Relevant bibliographies by topics / Carcinogenesis

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Carcinogenesis'

Author: Grafiati
Published: 4 June 2021
Last updated: 29 July 2024

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Journal articles on the topic "Carcinogenesis"

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Grilli, S., S. Bartoli, P. Perocco, and A. Colacci. "Experimental carcinogenesis and anti-carcinogenesis." European Journal of Cancer Prevention 3, no. 4 (July 1994): 382. http://dx.doi.org/10.1097/00008469-199407000-00020.

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Jukes, Thomas H. "Carcinogenesis." Science 227, no. 4686 (February 1985): 466. http://dx.doi.org/10.1126/science.227.4686.466.d.

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Dipple, A. "Carcinogenesis." Current Opinion in ONCOLOGY 2, no. 1 (February 1990): 129–33. http://dx.doi.org/10.1097/00001622-199002000-00021.

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JUKES, T. H. "Carcinogenesis." Science 227, no. 4686 (February 1, 1985): 466. http://dx.doi.org/10.1126/science.227.4686.466-c.

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Dilly, S. "Carcinogenesis." Journal of Clinical Pathology 47, no. 6 (June 1, 1994): 572. http://dx.doi.org/10.1136/jcp.47.6.572-b.

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Casson, Phillip. "Carcinogenesis." Plastic and Reconstructive Surgery 86, no. 2 (August 1990): 376. http://dx.doi.org/10.1097/00006534-199008000-00040.

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Waalkes, Michael P., Jerrold M. Ward, and Serpil C. Erzurum. "Carcinogenesis." Journal of Bronchology 2, no. 2 (April 1995): 173. http://dx.doi.org/10.1097/00128594-199504000-00022.

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Dunsford, Harold A. "Carcinogenesis." Human Pathology 25, no. 11 (November 1994): 1258–59. http://dx.doi.org/10.1016/0046-8177(94)90051-5.

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McMillan, Susan C. "Carcinogenesis." Seminars in Oncology Nursing 8, no. 1 (February 1992): 10–19. http://dx.doi.org/10.1016/0749-2081(92)90004-m.

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Malone, Michael J., Joseph K. Izes, and Liam J. Hurley. "CARCINOGENESIS." Urologic Clinics of North America 24, no. 4 (November 1997): 723–28. http://dx.doi.org/10.1016/s0094-0143(05)70414-6.

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Dissertations / Theses on the topic "Carcinogenesis"

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Solano, Marize de Lourdes Marzo [UNESP]. "Lesões histológicas em ratos Wistar submetidos ao protocolo modificado do bioensaio DMBDD." Universidade Estadual Paulista (UNESP), 2010. http://hdl.handle.net/11449/95846.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Toxicam
Um ensaio de média-duração em múltiplos órgãos de roedores, baseado no paradigma iniciação-promoção da carcinogênese, foi proposto por pesquisadores japoneses como alternativa ao ensaio convencional de longaduração para detecção de cancerígenos químicos. Esse ensaio alternativo, denominado DMBDD (acrônimo para os 5 agentes iniciadores da carcingênese neste protocolo), foi originalmente padronizado com a linhagem de ratos Fischer 344. Em 1996, o IBAMA adotou oficialmente uma variação (DMBDDb), proposta por nosso laboratório, como fonte de evidência do potencial cancerígeno de praguicidas agrícolas. O protocolo adotado pelo IBAMA tem algumas particularidades, como o uso de ambos os gêneros de ratos da linhagem Wistar e dois grupos controle positivo (tratados com fenobarbital - FB ou com 2’-acetoaminofluoreno -2’-AAF). Este protocolo foi utilizado ao longo de seis anos em nosso laboratório (TOXICAN) para a realização de cinco bioensaios sob contratos com empresas do setor agroquímico. O presente estudo consiste da revisão dos diagnósticos de três órgãos desses ensaios - o fígado, rins e intestinos - escolhidos porque foram os que apresentaram mais lesões na análise de cada um daqueles ensaios. A capacidade indutora enzimática dos agentes do protocolo foi avaliada pela expressão imunohistoquímica das enzimas hepáticas CYP 2B1/2B2 e 1A2. Os resultados indicam atividade promotora do FB, embora menos evidente que a do 2’-AAF, particularmente nos ratos machos. Apesar da alta variabilidade da linhagem de rato Wistar , este estudo permitiu estabelecer um banco de informações sobre as lesões que caracteristicamente são encontradas naqueles órgãos dos animais Wistar submetidos ao protocolo DMBDDb.
A medium-term multi-organ rat bioassay based on the initiation-promotion carcinogenesis paradigm has been proposed by Japanese researchers as an alternative to the conventional long-term assay for chemical carcinogenesis detection. This alternative bioassay, designated DMBDD (after the five carcinogenic initiators of this protocol), was originally standardized with the male Fischer 344 strain of rats. In 1996, the Brazilian Agency for the Environment (IBAMA) officially recognized a variation (DMBDDb), proposed by our laboratory, as a valid source of evidence of the carcinogenic potential of agrochemicals. The protocol adopted by IBAMA has some modifications, such as the use of both sexes of the Wistar strain of rats and two positive controls (Phenobarbital – PB, 2’-acetoaminofluorene - 2’-AAF). During six years, five different bioassays managed under contract with agrochemical companies were developed by our laboratory (TOXICAN). This study presents the revised results obtained from three organs of this protocol – liver, kidney and intestines –, chosen because they most frequently presented lesions through those assays analyses. Besides, the induction of the CYP 2B1/2B2, 1A2 isoforms was also immunohistochemically evaluated in the liver. Our results document the promoting activity of PB, otherwise less evident than 2’-AAF, especially in male rats. Although a high variability of the Wistar rat strain tested was evident, this study allowed building up a data bank of characteristic lesions in those selected organs of Wistar rats under the DMBDDb protocol treatment.
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Fischer, Heléne. "Gene expression in carcinogenesis /." Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4961-1/.

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Toft, Neil John. "MSH2, apoptosis, and carcinogenesis." Thesis, University of Edinburgh, 1998. http://hdl.handle.net/1842/22693.

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Tumour cells which lack DNA mismatch repair are resistant to the cytotoxic effects of DNA methylating agents and Cisplatin. To address whether this resistance is mediated through loss of an MSH2-dependent apoptotic pathway, the apoptotic response of the murine small intestine to DNA methylating agents and Cisplatin was studied. MSH2 was found to play a significant role in the initiation of apoptosis in vivo. The immediate apoptotic response to these agents was p53-dependent in the first 24 hours, however a smaller p53-independent apoptotic response was observed beyond this point. Mice doubly null for both MSH2 and p53 revealed that this delayed p53-indepdnent response was entirely MSH2-dependent. These results demonstrate the existence of a pathway to apoptosis following DNA methylation which is dependent upon both MSH2 and p53. The DNA repair enzyme O6-Alkylguanine-DNA-alkyltransferase (AGT), which removes potentially mutagenic methyl groups from guanine residues, was found to play no role in modulating the MSH2-dependeent apoptotic response of intestinal cells to methylating agents or Cisplatin, indicating that the rate of removal of methylated bases is not a major factor in the decision to enter this pathway. O6-Benzylguanine, a competitive inhibitor of AGT, prevented the metabolic activation of Dacarbazine probably through the inhibition of cytochrome P450 enzymes. This novel finding has adverse implications towards the potential clinical use of O6-Benzylguanine. The data presented in this thesis demonstrate that MSH2 plays a pivotal role in determining both the apoptotic response and mutation frequency of the murine intestine to methylating DNA damage and suggests that the consequences of MSH2-deficiency may be more significant to the initial stages of carcinogenesis that loss of p53.
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Silva, Juliana Ferreira da [UNESP]. "Efeitos da temperatura e do mate (Ilex paraguariensis) sobre o processo de carcinogênese de esôfago em ratos wistar machos." Universidade Estadual Paulista (UNESP), 2008. http://hdl.handle.net/11449/87778.

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Universidade Estadual Paulista (UNESP)
O consumo de mate em altas temperaturas tem sido considerado um fator de risco para o desenvolvimento do carcinoma epidermóide de esôfago (CE) na América do Sul. Desta forma, os efeitos da ingestão de mate sobre danos de DNA e a carcinogênese de esôfago, induzidos pela dietilnitrosamina (DEN) e injúria térmica, foram avaliados em ratos Wistar machos. Na fase de iniciação, os animais foram iniciados com injeções i.p. da DEN (8 x 80 mg/Kg p.c.) e submetidos a injúria térmica (água a 65°C, lmIlrato, instilado no interior do esôfago) e receberam, concomitantemente, mate (2.0% p/v, grupo teste) ou chá-verde (2.0% p/v, grupo controle positivo) como única fonte de líquidos por oito semanas. Nenhum tratamento adicional foi introduzido durante a fase de pós-iniciação (nona a vigésima semana do experimento). Amostras de sangue periférico foram coletadas quatro horas após a última administração da DEN para o teste do cometa na oitava semana e amostras de esôfago e fígado foram coletadas na oitava e vigésima semanas do experimento. Na oitava semana, a ingestão de mate e chá-verde por si não foi genotóxica e reduziu de forma significativa os níveis de danos no DNA de leucócitos de sangue periférico nos animais tratados com a DEN. Além disso, uma redução significativa nos níveis de proliferação celular no epitélio do esôfago e no parênquima hepático e no número de lesões hepáticas pré-neoplásicas foram também observadas nos grupos iniciados e que receberam mate ou chá-verde. Na vigésima semana, uma menor incidência de neoplasias de esôfago e fígado foi observada nos grupos que receberam previamente mate e chá-verde quando comparado ao grupo iniciado pela DEN e submetido à injúria térmica. Os resultados do presente estudo indicam que a ingestão de mate se mostrou benéfica contra danos no DNA e a carcinogênese de esôfago e fígado induzidos pela DEN.
Drinking hot mate has been associated with risk for esophageal squamous cell carcinoma m South America. Thus, the modifying effects of mate tea intake on DNA damage and esophageal carcinogenesis induced by diethylnitrosamine (DEN) plus thermal injury were evaluated in male Wistar rats. In the initiation phase, rats were treated with DEN injections (8 x 80 mg/Kg b.w.) plus thermal injury (water 65°C, lml/rat, instilled into the esophagus) and concomitantly received mate tea (2.0% w/v, test group) or green tea (2.0% w/v, positive control group) as the sole source of drinking fluid for 8 weeks. Any additional treatment was introduced at post-initiation until week 20. Peripheral blood was collected 4 hr after the last DEN application for comet assay at week 8 and samples from esophagus and liver were collected at weeks 8 and 20. At week 8, mate or green tea intake itselfwere non-genotoxic and significantly decreased DNA damage levels in peripheral blood leucocytes from DEN-treated animaIs. Also, a significant reduction of cell proliferation rates in both esophageal epithelium and liver parenchyma and on the number of putative preneoplastic liver lesions were observed in initiated and mate or green tea-treated animaIs at week 8. A significant lower incidence of esophageal and liver neoplasms and tumor multiplicity was observed in the groups previously treated with mate or green tea when compared to the DEN initiated/thermal injury group at week 20. These data indicate that mate tea presented protective effects against DNA damage and esophageal and liver carcinogenesis induced by DEN.
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Bowman, Rayleen Veronica. "Mechanisms of human bronchial carcinogenesis /." [St. Lucia, Qld.], 2005. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe19353.pdf.

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TOYOKUNI, SHINYA. "MECHANISMS OF ASBESTOS-INDUCED CARCINOGENESIS." Nagoya University School of Medicine, 2009. http://hdl.handle.net/2237/11331.

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Stefanius, K. (Karoliina). "Colorectal carcinogenesis via serrated route." Doctoral thesis, Oulun yliopisto, 2011. http://urn.fi/urn:isbn:9789514293993.

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Abstract Colorectal cancer is the third most common cancer in the developed countries. Originally, development of CRC was thought to proceed by a sequence of steps known as an adenoma-carcinoma sequence. At present CRC is recognized as a disease developing through diverse pathways. Serrated adenocarcinoma represents an endpoint of tumors developing from serrated pathway. This thesis focuses on studying the molecular alterations in serrated adenocarcinoma. Microsatellite instability, hypermethylation of promoter region in DNA repair genes hMLH1 and MGMT, frequency of KRAS and BRAF mutations and mutation spectrum of PTCH1 was determined in serrated adenocarcinomas (n=42) and compared to non-serrated adenocarcinomas (n=75). MSI, particularly low level of MSI (p=0.02) and methylation of both hMLH1 and MGMT promoters (p=0.004, p=0.026) were found to be more prevalent for serrated CRC. BRAF mutation was frequent and specific to serrated adenocarcinomas (p<0.001) and KRAS mutations were more frequent in serrated adenocarcinomas than in non-serrated cancers (p=0.002). A significant association between BRAF mutation, hMLH1 and MGMT methylation and MSI-H phenotype was found in serrated carcinomas. KRAS mutation was seen in association with MSS/MSI-L phenotype; in fact, if serrated adenocarcinoma presents with MSI-L there always seems to be a KRAS mutation as well. Negative immunohistochemical staining of the hMLH1 enzyme was in association with methylation of the gene and proved reliable in the detection of MSI-H phenotype (p<0.0001). Sequencing analysis of the whole coding regions of the PTCH1 gene did not reveal any truncating mutation to explain the previously detected downregulation of the gene in serrated CRCs. In conclusion, serrated adenocarcinomas proved to be an independent, but heterogeneous subtype of CRCs. High combined mutation rate (79–82%) of KRAS and BRAF in serrated adenomas and adenocarcinomas indicates that MAPK activation is a crucial part of the serrated pathway. BRAF mutations are specific for serrated adenocarcinoma, and identify a subset of serrated adenocarcinomas with gene methylation and a tendency for MSI-H. High frequency of KRAS mutations in serrated adenocarcinomas suggests that a significant proportion of KRAS-mutated CRCs originate from serrated precursors
Tiivistelmä Paksu- ja peräsuolisyöpä eli kolorektaalisyöpä on Suomessa kolmanneksi yleisin syöpätyyppi. Syöpää edeltävien muutosten tunnistaminen on tärkeää, jotta sen ehkäisy ja seuranta olisi tehokasta. Tavallisia adenoomapolyyppeja on pidetty tärkeimpinä kolorektaalisyövän esiastemuutoksina. 2000-luvulla on havaittu, että nk. sahalaitapolyypit edustavat tärkeää osaa esiastemuutoksista, ja näistä kehittyvää syöpää kutsutaan sahalaitaiseksi syöväksi. Sahalaitaisen syövän kehittymismekanismit eroavat huomattavasti tavallisesta kolorektaalisyövästä. Tässä väitöskirjassa keskityttiin tutkimaan sahalaitaiselle syövälle tyypillisiä morfologisia piirteitä sekä geneettisiä muutoksia. Työssä selvitettiin DNA mikrosatelliitti-instabiliteetin sekä DNA korjausgeenien hMLH1 ja MGMT promoottorialueiden hypermetylaation esiintyminen, nk. MAPK –signaalinsiirtoreitin komponenttien, KRAS ja BRAF -geenien, mutaatioiden yleisyys sekä PTCH1 geenin mutaatiokirjo sahalaitaisissa (n=42) ja tavallisissa kolorektaalisyövissä (n=75). DNA:n mikrosatelliitti-instabiliteetti, erityisesti matala-asteisena (MSI-L) (p=0.02) sekä MLH1 ja hMGMT -geenien metylaatio (p=0.004, p=0.026) olivat yleisempiä sahalaitaisissa syövissä. BRAF mutaatio oli yleinen sekä spesifinen sahalaitasyöville (p<0.001). Myös KRAS -mutaatiot olivat yleisempiä sahalaitaisissa syövissä (p=0.002). BRAF mutaatio, hMLH1 sekä MGMT metylaatio ja korkea-asteinen mikrosatelliitti-instabiliteetti (MSI-H) esiintyivät hyvin usein yhdessä sahalaitaisissa syövissä. Sahalaitaisissa syövissä KRAS –mutaatiot liittyivät MSI-L fenotyyppiin. hMLH1 geenin ilmentyminen tutkittiin myös immunohistokemiallisesti. Sahalaitaisissa syövissä MLH1 –proteiinin häviäiminen oli yhteydessä metylaatioon ja liittyi spesifisesti MSI-H:n esiintymiseen (p < 0.0001). PTCH1 geenin sekvensointi ei paljastanut proteiinin toimintaa vahingoittavia muutoksia, eikä tuloksen perusteella pystytä selittämään aikaisemmin havaittua geenin ilmentymisen häviämistä sahalaitaisessa syövässä. Tulosten perusteella sahalaitainen syöpä on oma, mutta heterogeeninen kolorektaalisyövän alatyyppi. KRAS ja BRAF –geenien aktivoivien mutaatioiden yleisyys (79–82%) osoittaa, että MAPK -reitin aktivaatio on tärkeää sahalaitaisen syövän kehityksessä. BRAF -mutaatiot ovat spesifisiä sahalaitaisille syöville, ja yhdessä metylaation sekä MSI-H:n kanssa identifioi osan sahalaitasyövistä omaksi ryhmäkseen. KRAS –mutaatioiden yleisyys sahalaitaisissa syövissä antaa aiheen epäillä, että merkittävä osa KRAS –mutaation sisältävistä kolorektaalisyövistä kehittyy sahalaitapolyypeista
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De, Buck Stefan. "Immunoprophylactic approaches against chemical carcinogenesis." Doctoral thesis, Universite Libre de Bruxelles, 2005. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210984.

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Cooper, Kumarasen. "Human papillomavirus and cervical carcinogenesis." Thesis, University of Oxford, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.306091.

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Al-Damouk, Jawdet Dakhel. "Malnutrition and experimental oral carcinogenesis." Thesis, University of Glasgow, 1988. http://theses.gla.ac.uk/2731/.

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The work was undertaken to examine the effects of nutritional deficiencies on cancer induction. Two of the most common and widely distributed nutrients, iron and folic acid, were examined to evaluate the effects of their deficiency on animals. The Syrian golden hamster was the animal model for all experimental work. In the first part of the study an attempt was made to induce iron deficiency in young adult male hamsters by feeding iron deficient diet coupled with repeated venesection of 1.5ml every two weeks. Following twelve weeks on this regime a superficial biopsy was taken, on week 13, from the medial wall of one pouch in each hamster in order to evaluate the effect of iron depletion on the epithelial compartment thicknesses. After allowing the biopsy sites to heal for two weeks, a solution of 0.25% DMBA in acetone was painted, three times per week, for eight weeks, on a defined one square centimetre area in each pouch of each hamster of the experimental and control groups. The hamsters were then maintained on the same dietary regimes for twelve weeks before being killed at the beginning of week 37 for analysis. Iron deficiency anaemia could not be induced in the experimental animals of this study. The effect of the iron deficient diet on epithelial compartment thicknesses at the stage of the biopsy was not clear. However, restriction of iron intake did cause animals to develop significantly fewer grossly seen tumours and histologically identified carcinomas than control animals. In the second part of this thesis an attempt was made to investigate alternative hamster dietary components that have less iron contamination than the diet given in the first part of this thesis. Casein and calcium lactate were the main contributers to iron in the hamster diet. Casein could not be substituted by another source of protein for hamsters. However, other sources for calcium with less iron contamination were available and therefore investigated in this part of the study. Three groups of young adult male and female hamsters were given the fully nourishing powdered diet used in previous studies. However, calcium lactate was substituted for by either calcium acetate, calcium chloride or calcium sulphate in each group. None of the three diets was accepted by the animals and many of them died of starvation. When calcium salts were replaced by calcium lactate the surviving animals accepted the diet and recovered quickly afterwards. This study proved that calcium lactate could not be substituted by any other calcium salt with less iron content and therefore iron contamination in the hamster diet could not be further reduced by this method. In the third part of this thesis the effect of nutritional folate deficiency on cancer induction was studied. A group of young adult female hamsters was given folate deficient diet for four weeks. On week 5, DMBA in acetone at a concentration of 0.25% was painted on a defined one square centimetre area of the medial wall of each pouch in each hamster in folate deficient and control groups. The carcinogen was applied three times per week for eight weeks following which animals were maintained on the same dietary regimes for a further 13 weeks before being killed at the beginning of week 27 for the final analysis of the study. It was found that nutritional folate deficiency had significantly reduced the number of animals developing grossly counted tumours and histologically identified carcinomas. The folate deficient animals also developed significantly less tumours and carcinomas compared to control groups. In the last part of this thesis, the effect of combined iron and folate deficiency was examined for its role in carcinogenesis of the hamster cheek pouch. Two groups of young adult male hamsters were fed powdered diet lacking iron and folic acid and a third group was fed diet lacking iron only. One of the combined deficiency groups and the iron deficiency group were bled 1.0-1.3ml every week. On week 6 of the study DMBA in acetone at a concentration of 0.25% was painted three times per week for eight weeks on the same area of the pouch used in the previous studies. The animals were then maintained on the same experimental regimes for a further eleven weeks before being sacrificed, on week 25, for the final analysis of the study. In this study, iron deficiency anaemia was induced in animals of the bleeding groups. Animals in the group with combined iron and folate deficiency without bleeding showed low normal folate levels and normal haemoglobin levels. The two groups that were bled repeatedly showed iron deficiency anaemia. In all groups, the numbers of tumours counted grossly and the numbers of carcinomas identified histologically were significantly reduced compared to control animals in the previous studies. The folate deficient diet did not appear to influence the induction of iron deficiency. The studies reported in this thesis proved that nutritional folate deficiency not only reduces the incidence, but it also reduces the numbers of tumours and carcinomas in the hamster cheek pouch. Iron deficiency anaemia was also found to significantly reduce the numbers of tumours and carcinomas of the hamster cheek pouch. It was not possible to produce combined iron and folate deficiency under the conditions of these studies. However, animals fed on a diet lacking iron and folic acid had significantly reduced numbers of grossly seen tumours and histologically identified carcinomas in the cheek pouch in response to DMBA applications. In each of the reported studies, the nutritional deficiency of iron and folic acid, whether individually or combined was found to significantly reduce the growth rate of affected animals.
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Books on the topic "Carcinogenesis"

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P, Waalkes Michael, and Ward Jerrold Michael 1942-, eds. Carcinogenesis. New York: Raven Press, 1994.

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Tanaka, Takuji, and Hiroyuki Tsuda. Carcinogenesis and modification of carcinogenesis. Kerala, India: Research Signpost, 2005.

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Penning, Trevor M. Chemical carcinogenesis. New York: Humana Press/Springer, 2011.

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Cockburn, Andrew, and Lewis Smith, eds. Nongenotoxic Carcinogenesis. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-662-03022-6.

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Skouteris, George G., ed. Liver Carcinogenesis. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-79215-1.

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Li, Jonathan J., Satyabrata Nandi, and Sara Antonia Li, eds. Hormonal Carcinogenesis. New York, NY: Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4613-9208-8.

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Feo, Francesco, Paolo Pani, Amedeo Columbano, and Renato Garcea, eds. Chemical Carcinogenesis. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4757-9640-7.

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Pokorski, Mieczyslaw, ed. Respiratory Carcinogenesis. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-16922-4.

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Penning, Trevor M., ed. Chemical Carcinogenesis. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61737-995-6.

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1923-, Upton Arthur C., ed. Radiation carcinogenesis. New York: Elsevier, 1986.

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Book chapters on the topic "Carcinogenesis"

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Muro-Cacho, Carlos A. "Carcinogenesis." In Hamilton & Hardy's Industrial Toxicology, 1135–72. Hoboken, New Jersey: John Wiley & Sons, Inc., 2015. http://dx.doi.org/10.1002/9781118834015.ch107.

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Schmähl, D., S. Yuspa, and G. C. Orth. "Carcinogenesis." In Dermatology in Five Continents, 714–15. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-83360-1_75.

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Weinstein, I. Bernard. "Carcinogenesis." In Encyclopedia of Cancer, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_843-2.

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Norris, James, and Deanne King. "Carcinogenesis." In Basic Science of Cancer, 154–67. London: Current Medicine Group, 2000. http://dx.doi.org/10.1007/978-1-4684-8437-3_8.

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Weinstein, I. Bernard. "Carcinogenesis." In Encyclopedia of Immunotoxicology, 142–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-54596-2_208.

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Weinstein, I. Bernard. "Carcinogenesis." In Encyclopedia of Cancer, 795–96. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46875-3_843.

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Rashid, Summya. "Carcinogenesis." In Cancer and Chemoprevention: An Overview, 21–25. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-2579-2_5.

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Schiller, Erich. "Carcinogenesis." In Free Radicals and Inhalation Pathology, 699–734. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18619-6_19.

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Mohammad, Akheel, and Ashmi Wadhwania. "Carcinogenesis." In Head and Neck Oncology, 1–6. Boca Raton: CRC Press, 2021. http://dx.doi.org/10.1201/9780367822019-1.

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Tsugawa, Hitoshi, and Hidekazu Suzuki. "Gastric Carcinogenesis." In Gastric Cancer, 51–62. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-1120-8_4.

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Conference papers on the topic "Carcinogenesis"

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Shvedsky, M. S., V. G. Bychkov, V. V. Matvienko, O. G. Solovyova, R. I. Duboshinsky, and D. A. Vagina. "On the question of carcinogenesis in superinvasive opisthorchiasis." In VIII Vserossijskaja konferencija s mezhdunarodnym uchastiem «Mediko-fiziologicheskie problemy jekologii cheloveka». Publishing center of Ulyanovsk State University, 2021. http://dx.doi.org/10.34014/mpphe.2021-226-229.

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Retrospective analysis of foreign literature present in PubMed was carried out with the purpose to define possible influence of superinvasive opisthorchiasis on possible development of cholangiocellular carcinoma. After the research we conclude that O. Felineus doesn’t have an entry point during the initiation stage of carcinogenesis but rather acts as a promotor of cholangiocarcinoma (СС), and therefore cannot be considered a primary cause of the disease without additional influence of another carcinogens and specific factors that increase the probability of cholangiocarcinoma development (chronic inflammation, free radicals). Keywords: superinvasive opisthorchiasis, parasitism, immune system, carcinogenesis.
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Souchelnytskyi, Serhiy. "Systemic properties of Carcinogenesis: Lessons from studies on the Earth and in the Space." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0118.

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proteins and genes act in coordinated ways, and their relations are visualized as networks. Networks are more accurate descriptions of cancer regulatory mechanisms, in comparison to lists of oncogenes and tumor suppressors. To extract essential regulators (nodes) and connections (edges), interrogations of these networks are performed, e.g. cancer cells are subjected to different treatments. Interrogations force cancer cells to engage nodes and edges essential for maintaining cancer properties, i.e. drivers, and nonessential followers. The challenge is to discriminate which of the mechanisms drive tumorigenesis, and which are followers. Interrogation of cancer cells under variable g-forces is the treatment to which cancer cells are not normally exposed. Therefore, low (weightlessness) and high (acceleration) g-forces may trigger responses, which may differ in part of followers from responses on the Earth, but still engage carcinogenesis-essential drivers nodes and edges. Methodology: Experimental interrogation of human cancer cells to generate carcinogenesis-related regulatory networks was performed by using proteomics, cell biology, biochemistry, immunohistochemistry and bioinformatics tools. We used also reported datasets deposited in various databases. These networks were analyzed with algorithms to extract drivers of carcinogenesis. Results: Systemic analysis of human breast carcinogenesis has shown mechanisms of engagement of all known cancer hallmarks. Moreover, novel hallmarks have emerged, e.g. involvement of mechanisms of virus-cell interaction and RNA/miR processing. The breast cancer networks are rich, with >6,000 involved proteins and genes. The richness of the networks may explain many clinical observations, e.g. personalized response to treatments. Systemic analysis highlighted novel opportunities for treatment of cancer, by identifying key nodes of known and novel hallmark mechanisms. Systemic properties of the cancer network provides an opportunity to study compensatory mechanisms. These compensatory mechanisms frequently contribute to development of resistance to treatment. These mechanisms will be discussed. Cancer cells are not “wired” to function in weightlessness. The cells would have to adapt. This adaptation will include preserving mechanisms driving carcinogenesis, in addition to the space-only-related adaptation. Key carcinogenesis regulators in the space would be the same as on the Earth, while “passenger”-mechanisms would differ. Systems biology allows integration of a space- and the Earth-data, and would extract key regulators, and, subsequently lead to better diagnostic. Conclusion: Systemic analysis of carcinogenesis studies with different ways of interrogation delivered better diagnostic and novel modalities of treatment.
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Boppart, Stephen A. "Multimodal Multiphoton Microscopy of Carcinogenesis." In Cancer Imaging and Therapy. Washington, D.C.: OSA, 2016. http://dx.doi.org/10.1364/cancer.2016.cth2a.1.

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Shin, Jin Woo. "Nedd4-1 in cervical carcinogenesis." In ASGO 2023. Korea: Korean Society of Gynecologic Oncology, 2024. http://dx.doi.org/10.3802/jgo.2024.35.s1.0032.

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Lane, Pierre, Sylvia F. Lam, Jessica McAlpine, Blake Gilks, Steve Kalloger, Dianne Miller, David Huntsman, and Calum MacAulay. "Autofluorescence Imaging of Fallopian Tube Carcinogenesis." In Biomedical Optics. Washington, D.C.: OSA, 2010. http://dx.doi.org/10.1364/biomed.2010.jma95.

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Shibata, Darryl. "Abstract CN12-02: Evolution in carcinogenesis." In Abstracts: Frontiers in Cancer Prevention Research 2008. American Association for Cancer Research, 2008. http://dx.doi.org/10.1158/1940-6207.prev-08-cn12-02.

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Nath, Raghu G., BR Sonawane, SV Vulimiri, and YS Lin. "Abstract 2738: Mechanisms of cadmium carcinogenesis." 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.am2015-2738.

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Hu, Yinling. "Abstract IA19: Fungal infection and carcinogenesis." In Abstracts: AACR Special Conference on the Microbiome, Viruses, and Cancer; February 21-24, 2020; Orlando, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.mvc2020-ia19.

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Deryagina, V. P., N. I. Ryzhova, L. A. Savluchinskaya, I. S. Golubeva, L. V. Krivosheeva, and K. I. Kirsanov. "eNOS INVOLVEMENT IN CARCINOGENESIS AND PROSPECTS FOR THE USE OF ENZYME INHIBITORS." In NOVEL TECHNOLOGIES IN MEDICINE, BIOLOGY, PHARMACOLOGY AND ECOLOGY. Institute of information technology, 2022. http://dx.doi.org/10.47501/978-5-6044060-2-1.310-321.

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The review discusses the literature data and the results of our own research on the role of endothelial NO synthase (eNOS) in carcinogenesis. The antitumor potential of eNOS inhibi-tors and the molecular mechanisms of their action are analyzed.
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Sokolov, Konstantin, Jesse Aaron, Sonia Kumar, Vivian Mack, Lezlee Coghlan, Ann Gillenwater, Karen Adler Storthz, Michele Follen, and Rebecca Richards Kortum. "Molecular imaging of carcinogenesis with metal nanoparticles." In Frontiers in Optics. Washington, D.C.: OSA, 2004. http://dx.doi.org/10.1364/fio.2004.fthk2.

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Reports on the topic "Carcinogenesis"

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Hayward, Simon W. Paracrine Regulation of Prostatic Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, January 2005. http://dx.doi.org/10.21236/ada435853.

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Coussens, Lisa M. Microenvironmental Regulation of Mammary Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, June 2009. http://dx.doi.org/10.21236/ada514035.

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Hayward, Simon W. Paracrine Regulation of Prostatic Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, January 2004. http://dx.doi.org/10.21236/ada423319.

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Patriotis, Christos F. Mechanisms and Chemoprevention of Ovarian Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, February 2005. http://dx.doi.org/10.21236/ada436431.

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Heffelfinger, Sue C. Mammary Stem Cell Susceptibility to Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, July 2005. http://dx.doi.org/10.21236/ada443556.

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He, Xi. WNT-1 Signaling in Mammary Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, April 2001. http://dx.doi.org/10.21236/ada395338.

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Cvetkovic, Dusica. Mechanisms and Chemoprevention of Ovarian Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, February 2008. http://dx.doi.org/10.21236/ada485054.

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Bianchi-Frias, Daniella. The Aged Microenvironment Influences Prostate Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, December 2008. http://dx.doi.org/10.21236/ada500681.

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Schafer, Melanie. Defining CCL20's Role in Carcinogenesis. Portland State University Library, January 2012. http://dx.doi.org/10.15760/honors.5.

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Patriotis, Christos. Mechanisms and Chemoprevention of Ovarian Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, February 2006. http://dx.doi.org/10.21236/ada449486.

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