième génération, et est actuellement approuvé pour cette indication. Le spectre complet de mécanismes de résistance au lorlatinib chez les patients reste à élucider. Il a récemment été rapporté que l'acquisition séquentielle de deux mutations ou plus dans le domaine kinase, également appelées mutations composées, est responsable de la progression de la maladie chez environ 35% des patients traités par le lorlatinib, principalement en altérant sa liaison au domaine kinase d’ALK. Cependant, l’effet de ces mutations sur la sensibilité aux différents inhibiteurs d’ALK peut varier, et les autres mécanismes de résistance survenant chez la plupart des patients restent inconnus. Mon travail de thèse avait pour but d’explorer la résistance au lorlatinib chez des patients atteints d'un cancer du poumon ALK réarrangé par la mise en œuvre de biopsies spatiales et temporelles et le développement de modèles dérivés de patients. Dans le cadre de l’étude institutionnelle MATCH-R (NCT02517892), nous avons effectué un séquençage à haut débit de l’exome, de l’ARN et ciblé, ainsi qu’un séquençage des ctDNA afin d’identifier les mécanismes de résistance. Nous avons établi des lignées cellulaires dérivées de patients et caractérisé de nouveaux mécanismes de résistance et identifiés de nouvelles stratégies thérapeutiques in vitro et in vivo. Nous avons identifié trois mécanismes de résistance chez quatre patients avec des biopsies appariées. Nous avons étudié l'induction de la transition épithélio-mésenchymateuse (EMT) par l'activation de SRC dans une lignée cellulaire, dérivée d’un patient, exposée au lorlatinib. Les cellules mésenchymateuses étaient sensibles à l’inhibition combinée de SRC et d'ALK, montrant que même en présence d'un phénotype agressif, des stratégies de combinaison peuvent surmonter la résistance aux ALK TKI. Nous avons identifié deux nouvelles mutations composées du domaine kinase d’ALK, F1174L / G1202R, C1156Y / G1269A survenues chez deux patients traités par le lorlatinib. Nous avons développé des modèles de cellules Ba / F3 exprimant les mutations simples et composées pour étudier leur effet sur la résistance au lorlatinib. Enfin, nous avons caractérisé un nouveau mécanisme de résistance provoqué par la perte de fonction de NF2 au moment de la progression du lorlatinib par l’utilisation de PDX et de lignées cellulaires dérivées de patients, et par CRISPR / CAS9 knock-out de NF2. Nous avons constaté que l'activation de mTOR par la perte de fonction de NF2 provoquait la résistance au lorlatinib et qu'elle pouvait être surmontée par le traitement avec des inhibiteurs de mTOR.Cette étude montre que les mécanismes de résistance au lorlatinib sont plus divers et complexes que prévu. Nos résultats démontrent également comment les études longitudinales de la dynamique tumorale permettent de déchiffrer la résistance aux TKI et d'identifier des stratégies thérapeutiques
The molecular study and classification of lung adenocarcinomas has led to the development of selective targeted therapies aiming to improve disease control and survival in patients. The anaplastic lymphoma kinase (ALK) is a tyrosine kinase receptor from the insulin tyrosine kinase receptor family, with a physiologic role in neural development. Gene rearrangements involving the ALK kinase domain occur in ~3-6% of patients with lung adenocarcinoma. The fusion protein dimerizes leading to transactivation of the ALK kinase domain in a ligand-independent and constitutive manner. Lorlatinib is a third generation ALK inhibitor with high potency and selectivity for this kinase in vitro and in vivo, and elevated penetrance in the central nervous system. Lorlatinib can overcome resistance mediated by over 16 secondary kinase domain mutations occurring in 13 residues upon progression to first - and second - generation ALK TKI. In addition, treatment with lorlatinib is effective for patients who have been previously treated with a first and a second generation or a second generation ALK TKI upfront and is currently approved for this indication. The full spectrum of biological mechanisms driving lorlatinib resistance in patients remains to be elucidated. It has been recently reported that the sequential acquisition of two or more mutations in the kinase domain, also referred as compound mutations, is responsible for disease progression in about 35% of patients treated with lorlatinib, mainly by impairing its binding to the ALK kinase domain. However, the effect of these compound mutations on the sensitivity to the repertoire of ALK inhibitors can vary, and other resistance mechanisms occurring in most patients are unknown. My PhD thesis aimed at exploring resistance to lorlatinib in patients with ALK-rearranged lung cancer through spatial and temporal tumor biopsies and development of patient-derived models. Within the institutional MATCH-R study (NCT02517892), we performed high-throughput whole exome, RNA and targeted next-generation sequencing, together with plasma sequencing to identify putative genomic and bypass mechanisms of resistance. We developed patient-derived cell lines and characterized novel mechanisms of resistance and personalized treatment strategies in vitro and in vivo. We characterized three mechanisms of resistance in four patients with paired biopsies. We studied the induction of epithelial-mesenchymal transition (EMT) by SRC activation in a patient-derived cell line exposed to lorlatinib. Mesenchymal cells were sensitive to combined SRC and ALK co-inhibition, showing that even in the presence of an aggressive and challenging phenotype, combination strategies can overcome ALK resistance. We identified two novel ALK kinase domain compound mutations, F1174L/G1202R, C1156Y/G1269A, occurring in two patients treated with lorlatinib. We developed Ba/F3 cell models harboring single and compound mutations to study the differential effect of these mutations on lorlatinib resistance. Finally, we characterized a novel mechanism of resistance caused by NF2 loss of function at the time of lorlatinib progression through the development of patients derived PDX and cell lines, and in vitro validation of NF2 knock-out with CRISPR/CAS9 gene editing. Downstream activation of mTOR was found to drive lorlatinib resistance by NF2 loss of function and was overcome by providing treatment with mTOR inhibitors.This study shows that mechanisms of resistance to lorlatinib are more diverse and complex than anticipated. Our findings also emphasize how longitudinal studies of tumor dynamics allow deciphering TKI resistance and identifying reversing strategies
APA, Harvard, Vancouver, ISO, and other styles
9

Baghai, Tabassom. "ATF3 as a Key Regulator of Cisplatin Cytotoxicity: Combining ATF3 Inducing Agents Enhances Cisplatin Activity in NSCLC." Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/37963.

Full text
Abstract:
Lung cancer is the leading cause of cancer and cancer deaths worldwide, with non-small-cell lung carcinomas (NSCLC) representing 85% of all diagnosed lung cancers. Platinum-combination chemotherapy is the current standard treatment for NSCLC, however, associated toxicities and resistance limit its efficacy. Our laboratory previously identified activating transcription factor 3 (ATF3), a stress-inducible gene whose elevated and sustained expression can trigger apoptosis to a wide variety of stressors, as a key regulator of cisplatin cytotoxicity as well. Thus, enhanced and sustained induction of ATF3 by combining platins with other ATF3 inducers potentially represents an effective therapeutic strategy. A chemical library screen identified vorinostat and topotecan as ATF3 inducers that also enhance cisplatin cytotoxicity. ATF3 plays a significant role in cisplatin, vorinostat and topotecan and their combinations cytotoxicity. Importantly, vorinostat and topotecan induced synergistic cytotoxicity with cisplatin in NSCLC cell lines and their cisplatin resistance sub-lines with enhanced ATF3 expression observed. Our study suggests a potential novel therapeutic approach where ATF3 inducing agents in combination with platins represents a rational combination based therapeutic strategy.
APA, Harvard, Vancouver, ISO, and other styles
10

Daskalos, Alexandros. "Deregulation of DNA methylation aand retrotransposon reactivation in NSCL." Thesis, University of Liverpool, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.539561.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "NSCLP"

1

U.S. Army Chemical Materiel Destruction Agency., ed. Non-Stockpile Chemical Materiel Program: NSCMP. [Aberdeen Proving Ground, MD: U.S. Army Chemical Materiel Destruction Agency, 1995.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

U.S. Army Chemical Materiel Destruction Agency., ed. Non-Stockpile Chemical Materiel Program: NSCMP. [Aberdeen Proving Ground, MD: U.S. Army Chemical Materiel Destruction Agency, 1995.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

U.S. Army Chemical Materiel Destruction Agency, ed. Non-Stockpile Chemical Materiel Program: NSCMP. [Aberdeen Proving Ground, MD: U.S. Army Chemical Materiel Destruction Agency, 1995.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

U.S. Army Chemical Materiel Destruction Agency, ed. Non-Stockpile Chemical Materiel Program: NSCMP. [Aberdeen Proving Ground, MD: U.S. Army Chemical Materiel Destruction Agency, 1995.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Cappuzzo, Federico. Guide to Targeted Therapies: EGFR mutations in NSCLC. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-03059-3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Kim, Ho-jung. array-CGH rŭl iyong han piso sepʻo pʻyeam ŭi chogi chaebal pʻyojija mit chindan mohyŏng kaebal =: Development of early-recurrence detection marker and diagnostic model using array-CGH in NSCLC. [Seoul]: Pogŏn Pokchibu, 2007.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Cappuzzo, Federico. Guide to Targeted Therapies : EGFR mutations in NSCLC: EGFR mutations in NSCLC. Adis, 2014.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Non-Stockpile Chemical Materiel Program: NSCMP. [Aberdeen Proving Ground, MD: U.S. Army Chemical Materiel Destruction Agency, 1995.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Krawczyk, Paweł Adam, Qing Zhou, Rafal Dziadziuszko, and Natasha Leighl, eds. Issues and Challenges in NSCLC Immunotherapy. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-816-0.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Northumberland Strait Crossing Project (NSCP). [Washington, DC]: Federal Highway Administration, 1996.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "NSCLP"

1

Shih, Helen. "BRAF in NSCLC." In Targeted Therapies in Lung Cancer: Management Strategies for Nurses and Practitioners, 39–49. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-16550-5_5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Du, Lingling, Saiama N. Waqar, and Daniel Morgensztern. "Multimodality Therapy for NSCLC." In Cancer Treatment and Research, 151–63. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-40389-2_7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Cappuzzo, Federico. "Therapy options for advanced NSCLC." In Guide to Targeted Therapies: Treatment Resistance in Lung Cancer, 5–25. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-20741-4_2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Doubre, H., C. Le Pechoux, and T. Le Chevalier. "Adjuvant Treatments in Resectable NSCLC." In Malignant Tumors of the Lung, 215–25. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18698-1_19.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Ramírez, J. L., M. F. Salazar, J. Gupta, J. M. Sánchez, M. Taron, M. Sänchez-Ronco, Vicente Alberola, and R. de las Peñas. "Methylation Patterns and Chemosensitivity in NSCLC." In New trends in cancer for the 21st century, 195–209. Dordrecht: Springer Netherlands, 2006. http://dx.doi.org/10.1007/978-1-4020-5133-3_17.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Blackhall, Fiona H. "Strategies in ALK Rearranged NSCLC Patients." In New Therapeutic Strategies in Lung Cancers, 147–56. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-06062-0_10.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Louie, Brian E., and Eric Vallières. "Minimally Invasive Surgery for Early NSCLC." In New Therapeutic Strategies in Lung Cancers, 27–32. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-06062-0_3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Pisters, Katherine. "Adjuvant and Neoadjuvant Therapy of NSCLC." In Lung Cancer, 139–59. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-524-8_6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Tsao, Anne S., and Jack A. Roth. "Novel and Emerging Agents in NSCLC." In Lung Cancer, 464–78. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2014. http://dx.doi.org/10.1002/9781118468791.ch30.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Das, Millie, and Heather Wakelee. "Anti-Angiogenic Agents in Metastatic NSCLC." In Lung Cancer, 527–40. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2014. http://dx.doi.org/10.1002/9781118468791.ch34.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "NSCLP"

1

Rauthan, Amit, Poonam Patil, Rajashree Aswath, Nitin Yashas, and Gaurav Ningade. "Immunotherapy in Patients with Lung Cancer with Driver Mutations: A Single-Centre Experience." In Annual Conference of Indian Society of Medical and Paediatric Oncology (ISMPO). Thieme Medical and Scientific Publishers Pvt. Ltd., 2021. http://dx.doi.org/10.1055/s-0041-1735365.

Full text
Abstract:
Abstract Introduction Immunotherapy has revolutionized treatment in metastatic nonsmall cell lung cancer (NSCLC) without driver mutations. Trial data shows that programmed death-1/PDL1 blockade in epidermal growth factor receptor (EGFR) and other driver mutation positive lung cancers is not beneficial; and instead maybe detrimental. Here, we evaluated the efficacy of immune check point inhibitors in a series of patients with EGFR and other driver mutation–positive advanced NSCLC. Objectives This study was aimed to evaluate the efficacy of immune check point inhibitors in a series of patients with EGFR and other driver mutation–positive advanced NSCLC. Materials and Methods We retrospectively analyzed 75 patients which received PD1/PDL1 inhibitors for advanced NSCL between January 2017 and January 2020. Ten patients were detected to have driver mutations on either tumor tissue or blood by next-generation sequencing (NGS). PDL1 status was assessed on SP263 ventana platform. Results Out of 10 patients, 7 were male and 3 were female. EGFR was detected in six patients (three on tumor and three in blood NGS), MET exon 14 skipping mutation in two patients, and RAS mutation in two patients on NGS in blood. Immunotherapy combined with chemotherapy was given in 5 (50%) patients, immunotherapy + bevacizumab + chemotherapy in two (20%) and immunotherapy alone in three patients (30%). Immunotherapy was started as first line in four patients as tumor tissue was negative for EGFR, ALK, and ROS1 by single gene testing. The remaining six patients received immunotherapy on progression in the second or subsequent lines. On NGS testing at progression, EGFR mutation was detected in one patient, MET exon 14 skip mutation was detected in two patients, and RAS mutation was detected in two patients. Immunotherapy alone was used in three patients in view of advanced age and multiple comorbidities. The median progression-free survival (PFS) was 5 months (range: 2–11 months). Two patients who received chemotherapy + bevacizumab + immunotherapy continue to do well without progression at 9 months. Conclusion PD1/PDL1 checkpoint inhibitors seem to have a limited impact in treatment in patients with driver mutations. Molecular testing by NGS is recommended either on tumor tissue or on blood by NGS if single gene testing for EGFR/ALK/ROS1 alterations is negative. We recommend not using single agent checkpoint inhibitors in molecular driven advanced NSCLC even with high PDL1 expression. We do see benefit in patients who received PD1/PDL1 inhibitors in combination with chemotherapy with bevacizumab. In conclusion, in patients with molecular-driven NSCLC who progress after standard therapy can be treated with PD1/PDL1 inhibitors, but this should always be given in combination with chemotherapy and bevacizumab.
APA, Harvard, Vancouver, ISO, and other styles
2

Benammar, Sarra, Fatima Mraiche, Jensa Mariam Joseph, and Katerina Gorachinova. "Glucose and Transferrin Liganded PLGA Nanoparticles Internalization in Non-Small Lung Cancer Cells." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0227.

Full text
Abstract:
Introduction: Recently, after a decade of confusing results, several studies pointed out that overexpression of GLUT1 (glucose transporter 1) is a biomarker of worse prognosis in NSCLC. Nonetheless, the presence of transferrin (Tf receptor), which is overexpressed in most cancer tissues and most lung cancers as well, in NSCLC is also an indicator of very poor prognosis. Therefore, these ligands can be used for active targeting of lung cancer cells and improved efficacy of internalization of cancer therapy using nanomedicines. Objectives: Having the background, the main goal of the project was the assessment of the influence of the glucose and transferrin ligands on the efficacy of internalization of the designed (i) glucose decorated PLGA (poly lactic-coglycolic acid) nanoparticles (Glu-PLGA NPs) and (ii) transferrin decorated PLGA nanoparticles (Tf-PLGA NPs) in comparison to (iii) non-liganded PLGA NPs using a A549 lung cancer cells. Methods: Glu-PLGA NPs, Tf-PLGA NPs and PLGA NP - fluorescently labelled), were designed using a sonication assisted nanoprecipitation method. Further, physicochemical properties characterization (particle size analysis, zeta potential, FTIR analysis, DSC analysis), cytotoxicity evaluation using MTT test, and cell internalization studies of DTAF labelled NPs using fluorimetry in A549 NSCLC cell line were performed. Results: The results pointed to a significantly improved internalization rate of the liganded compared to PLGA NPs. Glu-PLGA NPs showed higher internalization rate compared to Tf-PLGA and PLGA NPs, in the serum-supplemented and serumfree medium even at normal levels of glucose in the cell growth medium. Conclusion: The developed nanocarriers offer unique advantages of enhanced targetability, improved cell internalization and decreased toxicity, which makes them promising solution for current therapeutic limitations.
APA, Harvard, Vancouver, ISO, and other styles
3

Alam, Mohammed. "A Decision Analytical Model Investigating Cost-Effectiveness of Erlotinib." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0145.

Full text
Abstract:
Background: A decision analytical model investigating cost-effectiveness of Erlotinib was submitted to the UK NICE (National Institute for Health and Care Excellence), which was not based on actual health-state transition probabilities, leading to structural uncertainty in the model. The study adopted a Markov state-transition model for investigating the cost-effectiveness of Erlotinib versus Best Supportive Care (BSC) as a maintenance therapy for patients with non-small cell lung cancer (NSCLC). Methods: Unlike manufacturer submission (MS), the Markov model was governed by transition probabilities, and allowed a negative post-progression survival (PPS) estimate to appear in later cycle. Using published summary survival data, the study employs three fixed- and time-varying approaches to estimate state transition probabilities that are used in a restructured model. Results: Post-progression probabilities and probabilities of death for Erlotinib were different than fixed-transition approaches. The best fitting curves are achieved for both PPS and probability of death across the time for which data were available, but the curves start diverging towards the end of this period. The Markov model which extrapolates the curves forward in time suggests that this difference between a time-varying and fixed-transition becomes even greater. Our models produce an ICER of £54k -£66k per QALY gain, which is comparable to an ICER presented in the MS (£55k/QALY gain). Conclusions: Results from restructured Markov models show robust cost-effectiveness results for Erlotinib vs BSC. Although these are comparable to manufacturer submissions, in terms of magnitude, they vary, and which are crucial for interventions falling near a threshold value. The study will further explore the cost-effectiveness of therapies for NSCLC in Qatar.
APA, Harvard, Vancouver, ISO, and other styles
4

Gelbke, C. Konrad. "FRIB/NSCL Laboratory Update." In Sixth International Conference on Fission and Properties of Neutron-Rich Nuclei (ICFN6). WORLD SCIENTIFIC, 2017. http://dx.doi.org/10.1142/9789813229426_0030.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Ollosi, Stephen L., Margaret Soucheray, Jeffrey Becker, Ines Pulido, Annika Dalheim, Fatima Al-Shahrour, Wei Qui, et al. "Abstract 20: Inhibition of mutant EGFR in NSCLC promotes endothelin-1-mediated NSCLC disease progression and angiogenesis." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-20.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Shostak, E., R. Liberman, and D. Riker. "Stage I NSCLC: Risk Factors for Recurrence." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1107.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Pavicevic, R., and G. Bubanovic. "ERCC1 and RRM1 Expression in Resected NSCLC." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2679.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Wu, Yi-Long, and Robert van den Heuvel. "Sugemalimab offers PFS benefits for unresectable NSCLC." In IASLC 2022 World Conference on Lung Cancer, edited by Yi-Long Wu and Rachel Giles. Baarn, the Netherlands: Medicom Medical Publishers, 2022. http://dx.doi.org/10.55788/675f3ee0.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Molina-Pinelo, Sonia, Gabriel Gutierrez-Pozo, Maria D. Pastor, Marta Hergueta, Gema Moreno-Bueno, Rocio Garcia-Carbonero, Ana BS Nogal, et al. "Abstract 5305: Transcriptionalregulation by microRNAs in NSCLC." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5305.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

van den Heivel, Robert. "Confirmatory mediastinoscopy not needed in resectable NSCLC." In ERS International Congress 2022, edited by Richard Dekhuijzen. Baarn, the Netherlands: Medicom Medical Publishers, 2022. http://dx.doi.org/10.55788/5e8370b2.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "NSCLP"

1

Dawson, W., J. Boles, and K. Le Galloudec. NSLP-Final Report-Draft2022. Office of Scientific and Technical Information (OSTI), February 2022. http://dx.doi.org/10.2172/1860931.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Sherrill, Bradley, and Alexandra Gade. Operation of GRETINA at NSCL. Office of Scientific and Technical Information (OSTI), December 2017. http://dx.doi.org/10.2172/1427801.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Young, Jamey D., and Young M. Whang. Targeting Redox Homeostasis in LKB1-deficient NSCLC. Fort Belvoir, VA: Defense Technical Information Center, September 2014. http://dx.doi.org/10.21236/ada614534.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Peng, Yinglong, Jinwei Chen, Ziyan Wang, Yihui Cao, and Jie Zhao. A Systematic Review and meta-analysis of the efficacy of immunotherapy in the treatment of non-small cell lung cancer. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2022. http://dx.doi.org/10.37766/inplasy2022.6.0094.

Full text
Abstract:
Review question / Objective: This study aimed to compare the effectiveness of different ICIs in the treatment of NSCLC, and to provide a theoretical basis for clinical selection of different regimens. Condition being studied: Immunotherapy is a relatively new treatment method for non-small cell lung cancer (NSCLC), and clinical studies confirmed that immune checkpoint inhibitors (ICIs) showed prominent efficacy in the treatment of NSCLC patients. This study aimed to compare the effectiveness of different ICIs in the treatment of NSCLC, and to provide a theoretical basis for clinical selection of different regimens.
APA, Harvard, Vancouver, ISO, and other styles
5

Stiemerling, M., H. Tschofenig, C. Aoun, and E. Davies. NAT/Firewall NSIS Signaling Layer Protocol (NSLP). RFC Editor, October 2010. http://dx.doi.org/10.17487/rfc5973.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Freire, Mariana, Diana Martins, Maria Filomena Botelho, and Fernando Mendes. Biomarkers of resistance mechanisms in innovative lung cancer treatments - A systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0011.

Full text
Abstract:
Review question / Objective: This systematic review aims to provide an overview of the immunotherapy resistance mechanisms and identify potential biomarkers associated with immunotherapy response in NSCLC, as well as examine new treatment options to overcome this hurdle. Condition being studied: Lung Cancer (LC) remains one of the leading cancers worldwide. In 2020, were globally estimated 2 206 771 new cases and 1 796 144 deaths, representing the uttermost frequent cause of cancer death. LC is classified histologically into small cell lung cancer (SCLC) or non-small cell lung cancer (NSCLC), being the last one the most common, representing 80 to 85% of all LC. The three predominantly subtypes of NSCLC are lung adenocarcinoma (LUAD), lung squamous cell carcinoma (LUSC) and large cell carcinoma (LCLC). NSCLC is usually diagnosed in advanced-staged disease due to ambiguous and delayed severe symptoms.
APA, Harvard, Vancouver, ISO, and other styles
7

Winkles, Jeffrey A. GrB-TWEAK: A Potential Novel Biologic for NSCLC Therapy. Fort Belvoir, VA: Defense Technical Information Center, September 2015. http://dx.doi.org/10.21236/ada624531.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Ouyang, Zhiqiang, Qian Li, Guangrong Zheng, Tengfei Ke, Jun Yang, and Chengde Liao. Radiomics for predicting tumor microenvironment phenotypes in non-small cell lung cance: A systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0060.

Full text
Abstract:
Review question / Objective: Tumor microenvironment (TIME) phenotype is an important factor to affect the response and prognosis of immunotherapy in non-small cell lung cancer (NSCLC). Recently, accumulating studies have noninvasivly perdited the TIME phenotypes of NSCLC by using CT or PET/CT based radiomics. We will conduct this study by means of meta-analysis to eveluate the power and value of CT or PET/CT based radiomics for predicting TIME phenotypes in NSCLC patients. Condition being studied: At present, several recent prospective or retrospective cohort studies and randomized controlled studies have confirmed that CT or PET/CT-based radiomics were the potential tools to predict TIME phenotypes in NSCLC. However, this conclusion is controversial because of the difference of prediction profermance of different studies. The published and unpublished investigations will be included in this study. We will comprehensively evaluate the heterogeneity of these investigations, and the power and value of radiomics for predicting TIME phenotypes.
APA, Harvard, Vancouver, ISO, and other styles
9

Manner, J., G. Karagiannis, and A. McDonald. NSIS Signaling Layer Protocol (NSLP) for Quality-of-Service Signaling. RFC Editor, October 2010. http://dx.doi.org/10.17487/rfc5974.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Severin, Gregory, E. Paige Abel, and Hannah Clause. Closeout Report: Rare Isotope Generators at the NSCL and FRIB. Office of Scientific and Technical Information (OSTI), January 2022. http://dx.doi.org/10.2172/1837939.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'NSCLP' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography