Relevant bibliographies by topics / Cancer, n.e.c

Academic literature on the topic 'Cancer, n.e.c'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Cancer, n.e.c"

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Cohn, Allen Lee, Michael Seiden, Kathryn N. Kurtzman, Earl Hubbell, Samuel Gross, Oliver Venn, Eric T. Fung, et al. "The Circulating Cell-free Genome Atlas (CCGA) Study: Follow-up (F/U) on non-cancer participants with cancer-like cell-free DNA signals." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): 5574. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.5574.

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5574 Background: A noninvasive cell-free DNA (cfDNA)-based cancer detection assay offers the hope of a blood test that might reduce morbidity and mortality of cancers, particularly those without recommended screening tests (eg, some gynecologic cancers). CCGA (NCT02889978) is a prospective, multi-center, longitudinal, case-control study evaluating models for discriminating cancer versus non-cancer. Here, we report F/U of control participants (pts) who demonstrated a cancer-signal in CCGA. Methods: Clinically evaluable samples (N = 2508) from pts enrolled without a cancer diagnosis (dx; NC) and treatment-naive pts with newly diagnosed cancer (C) were divided into training (n = 1564; 580 NC, 984 C) and test (n = 944; 368 NC, 576 C) sets. Classification performance (cancer/non-cancer) was assessed via 3 prototype assays: whole-genome bisulfite (WGBS), whole-genome (WGS), and targeted (507 gene) sequencing. Notable outlier NC pts were identified with cancer-like scores in either ≥2 assay classification results or by the presence of known cancer drivers with ≥1 assay classification result suggesting cancer. All pts are currently in F/U in accordance with study protocol (to date: 80% with > 10 mo and 15% with > 22 mo F/U). Results: Among training and test sets, 8 ( < 1%) NC pts were identified with a cancer-like signal. To-date, 2 have been diagnosed with a gynecologic malignancy: 1 stage IIIc clear cell endometrial carcinoma and 1 stage IIIc ovarian cancer, 3 and 2 months (mo) post-enrollment [PE], respectively. Among C pts in the study, sensitivity (at 98% specificity; WGBS) in these cancer types was: uterine/endometrial: 11% (n = 27 train) and 22% (n = 9 test); ovarian: 82% (n = 17) and 71% (n = 7). In addition, a third NC pt was diagnosed with a stage IV lung cancer 15 mo PE. Conclusions: This cfDNA-based assay detected a cancer-like signal that anticipated a clinical presentation of cancer in undiagnosed pts as early as 15 months prior to the actual dx. High specificity ( > 99%) requires accounting for undiagnosed cancers in study design and analysis. Together, these data suggest that this prototype assay may have high performance detecting a variety of gynecological and other cancers. Clinical trial information: NCT02889978.
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Furihata, Chie, Akira Yamakoshi, Akiko Hatta, Masae Tatematsu, Hitoshi Iwata, Kenshi Hayashi, Kazuo Umezawa, and Taijiro Matsushima. "Induction of c-fos and c-myc oncogene expression in the pyloric mucosa of rat stomach by N-methyl-N′-nitro-N-nitrosoguanidine and taurocholate." Cancer Letters 83, no. 1-2 (August 1994): 215–20. http://dx.doi.org/10.1016/0304-3835(94)90322-0.

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DIAS, P., P. KUMAR, H. B. MARSDEN, H. R. GATTAMANENI, and S. KUMAR. "N-and c-myc Oncogenes in Childhood Rhabdomyosarcoma." JNCI Journal of the National Cancer Institute 82, no. 2 (January 17, 1990): 151. http://dx.doi.org/10.1093/jnci/82.2.151.

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Borrello, Maria G., Giusi Carbone, Marco A. Pierotti, Alessandra Molla, and Giuseppe Della Porta. "Activated c-K-ras and c-N-ras oncogenes in 3-methylcholanthrene-induced BALB/c fibrosarcomas." Carcinogenesis 9, no. 8 (1988): 1517–19. http://dx.doi.org/10.1093/carcin/9.8.1517.

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Putzrath, Resha. "Studying Cancer Human Carcinogenesis Curtis C. Harris Herman N. Autrup." BioScience 35, no. 1 (January 1985): 51. http://dx.doi.org/10.2307/1310088.

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Lin, D. X., M. Friesen, C. Malaveille, D. E. G. Shuker, and H. Bartsch. "Urinary excretion of S-benzylmercapturic acid as an indicator of N-nitroso-N-methylbenzylamine exposure." Cancer Letters 57, no. 3 (May 1991): 193–98. http://dx.doi.org/10.1016/0304-3835(91)90156-c.

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di Luccio, Eric, Masayo Morishita, and Takaaki Hirotsu. "C. elegans as a Powerful Tool for Cancer Screening." Biomedicines 10, no. 10 (September 23, 2022): 2371. http://dx.doi.org/10.3390/biomedicines10102371.

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Regular cancer screening is critical for early cancer detection. Cancer screening tends to be burdensome, invasive, and expensive, especially for a comprehensive multi-organ check. Improving the rate and effectiveness of routine cancer screenings remain a challenge in health care. Multi-cancer early detection (MCED) is an exciting concept and a potentially effective solution for addressing current issues with routine cancer screening. In recent years, several technologies have matured for MCED, such as identifying cell-free tumor DNA in blood or using organisms such as Caenorhabditis elegans as a tool for early cancer detection. In Japan, N-NOSE is a commercially available multi-cancer detection test based on the chemotaxis of C. elegans using a urine sample showing 87.5% sensitivity and 90.2% specificity. In this review, we focus on using C. elegans as a powerful biosensor for universal cancer screening. We review N-NOSE clinical research results, spotlighting it as an effective primary cancer screening test.
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Williams, Morwen, Adam I. Green, Julio Fernandez-Cestau, David L. Hughes, Maria A. O'Connell, Mark Searcey, Benoît Bertrand, and Manfred Bochmann. "(C^Npz^C)AuIII complexes of acyclic carbene ligands: synthesis and anticancer properties." Dalton Trans. 46, no. 39 (2017): 13397–408. http://dx.doi.org/10.1039/c7dt02804k.

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Tishchenko, V. K., V. M. Petriev, E. D. Stepchenkova, P. V. Shegai, S. A. Ivanov, and A. D. Kaprin. "The influence of temperature on biodistribution of N,N,N’,N’- ethylenediaminetetrakis(methylene phosphonic) acid labeled with gallium-68." Journal of Physics: Conference Series 2058, no. 1 (October 1, 2021): 012042. http://dx.doi.org/10.1088/1742-6596/2058/1/012042.

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Abstract Bone metastases are serious complication in the progression of various types of cancer. It determines the requirement of modern nuclear diagnostic tools, including positron emission tomography (PET). In this study the biodistribution of EDTMP labeled with gallium-68 (68Ga-EDTMP) prepared at different temperature (20, 50, and 95 °C) was investigated. All experimental studies were performed in healthy intact Wistar rats by measuring the radioactivity in organs and tissues with gamma counter. All 68Ga-EDTMP formulations accumulated predominantly in bones. Only in tibia the uptake of 68Ga-EDTMP prepared at 95 °C was higher (p < 0.05) than 68Ga-EDTMP prepared at 20 °C, but in other bones there weren’t any statistical differences in uptake of 68Ga-EDTMP formulations. The amounts of 68Ga-EDTMP formulations in soft organs and tissues were lower when compared with bones. In conclusion, a temperature of reaction mixture had an influence on the biodistribution of 68Ga-EDTMP in bones.
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Chu, Pei-Yi, Hsing-Ju Wu, Shin-Mae Wang, Po-Ming Chen, Feng-Yao Tang, and En-Pei Isabel Chiang. "MAT2A Localization and Its Independently Prognostic Relevance in Breast Cancer Patients." International Journal of Molecular Sciences 22, no. 10 (May 20, 2021): 5382. http://dx.doi.org/10.3390/ijms22105382.

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(1) Background: methionine cycle is not only essential for cancer cell proliferation but is also critical for metabolic reprogramming, a cancer hallmark. Hepatic and extrahepatic tissues methionine adenosyltransferases (MATs) are products of two genes, MAT1A and MAT2A that catalyze the formation of S-adenosylmethionine (SAM), the principal biological methyl donor. Glycine N-methyltransferase (GNMT) further utilizes SAM for sarcosine formation, thus it regulates the ratio of SAM:S-adenosylhomocysteine (SAH). (2) Methods: by analyzing the TCGA/GTEx datasets available within GEPIA2, we discovered that breast cancer patients with higher MAT2A had worse survival rate (p = 0.0057). Protein expression pattern of MAT1AA, MAT2A and GNMT were investigated in the tissue microarray in our own cohort (n = 252) by immunohistochemistry. MAT2A C/N expression ratio and cell invasion activity were further investigated in a panel of breast cancer cell lines. (3) Results: GNMT and MAT1A were detected in the cytoplasm, whereas MAT2A showed both cytoplasmic and nuclear immunoreactivity. Neither GNMT nor MAT1A protein expression was associated with patient survival rate in our cohort. Kaplan–Meier survival curves showed that a higher cytoplasmic/nuclear (C/N) MAT2A protein expression ratio correlated with poor overall survival (5 year survival rate: 93.7% vs. 83.3%, C/N ratio ≥ 1.0 vs. C/N ratio < 1.0, log-rank p = 0.004). Accordingly, a MAT2A C/N expression ratio ≥ 1.0 was determined as an independent risk factor by Cox regression analysis (hazard ratio = 2.771, p = 0.018, n = 252). In vitro studies found that breast cancer cell lines with a higher MAT2A C/N ratio were more invasive. (4) Conclusions: the subcellular localization of MAT2A may affect its functions, and elevated MAT2A C/N ratio in breast cancer cells is associated with increased invasiveness. MAT2A C/N expression ratio determined by IHC staining could serve as a novel independent prognostic marker for breast cancer.
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Dissertations / Theses on the topic "Cancer, n.e.c"

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He, Hua, and 何華. "Anti-tumor mechanisms of cyclooxygenase inhibitors and a c-Jun-N-terminal kinase inhibitor in gastrointestinal cancers." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B30075245.

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Arbesú, Andrés Miguel. "A novel regulatory unit in the N-terminal region of c-Src." Doctoral thesis, Universitat de Barcelona, 2018. http://hdl.handle.net/10803/543572.

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c-Src is a central player in several cellular signaling pathways. It controls impor- tant cellular processes like cellular proliferation, survival or motility. Therefore, a number of tumoral diseases have been related to abnormal c-Src activity. Among them, colorectal cancer stands out, as c-Src deregulation correlates with tumor progression and clinical outcome. This tyrosine kinase is part of a larger group of functionally and structurally related proteins termed Src Family Kinases. These proteins share the same domain architecture: a cassette formed by a catalytic domain (SH1), two reg- ulatory domains, SH2 and SH3, and a variable intrinsically disordered region (the Unique domain) that ultimately anchors to the inner face of the cellular membrane via the N-terminal SH4 domain, also disordered. The sequence and structure of the cassette are highly conserved, and thus unsurprisingly Src Family Kinases perform closely related and often overlapping functions. However, the role of intrinsically disordered regions has remained unclear, although they are known to be functionally relevant. In this work, the structural and functional relationship between the intrinsically disordered SH4 and Unique domains with the neighboring folded SH3 domain in c-Src is explored. Interactions between disordered and ordered proteins are often characterized by the formation of complexes that are specific and functional but structurally heterogeneous. Moreover, conformational plasticity is a fundamental feature for function. These assemblies are known as fuzzy complexes. Here this theoretical framework, usually applied to isolated partners, is extended to the intramolecular interface between covalently bound domains instead of isolated pairs. The concept of fuzzy binding is also used in order to describe interactions based on sets of dynamic, transient, and promiscuous contacts between ill-defined sets of interactors. In order to characterize the system, an integrative strategy using short and long range Nuclear Magnetic Resonance techniques and Small Angle X-ray Scattering is applied to several constructs containing different combinations of bound or isolated domains. It is demonstrated that the folded SH3 domain acts as a scaffold for the disordered region, which interacts in a specific manner with its partner. Both disordered domains, SH4 and Unique, are involved in the process albeit they contribute differently. Additionally, it is shown that the Unique domain is not a random coil, but contains a significant degree of pre-arrangement that is independent of the scaffold. Sequence determinants are then searched by comparison of the sequences of different Src Family Kinases. Four conserved phenylalanine residues are found and their implication in Unique domain pre-organization and Unique:SH3 domain interaction tested. All these amino acids are found to favor compaction of the intrinsically disordered region, and at the same time to perturb close contact with the scaffold. In addition, mutations in the interacting zones of the SH3 domain are also studied to test reciprocity. In all, the fuzzy complex model is proven for the SH4:Unique:SH3 system. Then, the results are extrapolated to the full-length c-Src to test its biological relevance. A co evolutionary analysis suggests that the fuzzy model may be a general feature for the whole Src Family, so the closest member of the family, Yes, is also tested experimentally. The initial results on long-range contacts suggests a similar arrangement between the scaffold and the disordered region. In all, it is suggested that plastic, fuzzy interfaces between ordered and disordered domains may be a relevant mode for the transmission of functional information within multidomain proteins. Finally, a first approach for a structural study of the c-Src fuzzy complex in a native-like lipid environment, including natural co-translational modifications, is presented. A protocol for sample preparation is developed and Dynamic Nuclear Polarization solid state NMR is shown to be an adequate tool for further analysis.
c-Src es una tirosina quinasa clave en múltiples rutas de señalización celulares. Su desregulación ha sido asociada a diversos procesos tumorales, entre los que destaca el cáncer de cólon. Una actividad anómala de c-Src se correlaciona con el desarrollo tumoral y pronóstico clínico desfavorable. c-Src forma parte de un grupo de proteínas relacionadas estructural y funcional- mente, la Familia de Quinasas Src. Todas ellas comparten la misma arquitectura modular, que incluye un dominio catalítico (SH1), dos dominios regulatorios, SH2 y SH3, y a continuación una región variable intrínsecamente desordenada que incluye los dominios Único y SH4. Mientras que el segmento ordenado está bien caracterizado, el papel de la región desordenada no está claro, aunque es funcionalmente relevante. En este trabajo se explora la relación estructural y funcional entre la región desordenada y el dominio ordenado adyacente SH3. Dado que este tipo de interacciones implican un grado significativo de heterogeneidad estructural, se ha aplicado el concepto de unión difusa para caracterizar este sistema. Este marco teórico permite modelar interacciones basadas en contactos dinámicos y transitorios entre múltiples interactores vagamente definidos, que sin embargo son específicos y funcionales. Para ello, se ha usado una estrategia que implica el uso combinado de técnicas de Resonancia Magnética Nuclear de largo y corto alcance, así como Dispersión de rayos X a Bajo Ángulo. Se demuestra así que el dominio plegado SH3 actúa como armazón para la región desordenada, que a su vez contiene un grado significativo de pre-organización estructural. Se han identificado cuatro fenilalaninas en el dominio Único responsables de esta pre-formación que también afectan a la interacción entre la región desordenada y el armazón. Los resultados demuestran que el conjunto de dominios SH4, Único y SH3 forman una unidad funcional que puede ser definida como un complejo difuso. Además, datos teóricos y experimentales de otros miembros de la familia sugieren que el modelo difuso es una característica común de todos ellos. Finalmente, se ha demostrado que la Resonancia Magnética de estado sólido con Polarización Dinámica Nuclear es una técnica adecuada para el estudio estructural de c-Src unida a una matriz lipídica similar a la natural.
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Yu, Lola. "Investigating the role of the c-Jun NH2-terminal kinase pathway in ErbB2-driven breast cancer and macrophage polarization." eScholarship@UMMS, 2020. https://escholarship.umassmed.edu/gsbs_diss/1094.

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Breast cancer is the second most common malignancy in the world, accounting for over 1.7 million new diagnoses and an estimated 500,000 deaths per year (1). Overexpression of the receptor tyrosine kinase ErbB2, also known as Her2 or Neu, occurs in over 30% of breast cancers and correlates with metastasis, poor prognosis, and decreased survival (1, 2). Although therapeutics targeting ErbB2 show clinical efficacy, many patients display no initial response or develop drug resistance over time (2). A deeper understanding of the molecular basis of ErbB2-driven tumorigenesis is thus required for the development of improved therapeutic strategies. In vitro experiments suggest that activation of the c-Jun NH2-terminal kinase (JNK) pathway, a mitogen-activated protein kinase pathway, promotes proliferation, cellular invasion, and stem cell expansion in ErbB2-driven breast cancer (3, 4). Furthermore, unpublished data from our lab using mammary epithelial cells expressing activated ErbB2 show that JNK is required for acinus formation in in vitro 3D cultures. In contrast to these studies showing a tumorigenic role for the JNK pathway, other data from our lab show that JNK loss results in accelerated breast tumor growth, suggesting a tumor suppressive role (5, 6). However, these studies were performed in p53 knockout mice with or without a Kras mutation, where the latter required extensive aging and genomic instability to occur before differences in tumor growth were observable. To date, limited in vivo studies exist to confirm the role of JNK in more biologically relevant breast tumor models, such as in ErbB2-mediated cancer, which accounts for over 30% of all human breast cancers. In addition, the molecular mechanisms by which JNK signaling promotes ErbB2-driven tumorigenesis remains poorly understood. To address the discrepancy in JNK function between the in vitro ErbB2-driven breast cancer data and the in vivo p53 knockout tumor data, I began the development of an in vivo murine model to confirm the role of JNK in ErbB2-driven breast cancer. This mouse model will also allow us to test a potential mechanism by which JNK regulates tumorigenesis. Studies show that ErbB2-mediated secretion of the inflammatory cytokine IL6 promotes transformation and tumor growth by activation of the STAT3 transcription factor, triggering an IL6/STAT3 autocrine signaling loop (7,8). A major regulator of Il6 gene expression includes activator protein 1 (AP-1), a transcription factor composed of downstream JNK targets in the Jun protein family (9). In vitro experiments using ErbB2-overexpressing mammary epithelial cell lines show that chemical inhibition of JNK suppresses secreted IL6 protein levels, supporting a role for the JNK pathway in IL6 regulation (7). Thus, I hypothesize that JNK drives ErbB2-driven breast cancer by promoting IL6-mediated tumor progression. Addressing this will increase our understanding of the role of JNK in ErbB2-driven breast cancer and reveal a potentially new mechanism by which JNK functions in tumor progression. Additionally, I began the development of a mouse model that will allow us to investigate the role of JNK in macrophage polarization as an alternative mechanism by which JNK regulates ErbB2-driven breast cancer. In addition to promoting STAT3-dependent tumor growth, IL6 can indirectly drive tumorigenesis by promoting expression of the IL4 receptor in macrophages, triggering STAT6-mediated macrophage polarization towards the pro-tumorigenic M2 phenotype (10, 11). Unlike classically activated M1 macrophages, which promote inflammation and anti-tumor immunity, alternatively activated M2 macrophages function in immunosuppression and metastasis and correlate with advanced stages of breast cancer (12, 13). Further evidence supporting a role for the JNK pathway in macrophage polarization includes a recent study suggesting that JunB, a downstream JNK target and component of the AP-1 complex, plays a crucial role in the induction of M2 macrophage polarization in human alveolar macrophages (13). I hypothesize that activation of the JNK signaling pathway induces IL6-dependent macrophage polarization towards the pro-tumorigenic M2 phenotype. Addressing this hypothesis will determine for the first time whether JNK functions in regulating macrophage polarization within the tumor microenvironment, offering a potentially new mechanism by which JNK can promote ErbB2-driven breast cancer. Determining the role of JNK in ErbB2-mediated breast cancer will have direct therapeutic relevance, as targeting JNK has the potential to inhibit ErbB2-driven breast cancer and other IL6-mediated diseases. Investigating the underlying mechanisms by which JNK functions in ErbB2-positive breast cancer can also offer new molecular targets and further contribute to effective drug design.
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Komati, Rajesh. "Cu (II) Catalyzed Gateways In The Synthesis of Acridine Derivatives and Their Biological Evaluation as Anti-Cancer Drugs." ScholarWorks@UNO, 2014. http://scholarworks.uno.edu/td/1818.

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Telomeres are nucleoprotein complexes found at the ends of linear eukaryotic chromosomes. Telomeres consist of a short sequence of repetitive double stranded DNA, TTAGGG repeats in humans (and all mammals), and a complex of 6 proteins, termed the shelterin complex. The length of the telomeres varies greatly between species, from approximately 300 base pairs in yeast to many 10-15 kilo bases in humans, because of the end replication problem this length get shorten with each cell division and ultimately leads to cell death. However the immortal eukaryotic cells and some transformed human cells over come this incomplete end replication problem with the use of enzyme called Telomerase. Telomerase is a ribonucleoprotein enzyme that adds a specific DNA sequence repeats (TTAGGG) to the 3¢ end of DNA strands in the telomere regions. However from the telomerase activity studies, it was concluded that telomerase is active in almost 90% of human cancers but not in normal somatic tissues. Finally, the low or transient expression of telomerase in normal tissues, including normal stem cells, and the generally longer telomeres in normal cells versus tumor cells provide a degree of tumor specificity to telomerase-based drugs and reduce the probability of toxicity to normal tissue. All of these factors suggest that cancer drugs based on telomerase might have a broad therapeutic window. This dissertation focusing on the synthesis of acridine derivatives that have the capability to inhibit the enzyme telomerase. Several N-acridyl maleimide (NAM), N-acridyl succinimide (NAS) and N-acridyl phthalimide (NAP) derivatives have been synthesized and evaluated for their anti cancer activity against various cancer cell lines. While synthesizing acridine derivatives it was required to form the C-N bonds at various stages. Developed a copper-nicotinic acid complex, which catalyzes the coupling of aryl halides with N-formyl amines and cyclic imides to form C-N bond. Explored Cu (II) catalyzed formation of C-N bond by coupling aryl halides with various N-nucleophiles such as formamide, N,N-dimethyl formamide, N-formyl amines and various cyclic imides.
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Le, Bihan Thomas. "Nouveaux radiopharmaceutiques à base de cyclams C-fonctionnalisés pour l'imagerie 64Cu-TEP et la thérapie des cancers." Thesis, Brest, 2019. http://www.theses.fr/2019BRES0009.

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Les polyazacycloalcanes sont largement utilisés pour l’élaboration de radiopharmaceutiques destinés à la médecine nucléaire. Ces structures, et plus particulièrement celles dérivées du cyclam, permettent une complexation idéale du cuivre et ainsi une application en imagerie TEP, avec l’utilisation du 64Cu, ou en radiothérapie grâce à l’isotope 67Cu. Le cyclam doit, en plus d’être N-fonctionnalisé par des bras coordinants, disposer d’une fonction supplémentaire permettant la bioconjugaison à une biomolécule pour un ciblage spécifique des cellules cancéreuses. Une première partie de cette thèse a porté sur la synthèse du cyclam monopicolinate C-fonctionnalisé par une fonction de bioconjugaison de type benzyle isothiocyanate. Cette synthèse, basée sur des travaux antérieurs du laboratoire, a nécessité la mise au point d’une méthode d’alkylation régiospécifique du cyclam C-fonctionnalisé par le biais de protections sélectives des atomes d’azote du macrocycle. Le ligand a ensuite été étudié in vitro et in vivo, par nos collaborateurs nantais du CRCINA, pour l’imagerie immuno-TEP du myélome multiple.La seconde partie de ce travail s’est consacrée à l’élaboration d’un dérivé polyfonctionnel du cyclam possédant deux fonctions permettant le ciblage des cellules tumorales. Ce composé a été synthétisé au sein du laboratoire brestois puis étudié, in vitro et in vivo, dans les locaux de la NECSA en Afrique duSud pour l’imagerie TEP du cancer du sein.Ces deux projets ont permis d’obtenir une preuve de concept en imagerie TEP ce qui confirme le potentieldes ligands dérivés de cyclam C-fonctionnalisés pour l’élaboration de radiopharmaceutiques à base de cuivre pour la médecine nucléaire
Polyazacycloalkanes are wildly used in the conception of radiopharmaceuticals for nuclear medicine. These structures, and especially cyclam derivatives, provide ideal complexation properties of copper, which can be applied in nuclear medicine applications with the 64Cu isotope for PET imaging or with 67Cu for radiotherapy purpose. Cyclams derivatives have to be N-functionalized with coordinative arms, and moreover include an additional function especially introduced for the bioconjugation of a biomolecule in the aim to preferentially target cancer cells.The first project treated in this manuscript consisted of the synthesis of a monopicolinate cyclam C-functionalized with a benzyl isothiocyanate function for the bioconjugation. Based on precedent results obtained in the Lab, a regiospecific alkylation method has been developed for the synthesis of this ligand.This method implies the selective protection and deprotection of the macrocycle nitrogen atoms. This ligand, once obtained, has been studied in vitro and in vivo, by our collaborators of the CRCINA in Nantes, for multiple myeloma immuno-PET imaging.The second project of this work is dedicated to the conception of a radiopharmaceutical based on apolyfunctionnal cyclam which bear two different moieties allowing the targeting of cancer cells. This ligand has been synthesized in our Lab in Brest and studied, in vitro and in vivo, in the South African NECSA company for breast cancer PET imaging.These two projects were elaborated in the aim to obtain a proof of principle in PET imaging and to confirm the high potential of C-funcitonnalized cyclam derivatives for nuclear medicine applications
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Ma, Qiuping. "Role of FoxO Factors as the Nuclear Mediator for PTEN-AR Antagonism in Prostate Cancer Cells." [Tampa, Fla] : University of South Florida, 2008. http://purl.fcla.edu/usf/dc/et/SFE0002559.

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Herbert, Brittney-Shea. "Mechanisms of RRR-[alpha]-tocopheryl succinate- and N-(4-hydroxyphenyl)retinamide-induced apoptosis of human HL-60 myelocytic leukemia and MDA-MB-435 breast cancer cells : a role for TGF-[beta] and C-JUN /." Digital version accessible at:, 1998. http://wwwlib.umi.com/cr/utexas/main.

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Ahern, J. M. "Radical hydroacylation of C-C and N-N double bonds in air." Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1309819/.

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The formation of C-C and C-N bonds in modern organic synthesis is a key target for methodological advancement. Current methods of C-C and C-N bond formation often involve the use of expensive catalysts, or sub-stoichiometric reagents, which can lead to the generation of undesirable waste products. This thesis describes a novel and environmentally benign set of reaction conditions for the formation of C-C and C-N bonds by hydroacylation and this is promoted by mixing two reagents, an aldehyde and an electron-deficient double bond, under freely available atmospheric oxygen at room temperature Chapter 1 will provide an introduction to the thesis and mainly discusses methods for C-C bond formation, in particular, radical chemistry and hydroacylation. Chapter 2 describes the hydroacylation of vinyl sulfonates and vinyl sulfones (C-C double bonds) with aliphatic and aromatic aldehydes with a discussion and evidence for the mechanism of the transformation. Chapter 3 details the synthesis of precursors for intramolecular cyclisations and studies into aerobic intramolecular cyclisations. Chapter 4 describes the hydroacylation of vinyl phosphonates (C-C double bonds) and diazocarboxylates (N-N double bonds) with aliphatic and aromatic aldehydes bearing functional groups. In addition, the hydroacylation of diazocarboxylates with chiral aldehydes will be discussed. In conclusion, a new, facile and clean set of reaction conditions for the formation of C-C and C-N bonds has been developed via aerobic C-H activation of aldehydes providing access to unsymmetrical ketones.
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Qian, Xin. "Cobalt-Catalyzed C-C and C-N Coupling reactions." Phd thesis, Ecole Polytechnique X, 2013. http://pastel.archives-ouvertes.fr/pastel-00943479.

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Ce travail de these a permis le déveloippement de nouvelles reactions de couplage catalysées par des sels de cobalt(II) Le premier chapitre décrit l'allylation cobalta catalysée d'halogénures d'alkyles. La méthode est facile à mettre en œuvre, efficace avec une grande variété d'halogénures d'alkyes et des acétates ou carbonates d'allyle substitués. Les rendements vont de bons à excellents et la tolérance fonctionnelle élevée. Dans le cas d'acétates d'allyle substitués le produit linéaire est obtenu majoritairement ou exclusivement. Quelques expériences ont permis de mettre en lumière la formation d'espèce radicalaire lors du cycle catalytique. Les premiers essais pour étendre cette méthodologie aux couplages allyle-allyle et alkyle-alkyle sont également décrits. Le deuxième chapitre porte sur l'amination catalysée au cobalt d'organozinciques fonctionnalisés en utilisant des N-chloroamines. La procédure est simple et générale et demande des conditions plus douces que celles précédemment décrite, tout en tolérant un très large éventail de substrats, avec une bonne tolérance à de nombreux groupes fonctionnels. Les premiers essais pour étendre la méthodologie à la réaction entre un organozincique et une source électrophile de soufre en vue de former des liaisons C-S sont également exposés. Enfin le dernier chapitre décrit la réaction d'organozinciques engendrés par catalyse au cobalt avec une source " verte " de cyanure électrophile, N-cyano-N-phenyl-p-methyl-benzenesulfonamide (NCTS), pour conduire avec de bons rendements aux arylnitriles correspondants. Des sources analogues de CN+ ont également été testées.
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Simayi, Rena. "Synthesis and reaction chemistry of various N,N,C- and O,N,C- palladium pincer complexes." Thesis, University of Leicester, 2017. http://hdl.handle.net/2381/39392.

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In this thesis, the synthesis, characterisation and complexation chemistry of a series of related NNC and ONC pyridine based pincer ligands, together with some reaction chemistry of the metal complexes is described. The pro-ligands and the metal complexes have been characterised by a combination of multinuclear NMR spectroscopic techniques, IR spectroscopy, mass spectrometry and, for selected examples, by single crystal X-ray crystallography; remarkable spectroscopic and structural data are discussed. In Chapter 2, the synthesis and characterization of thirteen NNC and ONC pyridine based pincer ligands is described, including nine novel pincer ligands and four pyridine based pincers which have been previously reported. In Chapter 3, the palladium/platinum chemistry of NNCaryl and ONCaryl pyridine based pincer ligands is explored. Variation on the donor atoms has allowed an investigation of donor property influences on C-H activation, by giving peri-activated palladium pincer complexes for the ketimine-, aldimine-, amine- and biyridine-armed ligands and generating ortho-activated ONC palladium pincer complexes in the case of the alcohol-armed pro-ligand. Use of different palladium salts also led to different regioselective C-H activations. With the ketimine-armed naphthyl ligand (HL1ket-nap) as the example, the interconversion chemistry between the ortho- and peri-C-H activated products is also explored. In Chapter 4, sp3 C-H activation of the Et-armed ligand HL4Et with both palladium acetate and palladium chlorides has been unsuccessful, giving the N,N-coordinated bidentate species. The reaction of palladium acetate with the iPr-armed pro-ligand HL4iPr has resulted in minor amounts of C-H activated vinyl species with the major product being the non-activated palladium diacetate complex. Noticeably, upon reaction with Na2PdCl4, a mixture of the non-activated bis-chloride palladium complex and the sp3 C-H activated NNC-tridentate palladium species has been obtained, in a ratio of 1:1.5. Moreover, the sp3 C-H activation and the isolation of a rare sp3 C-H activated palladium complex have been achieved by reacting the tBu-armed pro-ligand HL4tBu with palladium acetate. The reaction of this ligand with Na2PdCl4 also resulted in the successful C-H activation of the tBu-arm to give a palladium pincer complex with a yield of 95%. Other than the NMR and FABMS analyses, the solid state X-ray structure of the latter complex confirmed the formation of the material as a rare sp3 C-H activated palladium complex. The stoichiometric reactivity of the (NNC/ONC)PdCl species towards AgBF4/AgPF6, and the subsequent ligand exchange reactions are disclosed in Chapter 5, together with the application of twelve palladium complexes as a series of promising catalysts in the allylic arylation of various allylic acetates with sodium tetraphenylborate.
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Books on the topic "Cancer, n.e.c"

1

Souci, Robert D. San. N. C. Wyeth's pilgrims. San Francisco: Chronicle books, 1991.

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Weyn, Suzanne. The N-C zone. New York, NY: Macmillan McGraw-Hill, 1998.

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The C-word. London: Arrow, 2010.

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Diamond, John. C. London: Ebury Publishing, 2001.

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Swan, Rebecca. The big C. Auckland: Hodder Moa Beckett, 1996.

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i, Hung Kha. Khu c tie u ai oa n: Truye n kich. [s.l.]: ♯o i Nay, 1988.

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Va n Xua n Nhi Ho . Ho n em hanh phu c: Ta p truye n. Los Alamitos, Calif: Xua n Thu, 1988.

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Matthias, Rath. Cancer. Santa Clara, CA: MR Pub., 2001.

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Bartsch, H., and I. K. O'Neill. Relevance of N-Nitroso Compounds to Human Cancer: Exposures and Mechanisms (I a R C Scientific Publication). IARC Scientific Publications, 1987.

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Walbridge, Charlie. The Nuts 'N' Bolts Guide to Outfitting Your Canoe or C-1 (Nuts 'N' Bolts - Menasha Ridge). Menasha Ridge Press, 1996.

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Book chapters on the topic "Cancer, n.e.c"

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Chou, Teh-Ying, and Gerald W. Hart. "O-Linked N-Acetylglucosamine and Cancer: Messages from the Glycosylation of C-Myc." In The Molecular Immunology of Complex Carbohydrates —2, 413–18. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1267-7_26.

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Walzog, B., S. Müller, and S. Nigam. "Enhancement of Phospholipase C and Phospholipase D Activity by Staurosporine in N-Formyl-Methionin-Leucin-Phenylalanine- Stimulated Human Neutrophils." In Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation and Radiation Injury, 243–47. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3520-1_48.

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"c-Jun N-Terminal Kinase." In Encyclopedia of Cancer, 1085. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_100558.

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"N- or C-Terminal Processing." In Encyclopedia of Cancer, 2447. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_5733.

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"C-Jun N-Terminal Kinase (JNK)." In Encyclopedia of Cancer, 873. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_1193.

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"Cancer C ell M etabolism , N utrition, and D iet." In Cancer Cell Metabolism and Cancer Treatment, 183–218. CRC Press, 2001. http://dx.doi.org/10.1201/9780203091906-13.

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". C arcinom aofU nkn ow n P rim a ry." In Chemotherapy Regimens and Cancer Care, 27–30. CRC Press, 2001. http://dx.doi.org/10.1201/9781498713313-7.

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Taber, Douglass. "Alkaloid Synthesis: Crispine A (Zhou), Cermizine C (Zhang), Tangutorine (Poupon), FR901483 (Kerr), Serratezomine A (Johnston)." In Organic Synthesis. Oxford University Press, 2011. http://dx.doi.org/10.1093/oso/9780199764549.003.0061.

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Enantioselective hydrogenation of enamides is a well-established transformation. The corresponding reduction of enamines has been elusive. Qi-Lin Zhou of Nankai University designed (J. Am. Chem. Soc. 2009, 131, 1366) an Ir catalyst that reduced 2 to the Carpus alkaloid Crispine A 3 in high ee. Direct conversion of C-H to C-C bonds is a powerful synthetic transformation. Liming Zhang, now at the University of California, Santa Barbara, observed (J. Am. Chem. Soc. 2009, 131, 8394) that a gold catalyst converted the N-oxide of 4 into 5, that was then deoxygenated to give Cermizine C 6. The gold catalyst and the N-oxide combined to convert the alkyne into an α-keto carbene, in the process reducing the N-oxide back to the amine. The carbene then abstracted a hydride from the carbon adjacent to the amine, generating an intermediate that collapsed to give 5 with high diastereocontrol. Tangutorine 10, isolated from the leaves of Nitraria tangutorum, affects the morphology of human colon cancer cells. In a biomimetic approach, Erwan Poupon of the Université Paris-Sud stirred (Organic Lett . 2009, 11, 1891) glutaraldehyde 7 with bicarbonate to give an unstable carbocyclic dimer. Addition of tryptamine in acetic acid delivered the pentacyclic product 9, that was reduced with borohydride to give the crystalline Tangutorine 10. FR901483, a potent immunosuppressive isolated from a Cladobotyrum fermentation broth, presents an challenging array of stereogenic centers in its tricyclic skeleton. Michael A. Kerr of the University of Western Ontario prepared (Organic Lett. 2009, 11, 777) the activated cyclopropane 11, then effected intramolecular dipolar opening with an intermediate imine, yielding the tricyclic 12. The Lycopodium alkaloid Serratezomine A 21 presents a similarly challenging array of stereogenic centers in its tetracyclic structure. Jeffrey N. Johnston of Vanderbilt University constructed (J. Am. Chem. Soc. 2009, 131, 3470) the pyrrolidine ring of 15 using the imine free radical acceptor that he had previously developed. Having the alkene-Sn bond in place then enabled coupling with the acid chloride 16. Oxidative deprotection of 17 freed the enamine, that added in a conjugate sense to the unsaturated ester, kinetically setting the axial branch of 18.
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SOARES, ADRIANA RAQUEL ARAÚJO PEREIRA, FÁBIO RODRIGO ARAÚJO PEREIRA, MARIA DO CARMO GUIMARÃES PORTO, and STEFFANY LARISSA GALDINO GALISA. "ESTUDO DA MORTALIDADE DE IDOSOS BRASILEIROS EM DECORRÊNCIA DO CÂNCER DE ESÔFAGO NO INTERVALO DE CINCO ANOS." In Envelhecimento baseado em evidências: Tendências e Inovações. Realize, 2020. http://dx.doi.org/10.46943/vii.cieh.2020.01.001.

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INTRODUÇÃO: O CANCER DE ESOFAGO (CE) É A TERCEIRA NEOPLASIA MALIGNA DO TRATO GASTRINTESTINAL MAIS FREQUENTE NA POPULA??O, SENDO DESENCADEADA POR FATORES END?GENOS E AMBIENTAIS. NO BRASIL, ? A OITAVA MAIS INCIDENTE E A SEXTA CAUSA DE MORTES MUNDIAIS. OBJETIVO: AVALIAR O PERFIL DE IDOSOS QUE MORRERAM NO BRASIL, POR CE (2014-2018). METODOLOGIA: ESTUDO QUANTITATIVO DA MORTALIDADE DE IDOSOS BRASILEIROS POR C?NCER DE ES?FAGO, SEGUNDO O SISTEMA DE MORTALIDADE/DATASUS (2014 A 2018). AVALIOU-SE OS VALORES A N?VEL DE BRASIL, POR REGI?O E UNIDADES DA FEDERA??O, SEXO, ESCOLARIDADE E RA?A DOS INDIV?DUOS. UTILIZOU-SE A ESTAT?STICA DESCRITIVA PARA EXPRESS?O E AN?LISE DOS DADOS. RESULTADOS: NO BRASIL (2014-2018) 160.355 MORRERAM POR CE, COM APROXIMADAMENTE 6.400 ?BITOS/ANO, SENDO O SUDESTE (51,87%) E SUL (21,31%) AS REGI?ES DE MAIOR OCORR?NCIA. NO NORDESTE (25.667 ?BITOS) A BAHIA (6.722), PERNAMBUCO (5.924) E CEAR? (4.884), FORAM, RESPECTIVAMENTE, OS ESTADOS COM MAIORES N?MEROS. A PARA?BA CONCENTROU APENAS 4,87% DOS ?BITOS. IDENTIFICOU-SE 55% (88.588) DAS MORTES ENTRE HOMENS E 45% (71.767) ENTRE MULHERES. IDOSOS COM BAIXA N?VEL EDUCACIONAL (ENSINO FUNDAMENTAL COMPLETO OU INCOMPLETO) FORAM A ?BITO EM MAIOR PROPOR??O (58,02%), QUANDO COMPARADOS COM AQUELES SEM ESCOLARIDADE (15,61%) E COM OS IDOSOS DE MAIOR N?VEL EDUCACIONAL (26,37%). NA AVALIA??O DA RA?A/COR, OBSERVOU-SE PREDOMIN?NCIA ENTRE BRANCOS (63,30%), SEGUIDO POR PARDOS (28,62%) E PRETOS (6,83%), RESPECTIVAMENTE.
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Aggarwal, P., and M. W. P. Bebbington. "Fragments N—N, C—C, C—N." In Six-Membered Hetarenes with Two Unlike or More than Two Heteroatoms and Fully Unsaturated Larger-Ring Heterocycles, 1. Georg Thieme Verlag KG, 2012. http://dx.doi.org/10.1055/sos-sd-117-00227.

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Conference papers on the topic "Cancer, n.e.c"

1

Du, Lili, Tinghu Zhang, Tamer Kaoud, Nathanael Gray, Kevin Dalby, and Kenneth Y. Tsai. "Abstract 1941: Distinct roles of c-Jun N-terminal kinase (JNK) isoforms in skin cancer." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1941.

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Palmieri, C., B. Rudraraju, A. Giannoudis, D. Moore, J. Shaw, S. Chan, IO Ellis, et al. "Abstract P5-08-17: A study of c-Jun N-terminal kinase (JNK) and c-Jun as biomarkers in early breast cancer." In Abstracts: Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 8-12, 2015; San Antonio, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.sabcs15-p5-08-17.

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Sikder, Rahmat K., Wafik S. El-Deiry, and Philip H. Abbosh. "Abstract 2307: Differential effects of N-terminal vs C-terminal truncatingCDKN1Amutations on cisplatin resistance in bladder cancer." 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.am2018-2307.

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Nasrazadani, A., S. Mitra, and C. Van Den Berg. "Knockdown of c-Jun N-terminal kinase 1 expression in murine mammary cancer cells leads to an increase in tumor growth and bone metastasis." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-1156.

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Ebelt, ND, and CL Ven Den Berg. "Abstract P4-06-13: c-Jun N-Terminal Kinase 1 (JNK1) Inhibits Tumor Progression and Regulates Embryonic Mammary Development." In Abstracts: Thirty-Third Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 8‐12, 2010; San Antonio, TX. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/0008-5472.sabcs10-p4-06-13.

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Dan, Peng, Wu Xiaobo, Lu Jin, Hao Qian, Hong Jingyan, and Li Yiguo. "Physics Design of Epi-Thermal Neutron Beam for BNCT Based on C-MNSR." In 2017 25th International Conference on Nuclear Engineering. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/icone25-67384.

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Boron Neutron Capture Therapy (BNCT) is a kind of the targeted therapy with two element. It can kill the cancer cells while the effect on normal cells is very small, and it is suitable for the treatment of the various stage cancer so it will be the ideal radiotherapy for cancer treatment in the future. And Commercial Miniature Neutron Source Reactor (C-MNSR) was designed and constructed by CIAE, which is used for Neutron Activation Analysis (NAA), Training and teaching. The reactor with thermal power 27kW is an under-moderated reactor with pool-tank type, U-AL alloy with High Enriched Uranium (HEU) as fuel, light water as coolant and moderator, and metal beryllium as reflector. The fission heat produced by the reactor is removed by the natural circulation. Design C-MNSR with a epi-thermal neutron beam for BNCT is studied while the conversion from HEU to LEU (Low Enrichment Uranium) (235U percent≤20%) is carried on. As it has the advantages of MNSR safety, economy, easy operation and its application, and it can improve the epi-thermal neutron flux density and meet the requirements of BNCT. The fuel cage of C-MNSR with size of φ230×248mm in the reactor core, there are ton rows of 355lattices are concentrically arranged, the central lattice is reserved for central control rod, and four tie rods are uniformly arranged at the eighth row which link the upper and lower grid plates, the rest 350 fuel lattices are for fuel pins or dummies. The diameter of the fuel meat is 4.3mm, the height is 230mm, with Uranium enrichment is 17%; the diameter of the fuel element is 5.5mm, the height is 248mm. The frame design of the epithermal neutron beam is: Fluental material used as neutron moderation layer with its thickness is 50cm and its density is 2.85g/cm3; Cd with thickness of 0.1cm used as thermal neutron absorption layer, Lead with thickness of 10cm used as gamma ray shielding layer. And the neutron collimator parts is a composition of graphite, Cd and polythene with boron. The total length of the beam is 114.5cm, and the distance from the exit of the beam to the core is 130cm. The results show that the epithermal neutron flux density at the exit is 1.58 × 109n·cm-2·s-1 at full power of 27kW. and the fast neutron density at the exit is 5.45 × 107n · cm-2 · s-1 at full power. Fast neutron dose contamination (Df/ φepi) is 2.88 × 10−11Gy · cm2 · n−1 and gamma dose contamination (Dγ/φepi) 2.18× 10−14 Gy·cm2·n−1.
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Munagala, Rohit, Carol Joseph, Annie Liu, Kebin Liu, Muthusamy Thangaraju, and Patricia V. Schoenlein. "Abstract 3318: A critical role for c-Jun N-terminal kinase in autophagy and cell survival of breast cancer cells." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3318.

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McCoy, Francis G. P., Ian Paul, Jane L. Hurwitz, Barry O'Hagan, Krzysztofa Odrzywol, James T. Murray, George McKerr, and Dean A. Fennell. "Abstract B30: Phosphorylation of c‐jun N terminal kinase (JNK) regulates induction of mitochondrial apoptosis by pro‐suvival BCL‐2 antagoinist obatoclax." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-b30.

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Nasrazadani, A., and CL Van den Berg. "Abstract P4-06-02: Systemic Deletion of c-Jun N-Terminal Kinase 1 or 2 Is Protective in Breast Cancer Bone Metastasis." In Abstracts: Thirty-Third Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 8‐12, 2010; San Antonio, TX. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/0008-5472.sabcs10-p4-06-02.

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Zhang, Xiaolong, Xiaolin Chen, and Hua Tan. "A Numerical Study on Highly Viscous Compound Cancer Cell Microfiltration." In ASME 2016 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/imece2016-66953.

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Cancer is a leading cause of death worldwide. There has been extensive research on cancer in recent decades, with many studies focusing on Circulating Tumor Cells (CTCs), i.e., cancer cells shed into the circulating bloodstream from a primary tumor site. CTCs are mainly responsible for initiating metastases, and can be used as an indicator for early cancer detection. Investigating CTCs and the related detection methods such as microfiltration is of great importance. CTCs as well as other cells are normally composed of highly viscous nucleus and cytoplasm which are encapsulated by the outermost layer of cortical membrane. In order to account for the effects of viscous nucleus and cytoplasm on the microfiltration process and study the dynamic characteristics comprehensively, a realistic model is preferred. In this research, we employ the compound droplet model consisting of three layers, the layer of cell membrane, cytoplasm and nucleus, to capture the full range of CTCs behavior during the microfiltration process. The compound cell deformation and pressure signature during microfiltration are studied numerically. Also discussed are the effects of nucleus-cytoplasm ratio (N/C ratio), their viscosity as well as surface tension on the cell behavior when it squeezing through the filter channel. Our results can gain insight into the physics behind the filtering process and provide some guidance to the design and optimization of such devices.
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Reports on the topic "Cancer, n.e.c"

1

Chen, Yi-Rong. C-Jun N-terminal Kinase and Apoptosis in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 1999. http://dx.doi.org/10.21236/ada374120.

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Chen, Yi-Rong. C-Jun N-terminal Kinase and Apoptosis in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 1998. http://dx.doi.org/10.21236/ada353790.

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Chen, Yi-Rong, and Tse-Hua Tan. C-Jun N-Terminal Kinase and Apoptosis in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2000. http://dx.doi.org/10.21236/ada392179.

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Gland, J. L. Hydrogen induced C-C, C-N, and C-S bond activation on Pt and Ni surfaces. Office of Scientific and Technical Information (OSTI), December 1992. http://dx.doi.org/10.2172/10102894.

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Gland, J. L. Hydrogen induced C-C, C-N, and C-S bond activation on Pt and Ni surfaces. Office of Scientific and Technical Information (OSTI), January 1992. http://dx.doi.org/10.2172/6915688.

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Gland, J. L. Hydrogen Induced C-C, C-N, & C-S Bond Activation on Pt & Ni Surfaces. Office of Scientific and Technical Information (OSTI), July 2004. http://dx.doi.org/10.2172/830711.

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Gland, J. L. [Hydrogen induced C-C, C-N, and C-S bond activities on Pi and Ni surfaces]: Summary. Office of Scientific and Technical Information (OSTI), December 1994. http://dx.doi.org/10.2172/10110807.

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Friend, J. P. High-speed tapping for N/C machining centers. Office of Scientific and Technical Information (OSTI), November 1991. http://dx.doi.org/10.2172/6114424.

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Ball, J. Timothy. Running Title: C and N Allocation in Pine. Office of Scientific and Technical Information (OSTI), December 1996. http://dx.doi.org/10.2172/762784.

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Joyner, Rex W. Diffractive Processes in 200-GeV/c $\pi^- N \to \pi^- \pi^- \pi^+ N$ Interactions. Office of Scientific and Technical Information (OSTI), August 1987. http://dx.doi.org/10.2172/1433220.

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