Relevant bibliographies by topics / Tumorigenesis

Academic literature on the topic 'Tumorigenesis'

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Published: 4 June 2021
Last updated: 6 July 2024

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Journal articles on the topic "Tumorigenesis"

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Felsher, Dean W. "Reversible tumorigenesis." Cancer Biology & Therapy 3, no. 10 (October 2004): 942–44. http://dx.doi.org/10.4161/cbt.3.10.1307.

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Park, Jin-Woo. "Thyroid Tumorigenesis." Korean Journal of Endocrine Surgery 10, no. 2 (2010): 79. http://dx.doi.org/10.16956/kjes.2010.10.2.79.

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Wells, William A. "Innate tumorigenesis." Journal of Cell Biology 175, no. 2 (October 16, 2006): 197. http://dx.doi.org/10.1083/jcb.1752rr4.

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Casanueva, Felix. "Pituitary Tumorigenesis." Hormone Research in Paediatrics 68, no. 5 (2007): 126. http://dx.doi.org/10.1159/000110606.

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BEUSCHLEIN, F., and M. REINCKE. "Adrenocortical Tumorigenesis." Annals of the New York Academy of Sciences 1088, no. 1 (November 1, 2006): 319–34. http://dx.doi.org/10.1196/annals.1366.001.

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Abbasi, A. M., I. C. Talbot, A. Forbes, and I. C. Talbot. "Colorectal tumorigenesis." Gut 36, no. 5 (May 1, 1995): 801. http://dx.doi.org/10.1136/gut.36.5.801-b.

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Williams, E. D. "Thyroid Tumorigenesis." Hormone Research 42, no. 1-2 (1994): 31–34. http://dx.doi.org/10.1159/000184141.

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Shih, Ie-Ming, and Robert J. Kurman. "Ovarian Tumorigenesis." American Journal of Pathology 164, no. 5 (May 2004): 1511–18. http://dx.doi.org/10.1016/s0002-9440(10)63708-x.

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Alderton, Gemma K. "Mediating tumorigenesis." Nature Reviews Cancer 14, no. 6 (May 23, 2014): 382. http://dx.doi.org/10.1038/nrc3757.

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Kim, In-Gyu, and Yun-Sil Lee. "Radiation-induced Tumorigenesis." BMB Reports 36, no. 1 (January 31, 2003): 144–48. http://dx.doi.org/10.5483/bmbrep.2003.36.1.144.

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Dissertations / Theses on the topic "Tumorigenesis"

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Rocchi, Laura <1982&gt. "mRNAs translation and tumorigenesis." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2012. http://amsdottorato.unibo.it/4363/1/Rocchi_Laura_tesi.pdf.

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Translational control has a direct impact on cancer development and progression. Quantitative and qualitative changes of cap-dependent translation initiation contribute to neoplastic transformation and progression. However, the idea that “alternative” mechanisms of translation initiation, such as IRES-dependent translation, can be involved in the tumorigenesis is emerging. Because the relevance of this kind of translation initiation in cancer progression is not so well clarified, the purpose of my work was to study the impact of IRES-dependent mRNA translation on tumourigenesis and cancer progression with particular regard for breast cancer. The data obtained clarify the function of cap-independent translation in cancer. Particularly they suggested that the deregulation of IRES-dependent translation can be considered a sort of pro-oncogenic stimulus characterized by the inhibition of the expression of some proteins that block cell growth and proliferation and by the over expression of other proteins that contributed to cell survival. In addition, under stress condition, such as a hypoxia, in immortalized epithelial cell lines, changes in cap-independent translation are associated with an induction of expression of stem cell markers, and with the selection of a sub group of cells that have an increased ability to self-renewing and therefore in the acquisition of a more aggressive phenotype.
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Rocchi, Laura <1982&gt. "mRNAs translation and tumorigenesis." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2012. http://amsdottorato.unibo.it/4363/.

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Translational control has a direct impact on cancer development and progression. Quantitative and qualitative changes of cap-dependent translation initiation contribute to neoplastic transformation and progression. However, the idea that “alternative” mechanisms of translation initiation, such as IRES-dependent translation, can be involved in the tumorigenesis is emerging. Because the relevance of this kind of translation initiation in cancer progression is not so well clarified, the purpose of my work was to study the impact of IRES-dependent mRNA translation on tumourigenesis and cancer progression with particular regard for breast cancer. The data obtained clarify the function of cap-independent translation in cancer. Particularly they suggested that the deregulation of IRES-dependent translation can be considered a sort of pro-oncogenic stimulus characterized by the inhibition of the expression of some proteins that block cell growth and proliferation and by the over expression of other proteins that contributed to cell survival. In addition, under stress condition, such as a hypoxia, in immortalized epithelial cell lines, changes in cap-independent translation are associated with an induction of expression of stem cell markers, and with the selection of a sub group of cells that have an increased ability to self-renewing and therefore in the acquisition of a more aggressive phenotype.
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Cripps, Kathryn Jane. "Genetic events in colorectal tumorigenesis." Thesis, University of Edinburgh, 1995. http://hdl.handle.net/1842/27836.

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More is known about the genes involved in colorectal tumorigenesis than for any other human cancer. Mutations have been identified in many genes, including the K-ras oncogene and the APC, MCC, DC and p53 tumour suppressor genes. However, whilst much is known about these events there are many questions that remain unanswered. Three specific questions involving p53, MCC and APC were addressed in this thesis. Firstly, it has been previously assumed that point mutation of the p53 gene inevitably resulted in a permanently stabilised protein product. To address this question in colorectal carcinomas, the relationship between p53 mutation and stabilisation of p53 protein was assessed by comparing stabilised product detected by immunocytochemistry (ICC) using p53 specific antibodies, with mutation as detected by single strand conformational polymorphism analysis (SSCP) and sequencing. The results suggest a high correlation between p53 protein stabilisation and gene mutation, but highlight specific incidences in which concordance is not absolute. In particular, mutations in exon 6 of p53 did not result in a stabilised protein and several tumours with a high degree of staining contained no apparent mutation within the entire coding region of the gene. Secondly, although MCC (for mutated in colorectal cancer) on chromosome 5q was amongst the first colorectal cancer genes to be identified and was shown to be mutated in a small number of colon tumours, its role is still uncertain. Finally, another gene has also been located on chromosome 5q and had been shown to be mutated in about 60% of sporadic colon tumours as well as in the germline of FPC patients and hence called APC (for adenomatous polyposis coli).
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Jonkers, Yvonne Margaretha Hendrika. "Molecular alternations during insulinoma tumorigenesis." [Maastricht : Maastricht : Universiteit Maastricht] ; University Library, Universiteit Maastricht [host], 2007. http://arno.unimaas.nl/show.cgi?fid=8685.

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Hobeika, Alice. "Notch1 signaling in mammary tumorigenesis." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=110389.

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Aberrant activation of Notch receptors has been implicated in breast cancer. We and other have shown that the expression of a mutant Notch transcript coding mostly for the intracellular domain of Notch1 (Notch1IC) causes transformation of cells in culture and development of tumors in transgenic mice. However, the mechanisms contributing to Notch1IC-induced tumor formation remain elusive and the long latency before the appearance of tumors in Tg mice seems to indicate that Notch requires the collaboration of secondary mutations to induce transformation and tumorigenesis. In the aim of studying direct downstream effects of Notch1IC expression, we generated a Tet-ON inducible expression system for Notch1IC in Hc11 mammary epithelial cells. In the inducible cell lines established, expression of the transgene is only activated upon addition of doxycycline (DOX) to the culture media. The inducible cells were capable of forming colonies in soft agar when subjected to continuous DOX induction and transplantation of the inducible cells in DOX-treated recipient mice caused tumor formation with metastasis to the lungs. We performed a genome-wide microarray-based expression analysis to compare gene expression following 24-hr Notch1IC induction to that of their uninduced counterparts. There were 26 genes identified as being upregulated 2-fold and more upon expression of Notch1IC, while 5 genes were found to be downregulated. Most of these genes identified represent novel candidate Notch1 targets. Of the candidate Notch1IC targets found to be upregulated, expression of the transcript for M-cadherin, also known as CDH15, was most significantly elevated with a change of over 19-fold. M-cadherin is a member of the cadherin family of type I single-pass transmembrane domain proteins that mediate calcium-dependent cell adhesion. M-cadherin, first identified in myogenic mouse cells, is found predominantly in developing skeletal muscles and is highly expressed during secondary myogenesis. In mature skeletal muscle, M-cadherin is mainly detectable in satellite cells. A role for M-cadherin in tumors of epithelial origin has not been previously documented, nor has it been associated with the Notch signaling pathway. We first confirmed that M-cadherin was significantly upregulated by semi-quantitative RT-PCR in the Notch1IC-inducible system. In a time-course experiment, M-cadherin upregulation was observed within 2 hours of Notch1IC induction. In vivo, Notch1IC expression in mammary tumors from Tg mice also correlated with strong expression of M-cadherin, whereas M-cadherin was undetectable in non-Tg mammary glands. We further determined that the transcriptional upregulation of M-cadherin occurs, at least in part, through the canonical CSL-dependent Notch1 pathway. Moreover, using shRNA-mediated depletion of M-cadherin in cell lines derived from mammary tumors from our MMTV/Notch1IC, we were able to investigate the function of M-cadherin in Notch1IC-induced oncogenesis. Through in vitro and in vivo assays, M-cadherin was shown to be required for the transformation of MMTV/Notch1IC cells as well as for their ability to form tumors in mice. In light of these findings, we also examined gene expression of M-cadherin in several human cancer cell lines, including different subtypes of breast cancers. M-cadherin expression was confirmed and appears to also be activated by Notch1IC in a number of breast cancer cell lines. A cursory survey of publicly available human cancer gene expression datasets further corroborated an implication for M-cadherin in human cancers, as well as a correlation between the levels of expression of M-cadherin and Notch1. A better understanding of the mechanisms of action of M-cadherin could shed light on targeted therapeutic approaches for the treatment of Notch1-overexpressing cancers and possibly other human carcinomas.
L'activation aberrante des récepteurs Notch a été impliqué dans le cancer du sein. Notre groupe ainsi que quelques autres ont démontré que l'expression d'un transcrit Notch1 muté, codant principalement pour le domaine intracellulaire de Notch1 (Notch1IC) provoque la transformation des cellules en culture et le développement de tumeurs chez les souris transgéniques. Cependant, les mécanismes contribuant à la tumorigénèse induite par Notch1IC demeurent méconnus et la longue période de latence avant l'apparition de tumeurs chez les souris Tg semble indiquer que Notch nécessite la collaboration des mutations secondaires pour engendrer la transformation cellulaire et la formation de tumeurs. Dans le but d'étudier les effets directs en aval de l'expression de Notch1IC, nous avons généré un système d'expression inductible Tet-ON pour Notch1IC dans les cellules épithéliales mammaires Hc11. Dans les lignées cellulaires inductibles établies, l'expression du transgène n'est activée que lors de l'addition de doxycycline (DOX) au milieu de culture. Les cellules inductibles sont capables de former des colonies en agar lorsqu'elles sont induites à la DOX en continu, et elles forment des tumeurs avec métastases aux poumons lorsque transplantées dans des souris traitées à la DOX. Nous avons effectué une analyse de l'expression du génome entier par micropuce dans le but de comparer l'expression des gènes à la suite de l'induction Notch1IC durant 24 heures, à celle de cellules homologues non-induites. 26 gènes ont été identifiés comme étant régulés à la hausse (2 fois et plus) suite à l'expression de Notch1IC, tandis que 5 gènes ont été identifiés comme étant régulés à la baisse. La plupart des gènes ainsi identifiés représentent de nouvelles cibles candidates de Notch1.Parmi ces cibles candidates, l'expression du transcrit pour M-cadhérine (CDH15) a été le plus significativement élevée (19 fois). M-cadhérine, une molécule d'adhésion cellulaire, a été identifiée dans les cellules myogéniques de souris; la protéine est principalement exprimée durant le développement de muscles squelettiques et au cours de la myogenèse secondaire. Dans le muscle squelettique mature, M-cadhérine est principalement détectable dans les cellules satellites. Fait intéressant, un rôle pour M-cadhérine dans les tumeurs d'origine épithéliale n'a pas été précédemment documenté, d'autant plus que M-cadhérine n'a pas été associée à la voie de signalisation Notch.Nous avons d'abord confirmé la surexpression de M-cadhérine par RT-PCR semi-quantitatif dans les cellules Notch1IC-inductibles. In vivo, l'expression de Notch1IC dans les tumeurs mammaires de souris Tg corrélait également avec une forte expression de M-cadhérine. Nous avons également déterminé que la régulation de la transcription de M-cadhérine se produit, au moins en partie, par la voie de signalisation canonique (CSL-dépendante) de Notch1. Par ailleurs, en utilisant des shRNA pour supprimer l'expression de M-cadhérine dans des lignées cellulaires dérivées de tumeurs mammaires provenant de nos souris MMTV/Notch1IC, nous avons pu étudier la fonction de M-cadhérine dans l'oncogénèse induite par Notch1IC. Par le biais d'essais in vitro et in vivo, nous avons démontré que M-cadhérine était requise pour la transformation des cellules MMTV/Notch1IC ainsi que pour leur capacité à former des tumeurs chez la souris. Par la suite, nous avons également confirmé l'expression de M-cadhérine dans plusieurs lignées cellulaires de cancer du sein. Un bref survol de bases de données d'expression génique dans des cancers humain suggère que M-cadhérine serait impliquée dans plusieurs types de cancers, et qu'il y aurait une corrélation entre les niveaux d'expression de M-cadhérine et de Notch1 dans certains cancers du sein.Une meilleure compréhension des mécanismes d'action de M-cadhérine pourrait mener à de nouvelles approches thérapeutiques ciblées pour le traitement des cancers surexprimant Notch1.
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Hong, Karen H. (Karen Hsiao-Ying) 1971. "Mouse modifiers of intestinal tumorigenesis." Thesis, Massachusetts Institute of Technology, 2001. http://hdl.handle.net/1721.1/8585.

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Thesis (Ph.D.)--Massachusetts Institute of Technology, Dept. of Biology, 2001.
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Colorectal cancer involves a series of molecular alterations as a normal cell progresses to malignancy. A large body of evidence points to the mutation of the APC gene as the pivotal event initiating intestinal tumorigenesis. Apdmin, an induced mutation in mouse homologue of APC, was identified several years ago by Moser et al., providing a genetic model system to study this process. We used the Apdmin system to identify additional genes influencing tumorigenesis. One of these genes,. Mom1 (Modifier of Min-1), involves the effect of genetic background on the Apdmin phenotype. On C57BL/6 (B6), the strain on which Apdmin arose, mice develop approximately 100 tumors. However, B6 X AKR Fl hybrids develop five-fold fewer tumors. Mom1 was identified as the major locus controlling this variation and localized to a 15 cM region on distal mouse chromosome 4 by Dietrich et al. To positionally clone Mom1, Gould et al created a B6.Mom1 AKR congenic strain isolating Mom1 from other AKR resistance factors. Separated from other loci, a single copy of Mom1 AKR reduced tumor number by 50% and two copies produced a 70% reduction. We have used recombinant lines derived from B6.Mom1 AKR to mapMom1 to a 4-cM interval containing one candidate gene, the group IIA secretory phospholipase a2 (sPLA2-IIA). Only tumor prone Mom1 strains, such as B6, contain a mutation in sPLA2-IIA abolishing expression. In order to rigorously measure the effect of sPLA2-IIA on the Apdmin tumor phenotype, we have created and analyzed transgenic lines that restore sPLA2-IIA expression. While we conclude that sPLA2-IIA is indeed protective, tumor number is only reduced by approximately 30%, suggesting that sPLA2-IIA is only part of Mom1. Analysis of additional Moml AKR recombinant strains containing and lacking sPLA2-IIA also implicates a separate distal modifier that accounts for the remaining resistance. To further probe how phospholipases impinge on intestinal cancers, we have studied tumorigen-sis in mice lacking group IV cytosolic phospholipase a2 (cPLA2). Crossing ApcMin into this background produces an 83% reduction in tumor number in ApcMin, cPLA2 -/- homozygotes, suggesting that cPLA2 expression promotes tumorigenesis, most likely via the production of arachidonic acid for downstream eicosanoid synthesis.
by Karen H. Hong.
Ph.D.
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Tam, Mandy Chi-Mun. "Genomic analysis of mouse tumorigenesis." Thesis, Massachusetts Institute of Technology, 2006. http://hdl.handle.net/1721.1/37454.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2006.
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The availability of the human and mouse genome sequences has spurred a growing interest in analyzing mouse models of human cancer using genomic techniques. Comparative genomic studies on mouse and human tumors can be valuable in two major ways: in validating mouse models and in identifying genes that are common to mouse and human tumorigenesis. Many analytic tools have emerged in recent years for human genome mining. Some of these tools have been translated to the murine versions. The work in this thesis described the application of two new whole-genome analytic techniques to study mouse tumorigensis: Representational Oligonucleotide Microarray Analysis (ROMA) for tumor DNA copy number asessment and single nucleotide polymorphism (SNP) genotyping using the SNaPshotM system (Applied Biosystems) to detect loss of heterozygosity (LOH) in mouse tumors. The murine version of ROMA was tested on DNA from early-stage KrasGJ2D-derived lung cancers and metastatic retinoblastoma in mice with retinal-specific Rb and p130 deletions. We were interested in identifying the additional genetic lesions that got positively selected during tumorigenesis of these mice.
(cont.) Several recurrent chromosomal copy number gains and losses were observed in the DNA of KrasGJ2D-derived lung tumors. In addition, a focal amplification of the murine N-Myc locus was detected in the metastatic retinoblastomas, demonstrating the capability of ROMA to detect copy number changes at a single-gene resolution. For genome-wide allelotyping, a panel of 147 mouse SNPs were individually validated in 129S4/SvJae vs. C57BL/6J strains and were chosen as markers in the genotyping panel. We worked out a multiplex protocol to genotype the SNPs in an efficient manner. Through this protocol, we generated low-density global LOH maps of lung tumors from mice expressing KrasG12D. LOH that spanned entire chromosomes was seen in a subset of the tumors. A loss of the wild-type p53 allele was also observed in some cases.
by Mandy Chi-Mun Tam.
Ph.D.
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Cabrerizo, Granados David 1993. "Endothelial Snail1 in angiogenesis and tumorigenesis." Doctoral thesis, Universitat Pompeu Fabra, 2020. http://hdl.handle.net/10803/670305.

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Snail1 is a transcriptional factor with a great relevance in tumor development as it is required for epithelial to mesenchymal transition and activation of cancer-associated fibroblasts (CAF). In this thesis, we reported that tumor endothelial cells did also express Snail1, being key for angiogenesis, by promoting endothelial cell migration, invasion and tubulogenesis in vitro. Those roles are associated to Snail1 induction by FGF2 and VEGFA, leading to gene expression profile change in endothelial cells and modulation of their activation status. Specific Snail1 depletion in the endothelium of adult mice does not promote an overt phenotype; however, it controls angiogenesis and vessel morphology in Matrigel plug assay. Moreover, endothelium-specific Snail1 depletion in the MMTVPyMT breast cancer murine model delays the initiation of neoplasms, being less advanced and with a papillary morphology, which was corroborated by orthotopic breast tumor inoculation model. These in vivo effects are associated to the inability of Snail1-deficient endothelial cells to promote a full in vitro and in vivo activation of fibroblasts through a reduced FGF2 and CXCL12 signaling; as well as to sustain a complete in vivo angiogenesis, with wider and less invasive neo-vessels. Similar changes on tumor onset and morphology are observed by pretreatment on MMTV-PyMT mice with the angiogenic inhibitor bevacizumab. Checking those results in human breast tumor samples, we could recapitulate most of the findings of our mouse models. Altogether, these findings establish a new role for Snail1 in endothelial cells, not only in angiogenesis but also in tumor onset, development and phenotype
Snail1 es un factor de transcripción con gran relevancia en el desarrollo tumoral, siendo necesario para la transición epitelio-mesénquima y la activación de fibroblastos asociados al cáncer (CAF). En esta tesis, hemos reportado la expresión de Snail1 en células endoteliales de tumor, jugando un papel fundamental en angiogénesis, promoviendo su migración, invasión y tubulogenesis in vitro. Estas funciones están asociadas a la inducción de Snail1 por FGF2 y VEGF-A, que generan un cambio en el perfil de expresión génica en las células endoteliales y modulan su estado de activación. La depleción específica de Snail1 en el endotelio de ratones adultos no supone un cambio fenotípico evidente; sin embargo, sí controla la angiogénesis y la morfología de los vasos en ensayos de plugs de Matrigel. Además, la eliminación específica de Snail1 en el endotelio del modelo murino de tumores de mama espontáneos MMTV-PyMT provoca el retraso en la iniciación de tumores, siendo éstos menos avanzados y con una morfología papilar. Estos efectos in vivo están asociados a la incapacidad de las células endoteliales sin Snail1 de promover una activación completa de fibroblastos in vitro e in vivo, debido a una señalización reducida de las vías de FGF2 y CXCL12; ni de generar una angiogénesis completa in vivo, con neovasos más anchos y menos invasivos. Cambios similares en la aparición de tumores y en su morfología se observaron en ratones MMTV-PyMT pretratados con el antiangiógenico bevacizumab. En muestras humanas de cáncer de mama pudimos recapitular la mayoría de los descubrimientos de los modelos animales usados. En resumen, estos hallazgos establecen un nuevo papel para Snail1 en las células endoteliales, no solo en angiogénesis, sino también en la aparición tumoral, el desarrollo y el fenotipo del tumor.
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Andræ, Johanna. "PDGF in cerebellar development and tumorigenesis." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2001. http://publications.uu.se/theses/91-554-4987-5/.

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Ball, Elizabeth Louise. "Molecular mechanisms of human thyroid tumorigenesis." Thesis, Cardiff University, 2008. http://orca.cf.ac.uk/55767/.

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Thyroid cancer is the commonest endocrine malignancy. Several of the initiating genetic events in thyroid tumorigenesis have been identified, although the exact molecular mechanisms are unclear. Our thyrocyte model has demonstrated that p16INK4A is up-regulated in RAS-induced colonies which resemble follicular adenomas. Affymetrix microarrays revealed that many interferon-stimulated genes (ISGs) are also up-regulated in these colonies. I hypothesised that p16 expression would be induced in follicular adenomas and lost in follicular cancers, consistent with their escape from growth control, and that ISG expression (HLA-DR, PKR, MxA) would be induced in follicular adenomas. I tested these hypotheses using immunohistochemistry, and correlated p16 expression with cyclin D1 and p21 expression to further investigate growth control. My original research demonstrates that p16 is expressed in adenomas, and surprisingly up-regulated in well-differentiated cancers. Loss of expression was only seen in poorly-differentiated carcinomas. Cyclin D1 expression increased during the transition from a benign to a malignant tumour, whereas p21 protein was expressed at a lower level in both adenomas and carcinomas. Unexpectedly, ISGS were not up-regulated in either the adenomas or carcinomas, but were expressed in some papillary carcinomas. PKR expression was positively correlated with p16 expression. I speculate that there must be two or more growth inhibitory pathways involved in thyroid tumorigenesis, one of which involves p16, and both must be inactivated for progression to a more aggressive phenotype. The cyclin D1 result is explained as a result of growth stimulation during tumorigenesis, whereas the basis and implication of p21 expression is uncertain. Thyroid cancers are unusual because the majority are slow-growing yet potentially fatal despite continued p16 expression. Further work is needed to elucidate the nature of the additional pathways controlling tumour growth, which will improve our understanding of thyroid tumorigenesis, and may potentially lead to the development of novel treatment strategies.
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Books on the topic "Tumorigenesis"

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Yang, Vincent W., and Agnieszka B. Bialkowska, eds. Intestinal Tumorigenesis. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-19986-3.

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Fanciulli, Maurizio. Rb and Tumorigenesis. Boston, MA: Springer US, 2006. http://dx.doi.org/10.1007/0-387-33915-9.

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K, Wong David, ed. Tumorigenesis research advances. New York: Nova Science Publishers, 2007.

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Zhang, Xiaobo, ed. Virus Infection and Tumorigenesis. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-6198-2.

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Kastan, Michael B., ed. Genetic Instability and Tumorigenesis. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60505-5.

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Dickson, Robert B., and Marc E. Lippman, eds. Mammary Tumorigenesis and Malignant Progression. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2592-9.

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Shen-Ong, Grace L. C., Michael Potter, and Neal G. Copeland, eds. Mechanisms in Myeloid Tumorigenesis 1988. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74623-9.

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Heber, David, and David Kritchevsky, eds. Dietary Fats, Lipids, Hormones, and Tumorigenesis. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1151-5.

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Domenico, Coppola. Mechanisms of oncogenesis: An update on tumorigenesis. Dordrecht: Springer, 2010.

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Shahi, Mehdi Hayat. Role of Signaling Pathways in Brain Tumorigenesis. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-15-8473-2.

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Book chapters on the topic "Tumorigenesis"

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Atkinson, Michael J., and Soile Tapio. "Tumorigenesis." In The Impact of Tumor Biology on Cancer Treatment and Multidisciplinary Strategies, 1–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-74386-6_1.

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Gala, Manish, and Daniel C. Chung. "Hereditary CRC Syndromes." In Intestinal Tumorigenesis, 1–28. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-19986-3_1.

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Nautiyal, Jyoti, Krystyn Purvis, and Adhip P. N. Majumdar. "Aging: An Etiological Factor in The Development of Intestinal Tumorigenesis." In Intestinal Tumorigenesis, 287–308. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-19986-3_10.

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Pulkoski-Gross, Ashleigh, Xi E. Zheng, Deborah Kim, Jillian Cathcart, and Jian Cao. "Epithelial to Mesenchymal Transition (EMT) and Intestinal Tumorigenesis." In Intestinal Tumorigenesis, 309–64. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-19986-3_11.

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Koyuturk, Mehmet, and Rod K. Nibbe. "Omics and Biomarkers Development for Intestinal Tumorigenesis." In Intestinal Tumorigenesis, 365–89. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-19986-3_12.

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Chiorean, E. Gabriela, Andrew Coveler, Jon Grim, and William M. Grady. "Targeted Therapies For Intestinal Tumorigenesis." In Intestinal Tumorigenesis, 391–440. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-19986-3_13.

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Prasad, Meena A., and Barbara Jung. "Microsatellite Instability and Intestinal Tumorigenesis." In Intestinal Tumorigenesis, 29–53. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-19986-3_2.

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Shroyer, Noah F., Kristin Bell, and Yuan-Hung Lo. "Biology of Intestinal Epithelial Stem Cells." In Intestinal Tumorigenesis, 55–99. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-19986-3_3.

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Harris, Jennifer W., Tianyan Gao, and B. Mark Evers. "The Role of PI3K Signaling Pathway in Intestinal Tumorigenesis." In Intestinal Tumorigenesis, 101–35. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-19986-3_4.

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Moreira, Leticia, Francesc Balaguer, and Ajay Goel. "The Epigenetics in Intestinal Tumorigenesis." In Intestinal Tumorigenesis, 137–68. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-19986-3_5.

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Conference papers on the topic "Tumorigenesis"

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Sung, Hyeran, Li Ding, Krishna L. Kanchi, Jane L. Messina, Vernon K. Sondak, Mulé J. James, Richard K. Wilson, Jeffrey S. Weber, and Minjung Kim. "Abstract 442:RASA1alteration promotes melanoma tumorigenesis." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-442.

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Ogasawara, Tatsuki, Yoichi Fujii, Nobuyuki Kakiuchi, Yusuke Shiozawa, Hiromichi Suzuki, Ryuichi Sakamoto, Yusaku Yoshida, Yuichi Shiraishi, Satoru Miyano, and Seishi Ogawa. "Abstract 3132: Tumorigenesis of MEN2 pheochromocytoma." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-3132.

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Rittling, Susan R., Brenda Bourassa, and Yanping Chen. "ROLE OF HOST OSTEOPONTIN IN TUMORIGENESIS." In 3rd International Conference on Osteopontin and SIBLING (Small Integrin-Binding Ligand, N-linked Glycoprotein) Proteins, 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.248.

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Naik, Shruti. "Abstract IA15: Inflammatory memory and tumorigenesis." In Abstracts: AACR Virtual Special Conference on Tumor Heterogeneity: From Single Cells to Clinical Impact; September 17-18, 2020. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.tumhet2020-ia15.

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Kopsiaftis, Stavros, Kathryn N. Phoenix, Katie L. Sullivan, John A. Taylor, and Kevin P. Claffey. "Abstract 4209: AMPK suppression in bladder tumorigenesis." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4209.

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Davoli, Teresa, Wei Xu, Peter Park, and Stephen J. Elledge. "Abstract SY36-03: How aneuploidy drives tumorigenesis." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-sy36-03.

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Chauhan, Subhash C., Mara C. Ebeling, Diane M. Maher, Michael D. Koch, Matthew H. Friez, Akira Watanabe, Hiroyuki Aburatani, Yuhlong Lio, Krishan K. Pandey, and Meena Jaggi. "Abstract 2358: MUC13 mucin augments pancreatic tumorigenesis." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2358.

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Chen, Lina, Sun-Mi Park, Alexei V. Tumanov, Annika Hau, Kenjiro Sawada, Christine Feig, Jerrold R. Turner, et al. "Abstract LB-341: CD95/FAS promotes tumorigenesis." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-lb-341.

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Rajurkar, Mihir, and Junhao Mao. "Abstract A91: IKBKE signaling in pancreatic tumorigenesis." In Abstracts: AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.panca2014-a91.

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Skobeltcin, A. S., A. V. Ryabova, Yu S. Maklygina, and V. B. Loschenov. "Tumorigenesis and metastasis scheme from photodynamic therapy perspective." In 2020 International Conference Laser Optics (ICLO). IEEE, 2020. http://dx.doi.org/10.1109/iclo48556.2020.9285734.

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Reports on the topic "Tumorigenesis"

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Lozano, Guillermina. Mdm2 Function in Tumorigenesis. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada384084.

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Wallace, Margaret R. Steroid Hormones in NF1 Tumorigenesis. Fort Belvoir, VA: Defense Technical Information Center, August 2005. http://dx.doi.org/10.21236/ada443895.

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Heffelfinger, Sue C. Leptin Regulation of Mammary Tumorigenesis. Fort Belvoir, VA: Defense Technical Information Center, September 2001. http://dx.doi.org/10.21236/ada402352.

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Wallace, Margaret R., David Muir, and Martha Campbell-Thompson. Steroid Hormones in NF1 Tumorigenesis. Fort Belvoir, VA: Defense Technical Information Center, August 2004. http://dx.doi.org/10.21236/ada428454.

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Wallace, Margaret R., David Muir, and Martha Campbell-Thompson. Steroid Hormones in NF1 Tumorigenesis. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada411283.

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Dickson, Robert B. TGFa-myc Interactions in Mammary Tumorigenesis. Fort Belvoir, VA: Defense Technical Information Center, September 1998. http://dx.doi.org/10.21236/ada360094.

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Dickson, Robert B. TGFa-myc Interactions in Mammary Tumorigenesis. Fort Belvoir, VA: Defense Technical Information Center, September 1997. http://dx.doi.org/10.21236/ada334931.

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Dickson, Robert B. TGFa-myc Interactions in Mammary Tumorigenesis. Fort Belvoir, VA: Defense Technical Information Center, September 1995. http://dx.doi.org/10.21236/ada301626.

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Stephens, Karen G. Genetic Factors That Affect Tumorigenesis in NF1. Fort Belvoir, VA: Defense Technical Information Center, November 2001. http://dx.doi.org/10.21236/ada400492.

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Spruck, Charles H. The Role of HCDC4 in Prostate Tumorigenesis. Fort Belvoir, VA: Defense Technical Information Center, August 2005. http://dx.doi.org/10.21236/ada447557.

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