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Готові списки джерел за темами / Cancerogenesi

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Добірка наукової літератури з теми "Cancerogenesi"

Автор: Grafiati

Опубліковано: 11 березня 2023

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Статті в журналах з теми "Cancerogenesi"

1

Roth, Milan. "Skeletal cancerogenesis." Rivista di Neuroradiologia 10, no. 3 (June 1997): 337–40. http://dx.doi.org/10.1177/197140099701000306.

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2

Ryazansky, S. S., and V. A. Gvozdev. "Small RNAs and cancerogenesis." Biochemistry (Moscow) 73, no. 5 (May 2008): 514–27. http://dx.doi.org/10.1134/s0006297908050040.

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3

Pajovic, Snezana, Zorica Saicic, Snezana Pejic, Jelena Kasapovic, Vesna Stojiljkovic, and Dusan Kanazir. "Antioxidative biomarkers and cancerogenesis." Jugoslovenska medicinska biohemija 25, no. 4 (2006): 397–402. http://dx.doi.org/10.2298/jmb0604397p.

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4

Lo Fiego, D. P., A. M. Belmonte, and F. Mezzetti. "Carne suina e salute: un binomio possibile?" Archivos de Zootecnia 67, Supplement (January 15, 2018): 141–45. http://dx.doi.org/10.21071/az.v67isupplement.3591.

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La carne e i prodotti carnei sono fonte importante di nutrienti essenziali per l’organismo, ma recenti studi epidemiologici hanno associato il consumo di carne rossa e di carne trasformata ad un incremento del rischio di comparsa di malattie cardiocircolatorie e del cancro al colon. Ciò a causa della presenza di acidi grassi saturi, di sale aggiunto, di prodotti dell’ossidazione, di nitroso derivati che si formano durante le fasi di trasformazione, e della capacità ossidativa del ferro-EME. Recentemente l’International Agency for Research on Cancer (IARC) ha definito le carni rosse come probabilmente cancerogene e i salumi come cancerogeni. Ciò ha creato un notevole allarmismo nei consumatori, una significativa riduzione dei consumi di questi prodotti e un grosso impatto negativo sul mercato. L’Europa, con circa 150 milioni di suini e una produzione annuale di circa 22 milioni di tonnellate di carcasse, è il secondo produttore mondiale di carne suina, e l’area Mediterranea è conosciuta in tutto il mondo per la produzione di salumi di alto pregio. Appare pertanto di notevole importanza studiare nuove strategie produttive e di trasformazione atte a migliorare le caratteristiche salutistiche della carne suina. Nella relazione verranno prese in esame alcune di queste strategie.

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5

Buendia, MA. "Hepatitis B viruses and cancerogenesis." Biomedicine & Pharmacotherapy 52, no. 1 (January 1998): 34–43. http://dx.doi.org/10.1016/s0753-3322(97)86239-7.

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6

Krustev, L., O. Poliakova-Krusteva, and M. Krusteva-Chichova. "Liver cancerogenesis and fasciola hepatica." Journal of Hepatology 11 (January 1990): S96. http://dx.doi.org/10.1016/0168-8278(90)91716-a.

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7

Grce, M., L. Magdić, and K. Pavelic. "Human cytomegalovirus in cervical cancerogenesis." Journal of Cancer Research and Clinical Oncology 121, S1 (January 1995): S19. http://dx.doi.org/10.1007/bf02559829.

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8

Glushkov, Andrew N. "Immune-hormonal imbalance in chemical cancerogenesis." Russian Journal of Immunology 25, no. 1 (August 3, 2022): 23–36. http://dx.doi.org/10.46235/1028-7221-1091-ihi.

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The present article deals with experimental and clinical aspects of immuno-hormonal interactions in chemical carcinogenesis i.e., formation of DNA-adducts with chemical carcinogens as a trigger of tumor initiation; synthesis of specific antibodies as markers of human exposure to environmental carcinogens; immunomodulation of chemical carcinogenesis by the specific antibodies in experimental studies; interactions of antibodies against environmental carcinogens with endogenous steroid hormones in human carcinogenesis; immunological interference and inversion of immuno-hormonal interactions by the action of antibodies against environmental carcinogens; immune stimulation of tumor progression in cancer patients. It is shown that antibodies specific to estradiol and progesterone participate in regulation of serum estradiol and progesterone levels in healthy women. Excessive production of antibodies against benzo[a]pyrene is associated with impaired physiological balance between the levels of antibodies to estradiol and progesterone, thus causing disturbed physiological balance between serum estradiol and progesterone. Immuno-hormonal imbalance promotes tumor initiation, its growth and progression. The new approaches to the personalized cancer immunoprediction and immune prevention are discussed. Coordinated synthesis of antibodies against benzo[a]pyrene and estradiol seems to reflect production of DNA-adducts with genotoxic metabolic effects of these compounds manifesting as synergistic carcinogenic effects upon the target cells. Hence, simultaneously increased levels of serum antibodies against benzo[a]pyrene and estradiol in healthy people may be considered an immunological marker of high oncological risk and an reason to use of new immunoprotective tools against polycyclic aromatic hydrocarbons and phytoestrogens. However, ability of these antibodies to raise the blood serum levels of environmental carcinogens and endogenous estradiol, as shown in vitro and in vivo, excludes the opportunity for active cancer immune prevention. Usage of anticarcinogen vaccines aimed for induction of protective secretory antibodies is likely to further increase high levels of procarcinogenic serum antibodies against benzo[a]pyrene and estradiol, followed by additional enhancement of immuno-hormonal imbalance and promotion of carcinogenesis. Development of probiotics transduced with genes encoding human antibodies against environmental carcinogens may present an alternative approach to cancer immune prevention. The antibodies produced by such probiotics would bind appropriate carcinogens and prevent their invasion into the organism, thus inhibiting emergence of DNA-adducts and suppressing synthesis of specific autoantibodies that may promote carcinogenesis. The aim is to substantiate the concept of immuno-hormonal imbalance for the carcinogen-induced hormone-dependent tumors.

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9

Uhoda, Isabelle, Pascale Quatresooz, Claudine Piérard-Franchimont, and Gérald E. Piérard. "Nudging Epidermal Field Cancerogenesis by Imiquimod." Dermatology 206, no. 4 (2003): 357–60. http://dx.doi.org/10.1159/000069957.

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10

Siewinski, Maciej, Jan Gutowicz, Andrzej Zarzycki, and Wojciech Mikulewicz. "Role of Cysteine Endopeptidases in Cancerogenesis." Cancer Biotherapy and Radiopharmaceuticals 11, no. 3 (June 1996): 169–76. http://dx.doi.org/10.1089/cbr.1996.11.169.

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Дисертації з теми "Cancerogenesi"

1

Gu, Zu-Wei. "La cancerogenese chimique : aspect methodologique et evaluation du potentiel cancerogene." Paris 7, 1987. http://www.theses.fr/1987PA077051.

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2

INNAMORATI, Giulio. "Integrazione temporale del segnale mediato da recettori accoppiati a proteine G: il potenziale ruolo di G15 nella cancerogenesi." Doctoral thesis, Università degli Studi di Verona, 2009. http://hdl.handle.net/11562/337361.

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G15 è una proteina G eterotrimerica della famiglia di Gq/11, specifica del sistema ematopoietico, la cui funzione è sostanzialmente ignota. In questo studio si descrive la sua eccezionale resistenza al generale processo di desensibilizzazione che virtualmente regola l’attività di ogni recettore accoppiato a proteine G (GPCR). Il segnale di G15 è infatti risultato refrattario alla desensibilizzazione del recettore β2 adrenergico indotta da sovraespressione di arrestina. Allo stesso modo, il livello d’espressione di arrestina non ha influito sul segnale mediato da G15 in risposta all’attivazione dei recettori V2 per la vasopressina e δ oppioide. Esperimenti di co-immunoprecipitazione hanno dimostrato che la subunità Gα15 dell’eterotrimero (a differenza di Gαq and Gαs) viene stabilmente reclutata da un recettore V2 che una mutazione rende costitutivamente desensibilizzato. L’arrestina oltre a rendere meno efficiente il signalling dei GPCR, ne favorisce l’internalizzazione in compartimenti endosomiali. La co-espressione di Gα15 ha parzialmente ristabilito la presenza sulla membrana plasmatica del mutante costitutivamente desensibilizzato ristabilendone anche parte delle capacità segnalatorie. Tuttavia, confrontando l’effetto dell’agonista sull’attività verso gli effettori di G15, quali PKD1 e PLC, con l’effetto sull’internalizzazione del recettore, sono state osservate alcune peculiarità funzionali che suggeriscono che G15 stabilizzi una struttura conformazionale intermedia al normale processo di attivazione. Nel loro insieme, questi risultati suggeriscono un nuovo meccanismo per cui la regolazione dei GPCR può essere aggirata e G15 può trasdurre segnali estremamente prolungati quando le cellule siano “cronicamente” esposte all’effetto di ormoni, neurotrasmettitori etc. Questo aspetto ci ha portato ad ipotizzare che la presenza di G15 possa essere associata a stati fisiologici caratterizzati da fenomeni di deregolazione, in particolare con la formazione di tumori. Uno screening ha dimostrato la presenza di G15 in 10 fra 40 linee cellulari tumorali analizzate, tutte derivate da tessuti che in origine risultano negativi. Il messaggero di Gα15 e la corrispondente proteina sono anche risultati presenti in biopsie di cancro prostatico e pancreatico. Particolarmente rilevante appare il fatto che Gα15 fosse presente nella frazione proliferante del tumore così come dimostrato con xenotrapianti di tumore in topi nudi.
G15 is a heterotrimeric G protein of the Gq/11 family. In this study, we describe its exceptional poor sensitivity to the general regulatory mechanism of G protein-coupled receptor (GPCR) desensitization. Enhancing β2 adrenergic receptor desensitization by arrestin overexpression, did not affect signalling to G15. Similarly, increased levels of arrestin did not affect G15 signalling triggered by the activation of V2 vasopressin and δ opioid receptors. Furthermore, co-immunoprecipitation experiments showed that G15 α subunit (as opposed to Gαq and Gαs) is recruited to a V2 vasopressin receptor mutant that is constitutively desensitized by β-arrestin. Interestingly, co-expression of G15 partially rescued cell surface localization and signalling capabilities of the same mutant and supported its sustained activity on downstream effectors including PKD1. However, differential modulation by the agonist was observed while comparing effectors activity to receptor internalization. Taken together, these findings provide evidence for a novel mechanism whereby GPCR desensitization can be bypassed and G15 can support sustained signalling in cells chronically exposed to hormones or neurotransmitters. This aspect led us to hypothesize that G15 presence could be associated to poorly regulated physiological states, and in particular with tumor formation. A screening demonstrated Gα15 presence in 10 out of 40 human cancer cell lines analyzed, all derived from a variety of tissues reported as negative. Gα15 mRNA and protein were also found in pancreatic and prostate tumor biopsies. Notably, Gα15 was present in the proliferating fraction of the tumor as demonstrated by xenotransplantation of the tumors in nude mice.

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3

FOCACCETTI, CHIARA. "Inibizione immunologica del processo di cancerogenesi nei tumori della mammella insorti in topi BALB/c transgenici per il prodotto dell'oncogene ErbB2/neu mediante immunoterapia attiva." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2009. http://hdl.handle.net/2108/802.

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Utilizzando il modello tumorale transgenico BALB-NeuT abbiamo analizzato la specifica interferenza, indotta dalla vaccinazione, della carcinogenesi causata in questo modello animale dal prodotto dell’oncogene neu. È stata confrontata l’inibizione della formazione di masse tumorali in seguito alla vaccinazione con neu di ratto normale (ErbB2/Neu) o con i recettori ErbB xenogenici umani (LTR-EGFR, LTR-ErbB2, LTR-ErbB3, LTR-ErbB4), espressi singolarmente in cellule murine NIH3T3, o in seguito alla vaccinazione con poxvirus ricombinante, Vaccinia virus (rV-neu). La vaccinazione precoce, allo stadio di iperplasia atipica con LTR-Neu, inibisce in maniera drastica la carcinogenesi mammaria mediata da neu e inoltre, la vaccinazione con cellule esprimenti i recettori ErbB umani interferisce, significativamente in tutti i casi, con lo sviluppo del tumore nei topi BALB-NeuT. L’aumento relativo nella sopravvivenza libera da tumore e la riduzione dell’incidenza dei tumori corrisponde alla conservazione strutturale condivisa tra i recettori umani e l’oncogene neu, infatti l’immunizzazione con cellule trasfettate con LTR-Neu è quella che ha mostrato la maggiore efficacia antitumorale seguita da LTR-ErbB2 e dagli altri tre recettori ErbB umani. Le vaccinazioni hanno dimostrato di indurre un alto, specifico e comparabile titolo anticorpale e gli effetti antitumorali indotti da questi anticorpi correlano con la cross reattività verso il dominio extracellulare, purificato in vitro, della proteina Neu. Inoltre una specifica risposta T cellulare verso epitopi del Neu di ratto, rilevabile per la reattività di queste cellule alla stimolazione con peptidi specifici, è stata anche stimolata nelle cellule di milza dei topi immunizzati con LTR-Neu e, in misura minore, nelle cellule dei topi immunizzati con LTR-ErbB2 e LTR-EGFR. L’inibizione tumorale più pronunciata in seguito alla vaccinazione con LTR-Neu è stata associata con l’infiltrato leucocitario e la necrosi tumorale in vivo, mentre i sieri immuni specificamente inducono citotossicità cellulo mediata dipendente dagli anticorpi e apoptosi delle cellule tumorali mammarie dei topi BALB-NeuT in vitro. Inoltre, valutando l’efficacia di un vaccino che usa come veicolo il virus vaccinico ricombinante per Neu, si è rilevata la capacità anche di questa immunizzazione di contrastare efficacemente la crescita dei tumori nei topi transgenici con un effetto più marcato per inoculi multipli. L’inibizione risultante è comparabile alla vaccinazione allogenica quando le somministrazioni sono effettuate agli stadi più precoci di sviluppo del tumore mentre induce una protezione superiore ad essa quando l’immunizzazione con il virus ricombinante è eseguita a partire da uno stadio tardivo di sviluppo della malattia.
Employing the transgenic animal model BALB-NeuT, the outcome of neu-mediated tumorigenesis was compared following vaccination with isogenic normal rat ErbB2/Neu (LTR-Neu) or xenogeneic human ErbB receptors (LTR-EGFR, LTR-ErbB2, LTR-ErbB3 and LTR-ErbB4), both recombinantly expressed in an NIH3T3 murine cell background, or following vaccination with neu-recombinant Vaccinia virus (rV-neu). Vaccination using rat LTR-Neu at the stage of atypical hyperplasia potently inhibited neu-mediated mammary tumorigenesis. Moreover, all human ErbB receptors specifically interfered with tumor development in BALB-NeuT mice. Relative increase in tumor-free survival and reduction in tumor incidence corresponded to structural similarity shared with the etiologic neu oncogene. The rat orthologue LTR-Neu proved most effective followed by the human homologue LTR-ErbB2 and then the other three human ErbB receptors. Vaccination resulted in high titer of specific serum antibodies whose tumor-inhibitory effects correlated with cross-reactivity to purified rat Neu extracellular domain in vitro. Furthermore, a T cell response specific for peptide epitopes of rat Neu was elicited in spleen cells of mice immunized with LTR-Neu and was remotely detectable for discrete peptides upon vaccination with LTR-ErbB2 and LTR-EGFR. The most pronounced tumor inhibition by LTR-Neu vaccination was associated with leukocyte infiltrate and tumor necrosis in vivo, while immune sera specifically induced cytotoxicity and apoptosis of BALB-NeuT tumor cells in vitro. Moreover, the multiple vaccination employing the neu-recombinant virus also resulted in a specific inhibition of neu-mediated tumorigenesis. The resulting inhibition was comparable with the allogeneic immunization schedule when started early in tumor development but gave higher protection when the vaccination was started later in tumor onset.

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4

SERRA, MARIA PAOLA. "Cell senescence and aging in carcinogenesis and liver repopulation." Doctoral thesis, Università degli Studi di Cagliari, 2012. http://hdl.handle.net/11584/266184.

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The studies presented in my thesis delve into the complex relationship between cancer and aging using analytical approaches shared with the field of regenerative medicine. We took advantage of a model of orthotopic cell transplantation to explore the basic question as to whether the contribution of aging to the risk of cancer is, at least in part, related to alterations in the tissue microenvironment. Previous investigations conducted by our research group had revealed that isolated normal hepatocytes form larger clones of daughter cells when transplanted into the liver of old animals as compared to those formed in young recipients. In a relatively simple experiment we then utilized a similar approach to transplant preneoplastic cells isolated from hepatic nodules into either young or old animals of a syngeneic strain. Results were striking: very limited expansion of transplanted nodular hepatocytes was observed in the liver of young animals, while the same cell preparations grew significantly upon injection into older hosts, with a few cases of progression to hepatocellular carcinoma (HCC). The relevance of these findings is twofold. Firstly, they clearly indicate that preneoplastic cell populations isolated from hepatic nodules are not endowed with any measurable degree of growth autonomy, in that they were unable to form nodules when transferred into the liver of young hosts. Thus, their focal growth is dependent on stimuli originating from the local microenvironment. In this respect they behave like normal hepatocytes. Secondly, it is evident from these results that the microenvironment of the aged liver is able to foster the growth transplanted syngeneic nodular hepatocytes, again reproducing analogous findings already obtained with normal cells. Having established this fundamental fact, it became important to explore possible biological and underlying molecular mechanisms explaining the growth-promoting nature of the aged liver microenvironment. To this end, intriguing insights came again from the field of regenerative medicine. Our research group is involved in the characterization of an experimental model of massive liver repopulation through hepatocyte transplantation. This approach was set up in our laboratory and is based on the administration of retrorsine (RS), a naturally occurring alkaloid, as a preconditioning treatment. Rat liver exposed to RS and then transplanted with isolated normal hepatocytes is entirely replaced by donor-derived cells within a few months. Importantly, transplanted nodular hepatocytes can also selectively expand in the RS-treated liver, rapidly evolving to HCC. Again, neither normal, nor nodular hepatocytes are able to proliferate when injected into the liver of untreated recipients, as already noted above. This pattern of findings is similar to that observed in the aged liver, although the magnitude of the observed phenomena is far greater following exposure to RS. Moreover, it is apparent from the foregoing discussion that the growth of normal and nodular hepatocytes is controlled by fundamentally similar biological mechanisms, such that carcinogenesis and liver repopulation represent in fact “two sides of the same coin”, as it has been proposed. Given the similarities of biological responses between the RS-treated and the aged liver, we then probed into possible cellular and molecular analogies shared by the two systems. Much to our surprise, it was found that exposure to RS is a powerful inducer of cell senescence in hepatocytes in vivo. As reported in the preceding section of this report, several markers of cell senescence were expressed by RS-exposed hepatocytes, including senescence-associated β-galactosidase (SA-β-gal), cell hypertrophy, a persistent block in the cell cycle coupled with activation of cell growth pathways. The picture emerging from these findings is that RS treatment, which sets the stage for the selective growth of both normal and nodular transplanted hepatocytes, leading to massive liver repopulation and emergence of HCC, respectively, is also associated with the induction of a senescent phenotype in resident hepatocytes. Such a senescence phenotype is commonly found in aged tissues including the liver, as also shown in our studies. This phenotype is likely to explain, at least in part, the similarities observed between the microenvironments of the aged liver and that of RS-exposed liver. The last section of this thesis describes studies aimed at reversing the RS-induced alterations in the liver microenvironment and, in doing so, at verifying whether this would modulate the growth of preneoplastic lesions promoted by RS. Animals given the genotoxic agent diethylnitrosamine (DENA) followed by RS developed large hepatocyte nodules within a few months. However, the growth of preneoplastic nodules was significantly delayed in animals receiving hepatocyte transplantation following the DENA+RS regimen. These results represent a proof of principle that an altered microenvironment is indeed a powerful driving force in neoplastic progression; most importantly, they clearly indicate that strategies aimed at “normalizing” such an altered microenvironment might impact on the rate of progression of the neoplastic process.

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5

HANSMAENNEL, GERARD. "Exposition au formaldehyde et cancer." Lille 2, 1988. http://www.theses.fr/1988LIL2M258.

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6

REIBEL, MOSER MARIE-CHRISTINE. "Role de l'alimentation dans la carcinogenese." Strasbourg 1, 1993. http://www.theses.fr/1993STR15064.

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7

Bois, Frédéric Vasseur Paule. "MODELISATION MATHEMATIQUE DE LA CANCEROGENESE PAR DES PRODUITS CHIMIQUES /." [S.l.] : [s.n.], 1988. ftp://ftp.scd.univ-metz.fr/pub/Theses/1988/Bois.Frederic.SMZ889.pdf.

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8

Manickan, Lakshmy. "Proteomics of bacteroides fragilis and enterobacter cancerogenus." Thesis, Northumbria University, 2010. http://nrl.northumbria.ac.uk/1253/.

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Bacteroides fragilis NCTC 9343 is a Gram-negative anaerobic bacterium with genomic DNA of 5205 Kb and a GC ratio of 43%. It is a commensal organism that can act as an opportunistic pathogen and is commonly present on the mucous membranes. It causes a variety of infections including intra abdominal infections, perirectal abscesses and decubitus ulcers. Enterotoxigenic forms are capable of causing diarrhoea in children and animals. Enterobacter cancerogenus ATCC 35316 is also a Gram-negative facultatively anaerobic bacterium with genomic DNA of 4602 Kb and a GC ratio of 55%. It is a naturally occurring human gut symbiont known to exhibit resistance to antibiotics like aminopenicillins. It has also been reported in cases of severe osteomyelitis and infections of bones and joints. This study aims to analyse the differential expression of proteins in the presence of mucin since it serves as the first site of adherence for the bacteria. The E. cancerogenus and B. fra gilis proteins were extracted and separated by two dimensional electrophoresis from logarithmic phase cultures grown in semi-defined media enriched with or without porcine gastric mucin Types II and III. The gel images were analysed using Bio-Rad PDQuest, Ludesi Redfin and Nonlinear Dynamics SameSpots softwares. It was observed that the presence of mucin in the media affected the expression of a number of proteins in E. cancerogenus and B. fragilis cells. The protein spots of interest were excised, hydrolysed using trypsin and subjected to electrospray ionisation based LC-MS analysis in order to determine the identity of the digested proteins and obtain a better understanding of the interactions of B. fra gilis and E. cancero genus with mucin. The outer membrane protein surface antigen X was found to be up-regulated in both mucin Type II and III enriched media in E. cancerogenus. Some of the other proteins that were differentially regulated in both E. cancerogenus and B. fra gilis included the elongation factor Ts, malate dehydrogenase, triose phosphate isomerase and thiol peroxidase proteins indicating that these proteins may be associated with the ability of bacteria to grow in mucin and may be potential virulence factors. Genes encoding the proteins CAH06598 and CAH09443 from the glycoside hydrolase families 95 and 97 in B. fra gilis strain NCTC9343 were cloned, overexpressed and purified using nickel affinity and gel filtration chromatography. The enzymes were found to be active by performing fluorimetric assays using methyl-umbelliferyl sugar substrates. Diffracting crystals of CAH09443 were obtained from the PACT ANION screens containing polyethylene glycol and sodium malonate as a precipitant. Structure determination was achieved via molecular replacement using the glycoside hydrolase Family 97 α-galactosidase, BtGH97b, from Bacteroides thetaiotaomicron as a starting model. The structure of CAH09443 was shown to be composed of a N-terminal β-super-sandwich domain and a canonical (β/α)₈ barrel, similar to the two other glycoside hydrolase family 97 enzyme structures reported.

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9

Bektas, Yasin [Verfasser]. "Role of protein kinase D1 in pancreatic cancerogenesis / Yasin Bektas." Ulm : Universität Ulm, 2021. http://d-nb.info/1235527883/34.

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10

Chaudoreille, Marie-Madeleine. "Contribution a l'etude de l'interaction des oestrogenes de synthese avec la tubuline." Aix-Marseille 2, 1991. http://www.theses.fr/1991AIX22951.

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Книги з теми "Cancerogenesi"

1

Pokorski, Mieczyslaw, ed. Advances in Respiratory Cancerogenesis. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-35098-1.

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2

Konrad, Müller-Hermelink Hans, Neumann H. -G, and Dekant W, eds. Risk and progression factors in carcinogenesis. Berlin: Springer, 1997.

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3

Binetti, Roberto. Gli agenti cancerogeni negli ambienti di lavoro: Classificazioni e valutazioni nazionali e internazionali. Roma: Istituto superiore di sanità, 1994.

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4

Commissione consultiva tossicologica nazionale (Italy). Elenco di sostanze e prodotti di uso industriale e processi produttivi cancerogeni: Aggiornato al 2 dicembre 1988. Roma: Istituto superiore di sanità, 1988.

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5

Luigi, Rossi, and Commissione consultiva tossicologica nazionale (Italy), eds. Elenco di sostanze e prodotti di uso industriale e processi produttivi cancerogeni (aggiornato al 1⁰ dicembre 1989). Roma: Istituto superiore di sanità, 1989.

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6

Luigi, Rossi, and Commissione consultiva tossicologica nazionale (Italy), eds. Elenco di sostanze e prodotti di uso industriale, processi produttivi e attività professionali cancerogeni (aggiornato al 30 novembre 1990). Roma: Istituto superiore di sanità, 1991.

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7

P, Klein-Szanto Andres J., ed. Comparative molecular carcinogenesis: Proceedings of the Fifth International Conference on Carcinogenesis and Risk Assessment held in Austin, Texas, November 19-22, 1991. New York: Wiley-Liss, 1992.

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8

Michael, McClain R., ed. Growth factors and tumor promotion: Implications for risk assessment : proceedings of the Seventh International Conference on Carcinogenesis and Risk Assessment, held in Austin, Texas, on December 1-4, 1993. New York: Wiley-Liss, 1995.

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9

Principles of cell proliferation. Malden, MA: Blackwell Science, 2001.

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10

Heath, John K. Principles of Cell Proliferation. New York: John Wiley & Sons, Ltd., 2008.

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Більше джерел

Частини книг з теми "Cancerogenesi"

1

Peters, Nils, Martin Dichgans, Sankar Surendran, Josep M. Argilés, Francisco J. López-Soriano, Sílvia Busquets, Klaus Dittmann, et al. "Cancerogenesis." In Encyclopedia of Molecular Mechanisms of Disease, 268–69. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_3410.

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2

Petrik, Jim J. "Challenges in Experimental Modeling of Ovarian Cancerogenesis." In Methods in Molecular Biology, 371–76. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-547-7_28.

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3

Raudenska, Martina, Jaromir Gumulec, Andrew M. Fribley, and Michal Masarik. "HNSCC Biomarkers Derived from Key Processes of Cancerogenesis." In Targeting Oral Cancer, 115–60. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-27647-2_7.

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4

Drobne, Damjana, Sara Novak, Andreja Erman, and Goran Dražić. "New Opportunities for FIB/SEM EDX in Nanomedicine: Cancerogenesis Research." In Biological Field Emission Scanning Electron Microscopy, 533–43. Chichester, UK: John Wiley & Sons, Ltd, 2019. http://dx.doi.org/10.1002/9781118663233.ch25.

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5

Ostrovsky, Olga, Israel Vlodavsky, and Arnon Nagler. "Mechanism of HPSE Gene SNPs Function: From Normal Processes to Inflammation, Cancerogenesis and Tumor Progression." In Advances in Experimental Medicine and Biology, 231–49. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-34521-1_8.

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6

Hecker, Erich, and Friedrich Rippmann. "Outline of a Descriptive General Theory of Environmental Chemical Cancerogenesis — Experimental Threshold Doses for Tumor Promoters." In Mechanisms of Environmental Mutagenesis-Carcinogenesis, 167–73. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4615-3808-0_13.

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7

Brown, Andreas, and Hartmut Geiger. "Role of Cell Cycle Control, Checkpoints and DNA Repair Mechanisms in Stem Cells and Changes with Aging and Cancerogenesis." In Geriatric Oncology, 1–17. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-44870-1_87-1.

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8

Brown, Andreas, and Hartmut Geiger. "Role of Cell Cycle Control, Checkpoints, and DNA Repair Mechanisms in Stem Cells and Changes with Aging and Cancerogenesis." In Geriatric Oncology, 37–53. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-57415-8_87.

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9

"Epidemiology and Carciongenesis of Lung Cancer Part B: Lung Cancer Cancerogenesis." In Lung Cancer: Clinical and Surgical Specifications, edited by Murat Kara, 13–20. BENTHAM SCIENCE PUBLISHERS, 2013. http://dx.doi.org/10.2174/9781608054428113010005.

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10

Černe, Katarina, and Borut Kobal. "Implications of Microvesicle and Cell Surface Protein Shedding for Biomarker Studies, Cancerogenesis, and Therapeutic Target Discovery in Ovarian Cancer." In Advances in Planar Lipid Bilayers and Liposomes Volume 16, 239–74. Elsevier, 2012. http://dx.doi.org/10.1016/b978-0-12-396534-9.00008-8.

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Тези доповідей конференцій з теми "Cancerogenesi"

1

Höpken, M., O. Schildgen, S. Maune, and V. Schildgen. "Human Bocavirus as a cofactor in cancerogenesis of tonsil squamous cell carcinomas." In Abstract- und Posterband – 89. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Forschung heute – Zukunft morgen. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1640047.

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2

Youfang Cao, Hammad Naveed, Claire Liang, and Jie Liang. "Modeling spatial population dynamics of stem cell lineage in wound healing and cancerogenesis." In 2013 35th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2013. http://dx.doi.org/10.1109/embc.2013.6610807.

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3

Bilke, Sven, and Paul S. Meltzer. "Abstract LB-291: Environment or accident? A more stringent bound on environmental contributions to cancerogenesis." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-lb-291.

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4

Akin, Ata, Kambiz Pourrezaei, and Britton Chance. "A proposal for a Real-time Handheld NIR Breast Tumor Imager." In In Vivo optical Imaging at the NIH. Washington, D.C.: Optica Publishing Group, 1999. http://dx.doi.org/10.1364/ivoi.1999.dis136.

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Анотація:

Near infrared (NIR) technology using laser light sources at an optical window from 700-900 nm is shown to carry diagnostic value for early detection of breast cancer. The basic principle behind a breast tumor imager depends on detecting the abnormal changes in the optical properties of the breast tissue during cancerogenesis. This imager operates on the well established principle of amplitude cancellation time multiplex system which features congruent images of angiogenesis and hyper-metabolism, two diagnostics for tumors which both may be prognostic as well. The proposed device is a much more compact hand-held, battery operated system that can be used in field studies which is much faster, giving an image every second of the underlying deviation of optical properties of the tumor bearing breast from normal. The image is displayed in real-time on the back of the hand-held optical probe. The imager is a microcontroller controlled, self-calibrating device that requires minimum user interface. It is designed to be operated by technicians.

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5

Buslaev, V. Yu, A. V. Torgunakova, Irina Milentyeva, Lyubov Dyshlyuk, and V. I. Minina. "POPYMORPHISM OF IMMUNE RESPONSE GENES AND LUNG CANCER RISK IN NON-SMOKING RESIDENTS OF KUZBASS." In I International Congress “The Latest Achievements of Medicine, Healthcare, and Health-Saving Technologies”. Kemerovo State University, 2023. http://dx.doi.org/10.21603/-i-ic-17.

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Анотація:

Lung cancer (LC) is leading oncological pathology, posing a serious threat for patient’s lives. Accordingly to World Health Organization (WHO) 2,1 million of new cases and 1,8 of deaths are annually registered. It was accumulated a lot of information about significant influence of smoking on increased risk of LC development. 80-90% of patients with LC are namely smokers. However at present time it was registered increased level of mortality from this pathology among non-smoking patients [1]. LC formation in non-smoking individuals can occur due to environmental pollution by industrial and household cancerogens and also because of molecular and genetical and cytogenetical dissimilarities. Since LC development can be associated with anomalous immunological response, immune genes can be considered as potential biological markers [2]. Objective: To assess the influence of polymorphic variants of innate immunity genes on LC development in non-smoking patients.

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