Gotowa bibliografia na temat „Carcinogenesis”
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Artykuły w czasopismach na temat "Carcinogenesis"
Grilli, S., S. Bartoli, P. Perocco i A. Colacci. "Experimental carcinogenesis and anti-carcinogenesis". European Journal of Cancer Prevention 3, nr 4 (lipiec 1994): 382. http://dx.doi.org/10.1097/00008469-199407000-00020.
Pełny tekst źródłaJukes, Thomas H. "Carcinogenesis". Science 227, nr 4686 (luty 1985): 466. http://dx.doi.org/10.1126/science.227.4686.466.d.
Pełny tekst źródłaDipple, A. "Carcinogenesis". Current Opinion in ONCOLOGY 2, nr 1 (luty 1990): 129–33. http://dx.doi.org/10.1097/00001622-199002000-00021.
Pełny tekst źródłaJUKES, T. H. "Carcinogenesis". Science 227, nr 4686 (1.02.1985): 466. http://dx.doi.org/10.1126/science.227.4686.466-c.
Pełny tekst źródłaDilly, S. "Carcinogenesis". Journal of Clinical Pathology 47, nr 6 (1.06.1994): 572. http://dx.doi.org/10.1136/jcp.47.6.572-b.
Pełny tekst źródłaCasson, Phillip. "Carcinogenesis". Plastic and Reconstructive Surgery 86, nr 2 (sierpień 1990): 376. http://dx.doi.org/10.1097/00006534-199008000-00040.
Pełny tekst źródłaWaalkes, Michael P., Jerrold M. Ward i Serpil C. Erzurum. "Carcinogenesis". Journal of Bronchology 2, nr 2 (kwiecień 1995): 173. http://dx.doi.org/10.1097/00128594-199504000-00022.
Pełny tekst źródłaDunsford, Harold A. "Carcinogenesis". Human Pathology 25, nr 11 (listopad 1994): 1258–59. http://dx.doi.org/10.1016/0046-8177(94)90051-5.
Pełny tekst źródłaMcMillan, Susan C. "Carcinogenesis". Seminars in Oncology Nursing 8, nr 1 (luty 1992): 10–19. http://dx.doi.org/10.1016/0749-2081(92)90004-m.
Pełny tekst źródłaMalone, Michael J., Joseph K. Izes i Liam J. Hurley. "CARCINOGENESIS". Urologic Clinics of North America 24, nr 4 (listopad 1997): 723–28. http://dx.doi.org/10.1016/s0094-0143(05)70414-6.
Pełny tekst źródłaRozprawy doktorskie na temat "Carcinogenesis"
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.
Pełny tekst źródłaCoordenação 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.
Fischer, Heléne. "Gene expression in carcinogenesis /". Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4961-1/.
Pełny tekst źródłaToft, Neil John. "MSH2, apoptosis, and carcinogenesis". Thesis, University of Edinburgh, 1998. http://hdl.handle.net/1842/22693.
Pełny tekst źródłaSilva, 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.
Pełny tekst źródłaUniversidade 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.
Bowman, Rayleen Veronica. "Mechanisms of human bronchial carcinogenesis /". [St. Lucia, Qld.], 2005. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe19353.pdf.
Pełny tekst źródłaTOYOKUNI, SHINYA. "MECHANISMS OF ASBESTOS-INDUCED CARCINOGENESIS". Nagoya University School of Medicine, 2009. http://hdl.handle.net/2237/11331.
Pełny tekst źródłaStefanius, K. (Karoliina). "Colorectal carcinogenesis via serrated route". Doctoral thesis, Oulun yliopisto, 2011. http://urn.fi/urn:isbn:9789514293993.
Pełny tekst źródłaTiivistelmä 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
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.
Pełny tekst źródłaCooper, Kumarasen. "Human papillomavirus and cervical carcinogenesis". Thesis, University of Oxford, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.306091.
Pełny tekst źródłaAl-Damouk, Jawdet Dakhel. "Malnutrition and experimental oral carcinogenesis". Thesis, University of Glasgow, 1988. http://theses.gla.ac.uk/2731/.
Pełny tekst źródłaKsiążki na temat "Carcinogenesis"
P, Waalkes Michael, i Ward Jerrold Michael 1942-, red. Carcinogenesis. New York: Raven Press, 1994.
Znajdź pełny tekst źródłaTanaka, Takuji, i Hiroyuki Tsuda. Carcinogenesis and modification of carcinogenesis. Kerala, India: Research Signpost, 2005.
Znajdź pełny tekst źródłaPenning, Trevor M. Chemical carcinogenesis. New York: Humana Press/Springer, 2011.
Znajdź pełny tekst źródłaCockburn, Andrew, i Lewis Smith, red. Nongenotoxic Carcinogenesis. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-662-03022-6.
Pełny tekst źródłaSkouteris, George G., red. Liver Carcinogenesis. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-79215-1.
Pełny tekst źródłaLi, Jonathan J., Satyabrata Nandi i Sara Antonia Li, red. Hormonal Carcinogenesis. New York, NY: Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4613-9208-8.
Pełny tekst źródłaFeo, Francesco, Paolo Pani, Amedeo Columbano i Renato Garcea, red. Chemical Carcinogenesis. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4757-9640-7.
Pełny tekst źródłaPokorski, Mieczyslaw, red. Respiratory Carcinogenesis. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-16922-4.
Pełny tekst źródłaPenning, Trevor M., red. Chemical Carcinogenesis. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61737-995-6.
Pełny tekst źródła1923-, Upton Arthur C., red. Radiation carcinogenesis. New York: Elsevier, 1986.
Znajdź pełny tekst źródłaCzęści książek na temat "Carcinogenesis"
Muro-Cacho, Carlos A. "Carcinogenesis". W Hamilton & Hardy's Industrial Toxicology, 1135–72. Hoboken, New Jersey: John Wiley & Sons, Inc., 2015. http://dx.doi.org/10.1002/9781118834015.ch107.
Pełny tekst źródłaSchmähl, D., S. Yuspa i G. C. Orth. "Carcinogenesis". W Dermatology in Five Continents, 714–15. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-83360-1_75.
Pełny tekst źródłaWeinstein, I. Bernard. "Carcinogenesis". W Encyclopedia of Cancer, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_843-2.
Pełny tekst źródłaNorris, James, i Deanne King. "Carcinogenesis". W Basic Science of Cancer, 154–67. London: Current Medicine Group, 2000. http://dx.doi.org/10.1007/978-1-4684-8437-3_8.
Pełny tekst źródłaWeinstein, I. Bernard. "Carcinogenesis". W Encyclopedia of Immunotoxicology, 142–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-54596-2_208.
Pełny tekst źródłaWeinstein, I. Bernard. "Carcinogenesis". W Encyclopedia of Cancer, 795–96. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46875-3_843.
Pełny tekst źródłaRashid, Summya. "Carcinogenesis". W Cancer and Chemoprevention: An Overview, 21–25. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-2579-2_5.
Pełny tekst źródłaSchiller, Erich. "Carcinogenesis". W 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.
Pełny tekst źródłaMohammad, Akheel, i Ashmi Wadhwania. "Carcinogenesis". W Head and Neck Oncology, 1–6. Boca Raton: CRC Press, 2021. http://dx.doi.org/10.1201/9780367822019-1.
Pełny tekst źródłaTsugawa, Hitoshi, i Hidekazu Suzuki. "Gastric Carcinogenesis". W Gastric Cancer, 51–62. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-1120-8_4.
Pełny tekst źródłaStreszczenia konferencji na temat "Carcinogenesis"
Shvedsky, M. S., V. G. Bychkov, V. V. Matvienko, O. G. Solovyova, R. I. Duboshinsky i D. A. Vagina. "On the question of carcinogenesis in superinvasive opisthorchiasis". W 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.
Pełny tekst źródłaSouchelnytskyi, Serhiy. "Systemic properties of Carcinogenesis: Lessons from studies on the Earth and in the Space". W Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0118.
Pełny tekst źródłaBoppart, Stephen A. "Multimodal Multiphoton Microscopy of Carcinogenesis". W Cancer Imaging and Therapy. Washington, D.C.: OSA, 2016. http://dx.doi.org/10.1364/cancer.2016.cth2a.1.
Pełny tekst źródłaShin, Jin Woo. "Nedd4-1 in cervical carcinogenesis". W ASGO 2023. Korea: Korean Society of Gynecologic Oncology, 2024. http://dx.doi.org/10.3802/jgo.2024.35.s1.0032.
Pełny tekst źródłaLane, Pierre, Sylvia F. Lam, Jessica McAlpine, Blake Gilks, Steve Kalloger, Dianne Miller, David Huntsman i Calum MacAulay. "Autofluorescence Imaging of Fallopian Tube Carcinogenesis". W Biomedical Optics. Washington, D.C.: OSA, 2010. http://dx.doi.org/10.1364/biomed.2010.jma95.
Pełny tekst źródłaShibata, Darryl. "Abstract CN12-02: Evolution in carcinogenesis". W 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.
Pełny tekst źródłaNath, Raghu G., BR Sonawane, SV Vulimiri i YS Lin. "Abstract 2738: Mechanisms of cadmium carcinogenesis". W 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.
Pełny tekst źródłaHu, Yinling. "Abstract IA19: Fungal infection and carcinogenesis". W 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.
Pełny tekst źródłaDeryagina, V. P., N. I. Ryzhova, L. A. Savluchinskaya, I. S. Golubeva, L. V. Krivosheeva i K. I. Kirsanov. "eNOS INVOLVEMENT IN CARCINOGENESIS AND PROSPECTS FOR THE USE OF ENZYME INHIBITORS". W 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.
Pełny tekst źródłaSokolov, Konstantin, Jesse Aaron, Sonia Kumar, Vivian Mack, Lezlee Coghlan, Ann Gillenwater, Karen Adler Storthz, Michele Follen i Rebecca Richards Kortum. "Molecular imaging of carcinogenesis with metal nanoparticles". W Frontiers in Optics. Washington, D.C.: OSA, 2004. http://dx.doi.org/10.1364/fio.2004.fthk2.
Pełny tekst źródłaRaporty organizacyjne na temat "Carcinogenesis"
Hayward, Simon W. Paracrine Regulation of Prostatic Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, styczeń 2005. http://dx.doi.org/10.21236/ada435853.
Pełny tekst źródłaCoussens, Lisa M. Microenvironmental Regulation of Mammary Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2009. http://dx.doi.org/10.21236/ada514035.
Pełny tekst źródłaHayward, Simon W. Paracrine Regulation of Prostatic Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, styczeń 2004. http://dx.doi.org/10.21236/ada423319.
Pełny tekst źródłaPatriotis, Christos F. Mechanisms and Chemoprevention of Ovarian Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, luty 2005. http://dx.doi.org/10.21236/ada436431.
Pełny tekst źródłaHeffelfinger, Sue C. Mammary Stem Cell Susceptibility to Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2005. http://dx.doi.org/10.21236/ada443556.
Pełny tekst źródłaHe, Xi. WNT-1 Signaling in Mammary Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, kwiecień 2001. http://dx.doi.org/10.21236/ada395338.
Pełny tekst źródłaCvetkovic, Dusica. Mechanisms and Chemoprevention of Ovarian Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, luty 2008. http://dx.doi.org/10.21236/ada485054.
Pełny tekst źródłaBianchi-Frias, Daniella. The Aged Microenvironment Influences Prostate Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, grudzień 2008. http://dx.doi.org/10.21236/ada500681.
Pełny tekst źródłaSchafer, Melanie. Defining CCL20's Role in Carcinogenesis. Portland State University Library, styczeń 2012. http://dx.doi.org/10.15760/honors.5.
Pełny tekst źródłaPatriotis, Christos. Mechanisms and Chemoprevention of Ovarian Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, luty 2006. http://dx.doi.org/10.21236/ada449486.
Pełny tekst źródła