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Relevant bibliographies by topics / Tumor Formation

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Academic literature on the topic 'Tumor Formation'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Tumor Formation"

1

Easter, Stephanie L., Elizabeth H. Mitchell, Sarah E. Baxley, Renee Desmond, Andra R. Frost, and Rosa Serra. "Wnt5a Suppresses Tumor Formation and Redirects Tumor Phenotype in MMTV-Wnt1 Tumors." PLoS ONE 9, no. 11 (November 17, 2014): e113247. http://dx.doi.org/10.1371/journal.pone.0113247.

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Riede, Isolde. "Genes in Tumor Formation." Journal of Hematology and Oncology Research 3, no. 2 (October 22, 2019): 18–22. http://dx.doi.org/10.14302/issn.2372-6601.jhor-19-2986.

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With the definition of four gene classes, all differences between tumor cells and normal cells can be explained. Proliferative mutations induce a shortcut, forcing the cell to divide. They allow replication without control, induce somatic pairing defects of chromosomes and genome instability. Intact Tumor Supressors or mutant Switch Functions can inhibit this process. Oncogene mutations optimize the growth of the cells.

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Korneva, Yulia S., and Roman V. Ukrainets. "Principles of premetastatic niche formation." Journal of Modern Oncology 21, no. 4 (May 7, 2020): 6–9. http://dx.doi.org/10.26442/18151434.2019.4.190715.

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The article is devoted to premetastatic niche as a complex term, including stromal cells, vessels, extracellular matrix and their changes during interaction with the primary tumor. On example of different malignant tumors authors describe as primary tumor through tumor exosomes prepares certain organs-recipients to metastatic clone implantation. In the area of premetastatic niche under the influence of tumorous exosomes polarization of macrophages towards M2 type takes place. The cells are the main agents, providing survival as well as migration of tumorous cells. Affecting extracellular matrix, macrophages change the microcirculatory bed permeability. This mechanism is directed towards increase of its permeability to entrance of metastatic clone cells form vessels into premetastatic niche. Besides macrophages fibroblasts and polypotent bone marrow stem cells are also reprogrammed, that results in metabolism and local immunity changes at the place of future implantation. As a result, only when tissue of recipient-organ is prepared for contact with metastatic clone, their interaction take place with consequent formation of secondary tumor metastatic niche. Thus, this review describes pathogenesis of metastasis, different from its early understanding as spread of metastatic clone with lymph and blood. These peculiarities may in future have significant impact in practical medicine, Blockage of signal spread from primary tumor through exosomes is one of the promising directions in pathogenetic therapy of malignant tumors. Investigation of principles of premetastatic niche formation may become a theoretical substantiation for prophylaxis of metastatic disease and inhibition of micrometastasis to macrometastasis transformation.

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Baggenstos, Martin A., John A. Butman, Edward H. Oldfield, and Russell R. Lonser. "Role of edema in peritumoral cyst formation." Neurosurgical Focus 22, no. 5 (May 2007): 1–7. http://dx.doi.org/10.3171/foc.2007.22.5.10.

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✓Peritumoral cysts (those arising immediately adjacent to the tumor mass) are frequently associated with benign and malignant tumors of the brain and spinal cord (syringomyelia). The cystic component of central nervous system (CNS) tumors and associated peritumoral cysts are often the cause of clinical symptoms. Because of the common occurrence of peritumoral cysts with CNS neoplasms and the morbidity associated with them, advanced imaging, histological, and molecular techniques have been used to determine the mechanism underlying cyst formation and propagation. Based on evidence from such studies, edema appears to be a common precursor to peritumoral cyst formation in the CNS. Mediators of vascular permeability acting locally in the tumor and/or hydrodynamic forces within abnormal tumor vascula-ture appear to drive fluid extravasation. When these forces overcome the ability of surrounding tissue to resorb fluid, edema and subsequent cyst formation occur. These findings support the concept that the tumor itself is the source of the edema that precedes cyst formation and that resection of tumors or medical therapies directed at decreasing their vascular permeability will result in the resolution of edema and cysts.

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Mamedova, S. M., M. A. Qarashova, E. M. Aliyeva, and S. Q. Sultanova. "The condition of the hypothalamic-pituitary-adrenal-ovarian system in women with tumors and tumoral formations of the organs of the reproductive system in the postmenopausal period." HEALTH OF WOMAN, no. 7(133) (September 30, 2018): 96–99. http://dx.doi.org/10.15574/hw.2018.133.96.

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The objective: of the study was to study the state of the hypothalamic-pituitary-adrenal-ovarian system in women with benign preinvasive and tumor-like formations of the reproductive system organs in the postmenopausal period. Materials and methods. 130 women with various tumors and tumoral formations of reproductive system organs in the postmenopausal period were examined. The parameters of follicle stimulating, luteinizing hormones, estradiol, estrone, prolactin, progesterone, testosterone, dehydroepiandosterone sulfate were studied. Results. It was established that out of 130 women with various tumors and tumoral formations of the organs of the reproductive system in the postmenopausal period, uterine myoma was defined in 39 (39%), endometrial hyperplasia in 23 (17.7%), tumor-like formation of ovaries in 17 (13.1%). It was found that in the postmenopausal period, the presence of hyperandrogenia, hyperprolactinemia, and a significant increase in the level of estrone were noted in women with benign, preinvasive and tumor-like formations of the organs of the reproductive system, regardless of tumor origin. Conclusion. The obtained results allowed to conclude that in the postmenopausal period the presence of uterine fibroids, endometrial hyperplasia and ovarian tumor formation is accompanied by hyperprolactinemia, hyperandrogenism and hyperestrogenism due to an increase in estrone level. Key words: postmenopausal period, uterine myoma, endometrial hyperplasia, tumor-like formations, hyperandrogenia, hyperprolactinaemia, estrone.

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Samara, Ghassan, Michael Hurwitz, Mark Sawicki, and Edward Passaro. "Molecular mechanisms of tumor formation." American Journal of Surgery 164, no. 4 (October 1992): 389–96. http://dx.doi.org/10.1016/s0002-9610(05)80911-0.

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Vinnitsky, V. B. "Oncogerminative hypothesis of tumor formation." Medical Hypotheses 40, no. 1 (January 1993): 19–27. http://dx.doi.org/10.1016/0306-9877(93)90191-r.

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Lee, Thomas C., and Shizuo Mukai. "Molecular Events in Tumor Formation." International Ophthalmology Clinics 37, no. 4 (1997): 215–32. http://dx.doi.org/10.1097/00004397-199703740-00018.

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Purkayastha, Sudarshana, Alexandra Berliner, Suraj Shawn Fernando, Buddima Ranasinghe, Indrani Ray, Hussnain Tariq, and Probal Banerjee. "Curcumin blocks brain tumor formation." Brain Research 1266 (April 2009): 130–38. http://dx.doi.org/10.1016/j.brainres.2009.01.066.

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Xu, Daozhi, Peixin Dong, Ying Xiong, Junming Yue, Kei Ihira, Yosuke Konno, Noriko Kobayashi, Yukiharu Todo, and Hidemichi Watari. "MicroRNA-361: A Multifaceted Player Regulating Tumor Aggressiveness and Tumor Microenvironment Formation." Cancers 11, no. 8 (August 7, 2019): 1130. http://dx.doi.org/10.3390/cancers11081130.

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MicroRNA-361-5p (miR-361) expression frequently decreases or is lost in different types of cancers, and contributes to tumor suppression by repressing the expression of its target genes implicated in tumor growth, epithelial-to-mesenchymal transition (EMT), metastasis, drug resistance, glycolysis, angiogenesis, and inflammation. Here, we review the expression pattern of miR-361 in human tumors, describe the mechanisms responsible for its dysregulation, and discuss how miR-361 modulates the aggressive properties of tumor cells and alter the tumor microenvironment by acting as a novel tumor suppressor. Furthermore, we describe its potentials as a promising diagnostic or prognostic biomarker for cancers and a promising target for therapeutic development.

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Dissertations / Theses on the topic "Tumor Formation"

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Liu, Dan. "The role of senescent fibroblasts in tumor formation : a dissertation /." San Antonio : UTHSC, 2006. http://proquest.umi.com/pqdweb?did=1257790121&sid=1&Fmt=2&clientId=70986&RQT=309&VName=PQD.

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Rangwala, Fatima. "Ras signalling in Schwann cell tumor formation neurofibromatosis type 1 /." Cincinnati, Ohio : University of Cincinnati, 2003. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=ucin1069774794.

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Ortiz, Myrna Lillian. "Immature Myeloid Cells Promote Tumor Formation Via Non-Suppressive Mechanism." Scholar Commons, 2014. https://scholarcommons.usf.edu/etd/5089.

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ABSTRACT Although there is ample evidence linking chronic inflammation with cancer, the cellular mechanisms involved in early events leading to tumor development remain unclear. Myeloid cells are an intricate part of inflammation. They consist of mature cells represented by macrophages, dendritic cells and granulocytes and a population of Immature Myeloid Cells (IMC), which in healthy individuals are cells in transition to mature cells. There is a substantial expansion of IMC in cancer and many other pathological conditions which is associated with pathologic activation of these cells. As a result, these cells acquire the ability to suppress immune responses and are termed Myeloid-derived Suppressor Cells (MDSCs). Although the role of MDSC in immune suppression in cancer and tumor progression is well established, their contribution to tumor development is still uncertain. The fact that cells with MDSC phenotype and function are observed in chronic inflammation raised the possibility that these cells can contribute to initial stages of tumor development. To address this question, we used an experimental system where the number of IMC was regulated by the expression of S100A9 protein. In this project, we used two different models of chronic inflammation in S100A9 transgenic (S100A9tg) and S100A9 knock-out (S100A9KO) mice. In the first model, we created the conditions for topical accumulation of these cells in the skin in the absence of infection or tissue damage using S100A9tg mice. Accumulation of IMC in the skin resulted in a dramatic increase in the formation of skin tumors during epidermal carcinogenesis. Conversely, lack of myeloid cell accumulation in S100A9KO mice substantially reduced the formation of skin papillomas. The effect of IMC was not associated with immune suppression but with the recruitment of CD4+ T cells mediated by CCL4 chemokine released by activated IMC. Elimination of CD4+ T cells or blockade of CCL4 abrogated the increase in tumor formation caused by myeloid cells. Thus, this study implicates the accumulation of IMC as an initial step in facilitating of tumor formation, which can mediate the recruitment of CD4+ T cells via the release of CCL4 chemokine. In the second model, we used inflammation-associated lung cancer caused by the chemical lung carcinogen urethane in combination with exposure to cigarette smoke referred to throughout as CS. Exposure of mice to CS alone resulted in a significant accumulation of cells with typical MDSC phenotype in different organs; however, these cells lacked immune suppressive activity and could not be defined as bona fide MDSC. When CS was combined with the single dose of urethane, it led to the accumulation of immune suppressive cells. The expansion of MDSC followed the onset of lung tumors development. This suggests that MDSC in this model is not the preceding factor but rather a consequence of tumor formation. Further studies are necessary to determine the relevance of targeting these cells for cancer treatment and prevention.

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RANGWALA, FATIMA ABDULLA. "RAS SIGNALING IN SCHWANN CELL TUMOR FORMATION: NEUROFIBROMATOSIS TYPE 1." University of Cincinnati / OhioLINK, 2003. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1069774794.

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Saelzler, Matthew P. (Matthew Paul). "The recruitment of stromal cells to the site of tumor formation." Thesis, Massachusetts Institute of Technology, 2009. http://hdl.handle.net/1721.1/57520.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, February 2010.
This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Cataloged from student submitted PDF version of thesis. Vita.
Includes bibliographical references.
Myofibroblasts are an alpha-smooth muscle actin ([alpha]-SMA)-expressing cell type found within human mammary carcinomas, but not in the normal mammary gland. Myofibroblasts can enhance tumor formation by promoting angiogenesis and invasion, and we therefore sought to better understand how myofibroblasts are incorporated into breast carcinomas. By identifying secreted factors that recruit myofibroblasts as well as the physical niche where they originated, we aimed to identify possible therapeutic targets to inhibit their incorporation. Using a newly developed mammary carcinoma model, termed BPLER, we identified CXCL1, VEGF, CCL5, and IL-6 as factors that may be important for the recruitment of myofibroblasts. We tested the ability of CXCL1, VEGF164, or CCL5 to affect tumor formation and induce the incorporation of a-SMApositive cells. We show that the expression in MCF-7-Ras modified human breast cancer cells of VEGF164, but not CXCL1 or CCL5, results in the promotion of primary tumor growth and the increased incorporation of [alpha]-SMA-positive cells. Furthermore, we demonstrate that these a-SMA-positive cells do not correlate with cells expressing CD34, a marker of endothelial cells, suggesting that these cells are not [alpha]-SMA-positive smooth muscle cells. Thus, we propose that VEGF is a critical factor that recruits myofibroblasts to the site of breast cancer formation. In another line of experiments, we examined the source of the [alpha]-SMA-positive cell population recruited to another mammary tumor model, termed BPHER-3.
(cont.) In order to investigate whether these cells are derived from the bone marrow, we utilized chimeric mice that express green fluorescent protein (GFP) in their bone marrow and blood cells in order to look for incorporation of GFP-labeled cells within the stroma of a subcutaneously grown tumor. We demonstrated that green bone marrow-derived cells are robustly recruited to the site of BPHER-3 tumor formation; however strikingly, almost 100% of the [alpha]-SMA positive cells analyzed were GFP negative. Our results demonstrate that the [alpha]-SMA-positive cell population recruited to BPHER-3 tumors is not bone marrow-derived, but is instead recruited from the adjacent tissue microenvironment.
by Matthew P. Saelzler.
Ph.D.

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Appleman, Victoria A. "Mechanisms of KRAS-Mediated Pancreatic Tumor Formation and Progression: A Dissertation." eScholarship@UMMS, 2012. https://escholarship.umassmed.edu/gsbs_diss/600.

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Pancreatic cancer is the 4th leading cause of cancer related death in the United States with a median survival time of less than 6 months. Pancreatic ductal adenocarcinoma (PDAC) accounts for greater than 85% of all pancreatic cancers, and is marked by early and frequent mutation of the KRAS oncogene, with activating KRAS mutations present in over 90% of PDAC. To date, though, targeting activated KRAS for cancer treatment has been very difficult, and targeted therapies are currently being sought for the downstream effectors of activated KRAS. Activation of KRAS stimulates multiple signaling pathways, including the MEK-ERK and PI3K-AKT signaling cascades, but the role of downstream effectors in pancreatic tumor initiation and progression remains unclear. I therefore used primary pancreatic ductal epithelial cells (PDECs), the putative cell of origin for PDAC, to determine the role of specific downstream signaling pathways in KRAS activated pancreatic tumor initiation. As one third of KRAS wild type PDACs harbor activating mutations in BRAF , and KRAS and BRAF mutations appear to be mutually exclusive, I also sought to determine the effect of activated BRAF (BRAF V600E ) expression on PDECs and the signaling requirements downstream of BRAF. I found that both KRAS G12D and BRAF V600E expressing PDECs displayed increased proliferation relative to GFP expressing controls, as well as increased PDEC survival after challenge with apoptotic stimuli. This survival was found to depend on both the MEK-ERK and PI3K-AKT signaling cascades. Surprisingly, I found that this survival is also dependent on the IGF1R, and that activation of PI3K/AKT signaling occurs downstream of MEK/ERK activation, and is dependent on signaling through the IGF1R. Consistent with this, I find increased IGF2 expression in KRAS G12D and BRAF V600E expressing PDECs, and show that ectopic expression of IGF2 rescues survival in PDECs with inhibited MEK, but not PI3K. Finally, I showed that the expression of KRAS G12D or BRAF V600E in PDECs lacking both the Ink4a/Arf and Trp53 tumor suppressors is sufficient for tumor formation following orthotopic transplant of PDECs, and that IGF1R knockdown impairs KRAS and BRAF-induced tumor formation in this model. In addition to these findings within PDECs, I demonstrate that KRAS G12D or BRAF V600E expressing tumor cell lines differ in MEK-ERK and PI3K-AKT signaling from PDECs. In contrast to KRAS G12D or BRAF V600E expressing PDECs, activation of AKT at serine 473 in the KRAS G12D or BRAF V600E expressing tumor cell lines does not lie downstream of MEK, and only the inhibition of PI3K alone or both MEK and the IGF1R simultaneously results in loss of tumor cell line survival. However, inhibition of MEK, PI3K, or the IGF1R in KRAS G12D or BRAF V600E expressing tumor cell lines also resulted in decreased proliferation relative to DMSO treated cells, demonstrating that all three signaling cascades remain important for tumor cell growth and are therefore viable options for pancreatic cancer therapeutics.

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Lähdesmäki, Aleksi. "Functional analysis of ATM with relevance for primary immunodeficiency and tumor formation /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-900-5/.

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Ueo, Taro. "The role of Hes genes in intestinal development, homeostasis and tumor formation." Kyoto University, 2012. http://hdl.handle.net/2433/158055.

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Branschädel, Marcus. "Analysis of molecular components essential for the formation of signaling competent TNF-TNFR complexes." [S.l. : s.n.], 2007. http://nbn-resolving.de/urn:nbn:de:bsz:93-opus-32358.

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Persa, Oana-Diana [Verfasser]. "The role of aPKC polarity in migration and tumor formation / Oana-Diana Persa." Köln : Deutsche Zentralbibliothek für Medizin, 2014. http://d-nb.info/1061094715/34.

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Books on the topic "Tumor Formation"

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Yosef, Shiloh, and SpringerLink (Online service), eds. The DNA Damage Response: Implications on Cancer Formation and Treatment. Dordrecht: Springer Netherlands, 2009.

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Gogichadze, G. K. Karyogamic theory of cancer cell formation from the view of the XXI century. Hauppauge, N.Y: Nova Science Publishers, 2009.

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T, Gogichadze, ed. Karyogamic theory of cancer cell formation from the view of the XXI century. New York: Nova Biomedical Books, 2010.

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Vásquez Rodríguez, Fernando, ed. La tutoría de la investigación. Bogotá. Colombia: Universidad de La Salle. Ediciones Unisalle, 2019. http://dx.doi.org/10.19052/9789585486331.

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Esta obra es de gran utilidad para los noveles tutores, quienes, en la mayoría de los casos, comienzan su labor apenas con los referentes de un profesor que los acompañó en su trabajo de grado, pero sin contar con una fuente de consulta en la que logren profundizar o capacitarse en este nuevo rol. A lo largo de las páginas de este texto se podrán apreciar y distinguir las características, los alcances, las dificultades y el itinerario formativo de un tutor; una labor académica que empieza en las vicisitudes de la conformación de un equipo de investigación, pasando por las extensas jornadas de diálogo, revisión y señalamiento de compromisos, hasta llegar a la supervisión formal y de contenido del trabajo final.

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Reader, Jocelyn, Sarah Lynam, Amy Harper, Gautam Rao, Maya Matheny, and Dana M. Roque. Ovarian Tumor Microenvironment and Innate Immune Recognition. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0004.

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Ovarian adenocarcinoma is typified by detection at late stages with dissemination of cancer cells into the peritoneal cavity and frequent acquisition of chemoresistance. A number of studies show the importance of the tumor microenvironment and innate immune recognition in tumor progression. Ovarian cancer cells can regulate the composition of their stroma to promote the formation of ascitic fluid rich in cytokines and bioactive lipids such as PGE2, and to stimulate the differentiation of stromal cells into a pro-tumoral phenotype. In response, cancer-associated fibroblasts, cancer-associated mesenchymal stem cells, tumor-associated macrophages, and other peritoneal cells can act through direct and indirect mechanisms to regulate tumor growth, chemoresistance via alteration of class III β‎ tubulin, angiogenesis and dissemination. This chapter deciphers the current knowledge about the role of stromal cells, associated secreted factors, and the immune system on tumor progression. This suggests that targeting the microenvironment holds great potential to improve the prognosis of patients with ovarian adenocarcinoma.

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Hatef, Jeffrey, and Russell R. Lonser. Hemangioblastoma. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190696696.003.0007.

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Hemangioblastomas are benign central nervous system tumors that are found primarily (99%) in the cerebellum, brainstem, and spinal cord. They can occur sporadically (67% of cases) or in the context of the familial neoplasia syndrome, von Hippel-Lindau disease (VHL; 33%). These lesions often remain quiescent or grow in a saltatory pattern. When these tumors cause signs or symptoms, the signs or symptoms are often associated with peritumoral cyst formation. Whether the tumor occurs sporadically or in the context of VHL, complete resection is the treatment of choice when necessary. This chapter describes the clinical, imaging, and treatment features of this neoplasm.

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Malyshev, Igor. Immunity, Tumors and Aging : The Role of HSP70: The Role of HSP70. Springer, 2013.

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Jordan, Nerissa. Non-metastatic neurological manifestations of malignancy. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0238.

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Neurological complications of systemic malignancy are frequent. They may reflect direct local effects of the tumour; CNS infection; side effects of chemotherapy or radiotherapy; nutritional or metabolic derangements; or a paraneoplastic syndrome. The paraneoplastic neurological syndromes are a group of disorders associated with a malignancy outside the nervous system. The pathophysiology is immune-mediated, with the tumour’s expression of neuronal proteins invoking antibody formation, which in turn results in neurological symptoms. This chapter will mainly focus on these syndromes.

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(Editor), James H. Finke, and Ronald M. Bukowski (Editor), eds. Cancer Immunotherapy at the Crossroads: How Tumors Evade Immunity and What Can Be Done (Current Clinical Oncology). Humana Press, 2003.

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Zhang, Quan. Temperature modulated aflatoxin B1 hepatic disposition, and formation and persistence of DNA adducts in rainbow trout. 1992.

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Book chapters on the topic "Tumor Formation"

1

de Almodovar, Carmen Ruiz, Serena Zacchigna, Monica Autiero, and Peter Carmeliet. "Guidance of Vascular and Neuronal Network Formation." In Tumor Angiogenesis, 47–65. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-33177-3_3.

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Deutsch, Andreas, and Sabine Dormann. "Tumor Growth and Invasion." In Cellular Automaton Modeling of Biological Pattern Formation, 257–92. Boston, MA: Birkhäuser Boston, 2017. http://dx.doi.org/10.1007/978-1-4899-7980-3_12.

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Sager, R., S. Sheng, P. Pemberton, and M. J. C. Hendrix. "Maspin: A Tumor Suppressing Serpin." In Attempts to Understand Metastasis Formation I, 51–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-61107-0_4.

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Nicolson, Garth L. "Cell Surfaces and Secondary Tumor Formation." In Influence of Tumor Development on the Host, 84–96. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-2528-1_9.

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Schirrmacher, V. "Cell Biology of Tumor Metastasis Formation." In Breast Diseases, 62–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-73523-3_7.

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Vignaud, Jean-Michel, Béatrice Marie, Evelyne Picard, Karim Nabil, Jöelle Siat, Francoise Galateau-Salle, Jacques Borrelly, Yves Martinet, and Nadine Martinet. "Tumor Stroma Formation in Lung Cancer." In Clinical and Biological Basis of Lung Cancer Prevention, 75–93. Basel: Birkhäuser Basel, 1998. http://dx.doi.org/10.1007/978-3-0348-8924-7_7.

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Johnson, J. P., M. M. Rummel, U. Rothbächer, and C. Sers. "MUC18: A Cell Adhesion Molecule with a Potential Role in Tumor Growth and Tumor Cell Dissemination." In Attempts to Understand Metastasis Formation I, 95–105. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-61107-0_7.

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Seiki, M. "Membrane Type-Matrix Metalloproteinase and Tumor Invasion." In Attempts to Understand Metastasis Formation I, 23–30. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-61107-0_2.

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Mescher, Melina, and Sandra Iden. "Par Proteins in Tumor Formation and Progression." In Cell Polarity 2, 145–65. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-14466-5_6.

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Powell, W. C., and L. M. Matrisian. "Complex Roles of Matrix Metalloproteinases in Tumor Progression." In Attempts to Understand Metastasis Formation I, 1–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-61107-0_1.

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Conference papers on the topic "Tumor Formation"

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Li, Hua, Hongyun Li, Eliza Raymundo, Rajesh Thangapazham, Taduru Sreenath, Albert Dobi, and Shiv Srivastava. "Abstract 4920: Effects ofPMEPA1in prostate tumor cell growth and tumor formation." 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.am10-4920.

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Moore, Lakisha D., Tatyana Isayeva, Jessica Gurley, and Selvarangan Ponnazhagan. "Abstract 541: TGF-β signaling in the tumor microenvironment promotes tumor formation and tumor progression." 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.am10-541.

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Hye-Jin Jin, Taeyoon Kim, Young-Ho Cho, Jin-Mo Gu, Jhingook Kim, and Yong-Soo Oh. "A multicellular tumor spheroid formation and extraction chip." In 2010 IEEE 10th Conference on Nanotechnology (IEEE-NANO). IEEE, 2010. http://dx.doi.org/10.1109/nano.2010.5697838.

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Eckert, Mark A., Thinzar M. Lwin, Andrew T. Chang, Jihoon Kim, Etienne Danis, Lucila Ohno-Machado, and Jing Yang. "Abstract 4747: Twist1-induced invadopodia formation promotes tumor metastasis." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4747.

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Rhim, Andrew D., Nicole M. Aiello, Emily T. Mirek, and Ben Z. Stanger. "Abstract IA5: EMT and dissemination precede pancreatic tumor formation." In Abstracts: AACR Special Conference on Pancreatic Cancer: Progress and Challenges; June 18-21, 2012; Lake Tahoe, NV. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.panca2012-ia5.

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Juratli, Mazen A., Ekaterina I. Galanzha, Mustafa Sarimollaoglu, Dmitry A. Nedosekin, James Y. Suen, and Vladimir P. Zharov. "Photoacoustic monitoring of clot formation during surgery and tumor surgery." In SPIE BiOS, edited by Alexander A. Oraevsky and Lihong V. Wang. SPIE, 2013. http://dx.doi.org/10.1117/12.2008035.

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Kang, Jin Muk, Sujin Park, Staci Jakyong Kim, and Seong-Jin Kim. "Abstract 25: CBL enhances breast tumor formation by inhibiting tumor suppressive activity of TGF-beta signaling." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-25.

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Eder, Noreen, Marie-Charlotte Dolmart, Suzanne Claxton, Jennifer Cotton, Jun-Hao Mao, Bram Snijders, Federico Roncaroli, Barry Thompson, and Sila Ultanir. "Abstract A01: YAP1 drives ependymoma-like tumor formation in the brain." In Abstracts: AACR Special Conference on the Hippo Pathway: Signaling, Cancer, and Beyond; May 8-11, 2019; San Diego, CA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3125.hippo19-a01.

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Jones, Dennis, Han-Sin Jeong, Shan Liao, Daniel A. Wattson, Cheryl H. Cui, Dan G. Duda, Christopher G. Willett, Rakesh K. Jain, and Timothy P. Padera. "Abstract B03: Formation of lymph node metastases is not angiogenesis dependent." In Abstracts: AACR Special Conference on Tumor Metastasis; November 30-December 3, 2015; Austin, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.tummet15-b03.

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Dominguez-Gutierrez, Paul R., Paul Crispen, and Sergei A. Kusmartsev. "Abstract 1521: Tumor-produced hyaluronan contributes to the formation tolerogenic immunosuppressive microenvironment." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1521.

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Reports on the topic "Tumor Formation"

1

Wellberg, Elizabeth. Regulation of Mammary Tumor Formation and Lipid Biosynthesis by Spot14. Fort Belvoir, VA: Defense Technical Information Center, October 2011. http://dx.doi.org/10.21236/ada555801.

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Wellberg, Elizabeth. Regulation of Mammary Tumor Formation and Lipid Biosynthesis by Spot 14. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada590676.

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Kim, Yongbaek. Participation of Bone Marrow-Derived Cells in the Formation of Tumor-Associated Stroma During Lung Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2011. http://dx.doi.org/10.21236/ada552887.

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Belches, Allison P., and Sarah J. Parsons. Investigations of Functional and Structural Interactions Between c-src and HER2: Involvement in Human Breast Tumor Formation. Fort Belvoir, VA: Defense Technical Information Center, July 1999. http://dx.doi.org/10.21236/ada382883.

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