Gotowe bibliografie tematyczne / Malignant Cells - Molecular Characetrization

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Gotowa bibliografia na temat „Malignant Cells - Molecular Characetrization”

Autor: Grafiati

Data publikacji: 7 września 2023

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Artykuły w czasopismach na temat "Malignant Cells - Molecular Characetrization"

Fredholm, Simon, Andreas Willerslev-Olsen, Özcan Met, Linda Kubat, Maria Gluud, Sarah L. Mathiasen, Christina Friese i in. "SATB1 in Malignant T Cells". Journal of Investigative Dermatology 138, nr 8 (sierpień 2018): 1805–15. http://dx.doi.org/10.1016/j.jid.2018.03.1526.

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Miller, W. H. "Molecular Targets of Arsenic Trioxide in Malignant Cells". Oncologist 7, nr 90001 (1.04.2002): 14–19. http://dx.doi.org/10.1634/theoncologist.7-2004-14.

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Miller, Wilson H. "Molecular Targets of Arsenic Trioxide in Malignant Cells". Oncologist 7, S1 (kwiecień 2002): 14–19. http://dx.doi.org/10.1634/theoncologist.7-suppl_1-14.

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Suzme, R., J.-C. Tseng, B. Levin, S. Ibrahim, D. Meruelo i A. Pellicer. "Sindbis viral vectors target hematopoietic malignant cells". Cancer Gene Therapy 19, nr 11 (7.09.2012): 757–66. http://dx.doi.org/10.1038/cgt.2012.56.

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BALIS, M. EARL. "Adenosine Deaminase and Malignant Cells". Annals of the New York Academy of Sciences 451, nr 1 (październik 1985): 142–49. http://dx.doi.org/10.1111/j.1749-6632.1985.tb27105.x.

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Cairo, Gaetano, Paolo Vezzoni, Lidia Bardella, Luisa Schiaffonati, Emilia Rappocciolo, Sonia Levi, Paolo Arosio i Aldo Bernelli-Zazzera. "Regulation of ferritin synthesis in malignant and non-malignant lymphoid cells". Biochemical and Biophysical Research Communications 139, nr 2 (wrzesień 1986): 652–57. http://dx.doi.org/10.1016/s0006-291x(86)80040-7.

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Postovit, Lynne-Marie, Elisabeth A. Seftor, Richard EB Seftor i Mary JC Hendrix. "Targeting Nodal in malignant melanoma cells". Expert Opinion on Therapeutic Targets 11, nr 4 (20.03.2007): 497–505. http://dx.doi.org/10.1517/14728222.11.4.497.

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Cheng, Sun-Long, Rosa Huang-Liu, Jin-Nan Sheu, Shui-Tein Chen, Supachok Sinchaikul i Gregory J. Tsay. "Toxicogenomics of A375 human malignant melanoma cells". Pharmacogenomics 8, nr 8 (sierpień 2007): 1017–36. http://dx.doi.org/10.2217/14622416.8.8.1017.

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Katsoulidis, Efstratios, Surinder Kaur i Leonidas C. Platanias. "Deregulation of Interferon Signaling in Malignant Cells". Pharmaceuticals 3, nr 2 (4.02.2010): 406–18. http://dx.doi.org/10.3390/ph3020406.

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Too, Catherine K. L., Christine Lee, Shirley M. Sangster i Peter W. Gout. "Malignant Progression of Rat Nb2 Lymphoma Cells". Cancer Genetics and Cytogenetics 110, nr 2 (kwiecień 1999): 115–23. http://dx.doi.org/10.1016/s0165-4608(98)00191-5.

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Rozprawy doktorskie na temat "Malignant Cells - Molecular Characetrization"

Endaya, Berwini B. "Detecting Proliferating Tumor Cells for their Molecular Characterisation". Thesis, Griffith University, 2016. http://hdl.handle.net/10072/367491.

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Uncontrolled proliferation is a fundamental trait that defines all malignant neoplasms. The acquisition of such ability for unrestrained growth is governed by mechanisms encompassing a multitude of complementary molecular events that include somatic mutations, epigenetic alterations, and constant phenotypic changes driven by the ever changing tumour microenvironment. In time, while going through the evolutionary process of tumourigenesis, tumours acquire and adapt unique sets of these molecular events driving proliferation and growth. As a result, a multitude of growth pathways, each unique in its molecular makeup, yet similar in conferring unlimited proliferative capacity can potentially arise. A major challenge therefore is to establish a way to pinpoint the specific molecular alterations actively driving proliferation and tumour growth. In this study, we design a method that has the ability to detect and isolate the proliferating tumour cells for their molecular characterisation.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
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Au, Wing-yan. "Pathogenesis and progression of malignant B cell neoplasms /". View the Table of Contents & Abstract, 2005. http://sunzi.lib.hku.hk/hkuto/record/B31540892.

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Joseloff, Elizabeth 1969. "AP-1 regulation during malignant progression of mouse keratinocyte cells". Diss., The University of Arizona, 1997. http://hdl.handle.net/10150/282562.

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The mouse skin model that has been used to study skin carcinogenesis can be divided into three stages: initiation, promotion, and progression. One genetic change observed during tumor promotion and malignant progression is increased transactivation of the transcription factor AP-1. AP-1 consists of Jun (c-Jun, Jun B, Jun D) and Fos (c-Fos, Fos B, Fra-1, Fra-2) proteins that form Jun:Jun homodimers or Jun:Fos heterodimers. AP-1 binds to a consensus cis-promoter element, the TRE, and transcriptionally regulate a number of genes with various biological functions. By studying the benign mouse keratinocyte cells, 308, and its malignant variant, 10Gy5, it has been shown that 10Gy5 cells have elevated AP-1 activity compared to 308 cells. Reduced AP-1 transactivation in 10Gy5 cells has been correlated with suppression of its malignant phenotype. This research examined the differential AP-1 transactivation in benign 308 and malignant 10Gy5 cells. By examing mechanisms of AP-1 regulation in the two cell lines, differences were observed with post-translational modifications of AP-1. There were differences in phosphorylation of one of the AP-1 family members, Jun B. In addition, AP-1 proteins in 10Gy5 cells appear to be in a fully reduced state, unlike AP-1 proteins in 308 cells. A third difference that was observed was in Jun B steady state protein levels, with decreased Jun B protein in malignant 10Gy5 compared to benign 308 cells. Reduced Jun B protein in 10Gy5 cells was the result of decreased Jun B protein synthesis. Jun B protein may inhibit AP-1 transactivation and cell proliferation. Experiments were performed to determine whether Jun B protein could modulate AP-1 transactivation, cell growth, and tumor formation in 308 and 10Gy5 cells. Altering Jun B protein levels in these keratinocytes affected AP-1 transactivation. Overexpression of Jun B protein in malignant 10Gy5 cells corresponded to an inhibition of cell growth and tumor development. However, overexpression of Jun B protein in 10Gy5 cells was not sufficient to reverse the malignancy, indicating that additional genetic changes are involved in malignant conversion of these keratinocytes. The results of this research suggest that Jun B protein levels may be important during malignant progression of mouse skin.

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Kårehed, Karin. "Signal Transduction in Malignant Cells – Transformation, Activation and Differentiation". Doctoral thesis, Uppsala University, Department of Genetics and Pathology, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-6346.

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All aspects of cell life are regulated by signal transduction mechanisms. This thesis describes the regulatory roles of a few key signal transduction molecules involved in three major biological responses. The studied pathways include platelet derived growth factor (PDGF)-BB induced transformation of murine fibroblasts, interferon (IFN)-γ stimulated monocyte activation and all-trans retinoic acid (ATRA) induced myeloid differentiation.

We found that intact phosphoinositide 3OH-kinase (PI3K) activity is essential in the signaling pathway that leads to the morphological alterations and migration pattern characteristic of PDGF-BB transformed NIH/sis and NIH/COL1A1 fibroblasts. Furthermore, our data indicated that the small Rho-GTPase, Rac1 is the predominant mediator of these signals downstream of PI3K.

The study of the IFN-γ induced activation of monocytic U-937 cells showed that upregulation of the high affinity receptor for IgG (FcγRI) is dependent on the coordination of several regulatory events: the PKR-mediated serine 727 phosphorylation of Stat1, the expression of the hematopoietic lineage specific transcription factor PU.I, and the activation of the NFκB pathway.

ATRA-induced differentiation and cell cycle arrest are impaired in U-937 sublines expressing phosphorylation deficient Stat1 (Stat1Y701F and Stat1S727A). The findings in paper III indicated that the expression pattern of the myeloid specific transcription factors Stat2, ICSBP and c/EBPε was altered in the sublines and that intact Stat1 activation is critical for maintaining the balance of the transcriptional network during ATRA induced terminal differentiation.

Finally, ATRA-induced differentiation and growth arrest were blocked by treatment with the IKKα/β inhibitor BMS345541 or by ectopic expression of the NFκB super repressor IκBα (S32A/S36A). The fact that IκB(AA) sublines differentiated normally in response to vitamin D3, showed that NFκB inhibition specifically affected ATRA induced responses. Notably we suggest that the activity of the NFκB pathway may interfere with the differentiation process via a direct effect on the RAR/RXR mediated transcription.

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Bouralexis, Stelios. "Molecular mechanisms of Apo2L/TRAIL induced apoptosis in normal and malignant cells /". Title page, contents and synopsis only, 2003. http://web4.library.adelaide.edu.au/theses/09PH/09phb766.pdf.

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Au, Wing-yan, i 區永仁. "Pathogenesis and progression of malignant B cell neoplasms". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B45007676.

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Solomon, Cynthia 1974. "Mechanisms of 1,25-dihydroxyvitamin D resistance in tumor cells as they progress from the normal to the malignant phenotype". Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=36710.

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Human retinoid X receptor alpha (hRXRalpha) plays a critical role in DNA binding and transcriptional activity through its heterodimeric association with several members of the nuclear receptor superfamily, including the vitamin D receptor (VDR). Several cancer cell lines derived from many tissues have been shown to be resistant to the growth inhibitory action of 1,25-dihydroxyvitamin D3, (1,25(OH)2D3), the biologically active metabolite of vitamin D3. In the malignant ras-transformed human keratinocyte cell line, HPK1Aras, 10--100 fold higher concentrations of 1,25(OH)2D3 are required than the non-malignant normal human epidermal keratinocytes to achieve comparable inhibition of cell growth. Here we show that in ras-transformed keratinocytes, ser260 of hRXRalpha is phosphorylated through the Ras-Raf-MAP kinase cascade. This phosphorylation event results in the inhibition of vitamin D signaling via VDR/hRXRalpha heterodimers. Strategies to reverse this resistance include the use of the MAP kinase inhibitor, PD098059, and a non-phosphorylatable hRXRalpha mutant, ala260, which completely abolishes RXR phosphorylation and restores the function of both 1,25(OH)2D3 and a specific RXR ligand, LG1069 (4-[1-(5,6,7,8-tetrahydro-3,5,5,8,8-pentamethyl-2-naphtalenyl)ethenyl]-benzoic acid). In addition, we show that a vitamin D analog with low calcemic activity (EB1089) is more potent than 1,25(OH)2D3 in inhibiting cancer cell growth in this system. Targeted therapy with selective analogs such as EB1089, in combination with the inhibition of phosphorylation of the RXR, could play a critical role in the therapeutic strategies of cancer biology. In addition, we also demonstrate that resistance to 1,25(OH)2D 3 can be acquired through genetic alterations in the VDR, implying that both components of the VDR/RXR heterodimer are potential targets for the induction of cellular resistance to 1,25(OH)2D3 and present two distinct mechanisms through which tumour cells can escape the growt

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Corradi, Giulia <1990&gt. "Molecular and functional characterization of the interplay between malignant and stromal cells in acute myeloid leukemia and myelodysplastic syndrome". Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2019. http://amsdottorato.unibo.it/8812/1/Corradi_Giulia_Tesi.pdf.

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In this thesis, we studied the cross-talk between malignant cells and stromal cells, with the aim to elucidate the respective contribution to myeloid neoplasm onset and progression. First, we characterized and compared mesenchymal stromal cells (MSCs) isolated from myelodysplastic syndrome (MDS-MSCs) and acute myeloid leukemia (AML-MSCs) patients. We demonstrated that, despite some unaltered functions, patient-derived MSCs show also intrinsic, distinct functional abnormalities, which could all potentially favor a leukemia-protective bone marrow (BM) niche in vivo. Second, we investigated the ability of AML cells to modulate the AML-MSC functions. In a GEP-screening, we found that 40% of BM-derived AML samples show a higher IFN-γ expression, compared to the mean IFN-γ expression in healthy BM-derived cells. We demonstrated that in co-culture experiments, IFN-γ+ AML cells modify AML-MSC gene expression and function, inducing the up-regulation of IDO1, and consequently the generation of T regulatory cells. Finally, we wondered if the transcriptome of stromal cells could be influenced by the hematopoietic-specific alterations, i.e. Dnmt3a and Asxl1 mutations, which occur early in MDS/AML patients. We found that Dnmt3a- and Asxl1-null BM cells, when transplanted in wild-type mice, induce profound and deletion-specific modifications in the transcriptome of wild-type BM stromal cells, suggesting the ability of Dnmt3a- and Asxl1-null BM cells to shape the niche. Furthermore, we compared the transcriptome of wild-type BM stromal cells, obtained from transplantation experiments, with that of MSCs isolated from low-risk MDS patients with DNMT3A and ASXL1 mutations, and we highlighted some common modifications, which could be potentially relevant for human disease and specific for DNMT3A/ASXL1 mutations. In conclusion, this thesis pointed out that there is a bi-directional cross-talk, in which stromal cells can influence malignant cells, and in turn malignant/pre-malignant cells can alter stromal cell gene expression and function. Both mechanisms could potentially contribute to the pathogenesis of myeloid malignancies.

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Li, Ge. "Cell physiology, biochemistry, and molecular biology of 5-aminolevulinic acid-induced protoporphyrin IX in normal, immortalized, transfected, and malignant cells". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0005/NQ27837.pdf.

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Eliasson, Pernilla. "Live and Let Die : Critical regulation of survival in normal and malignant hematopoietic stem and progenitor cells". Doctoral thesis, Linköpings universitet, Experimentell hematologi, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-52932.

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The hematopoietic stem cell (HSC) is characterized by its ability to self-renew and produce all mature blood cells throughout the life of an organism. This is tightly regulated to maintain a balance between survival, proliferation, and differentiation. The HSCs are located in specialized niches in the bone marrow thought to be low in oxygen, which is suggested to be involved in the regulation of HSC maintenance, proliferation, and migration. However, the importance of hypoxia in the stem cell niche and the molecular mechanisms involved remain fairly undefined. Another important regulator of human HSCs maintenance is the tyrosine kinase receptor FLT3, which triggers survival of HSCs and progenitor cells. Mutations in FLT3 cause constitutively active signaling. This leads to uncontrolled survival and proliferation, which can result in development of acute myeloid leukemia (AML). One of the purposes with this thesis is to investigate how survival, proliferation and self-renewal in normal HSCs are affected by hypoxia. To study this, we used both in vitro and in vivo models with isolated Lineage-Sca-1+Kit+ (LSK) and CD34-Flt3-LSK cells from mouse bone marrow. We found that hypoxia maintained an immature phenotype. In addition, hypoxia decreased proliferation and induced cell cycle arrest, which is the signature of HSCs with long term multipotential capacity. A dormant state of HSCs is suggested to be critical for protecting and preventing depletion of the stem cell pool. Furthermore, we observed that hypoxia rescues HSCs from oxidative stress-induced cell death, implicating that hypoxia is important in the bone marrow niche to limit reactive oxidative species (ROS) production and give life-long protection of HSCs. Another focus in this thesis is to investigate downstream pathways involved in tyrosine kinase inhibitor-induced cell death of primary AML cells and cell lines expressing mutated FLT3. Our results demonstrate an important role of the PI3K/AKT pathway to mediate survival signals from FLT3. We found FoxO3a and its target gene Bim to be key players of apoptosis in cells carrying oncogenic FLT3 after treatment with tyrosine kinase inhibitors. In conclusion, this thesis highlights hypoxic-mediated regulation of normal HSCs maintenance and critical effectors of apoptosis in leukemic cells expressing mutated FLT3.

On the day of the defence date the title of article II was "Hypoxia, via hypoxia-inducible factor (HIF)-1, mediates low cell cycle activity and preserves the engraftment potential of mouse hematopoietic stem cells" and one of the authors is no longer included in the article.

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Książki na temat "Malignant Cells - Molecular Characetrization"

T, Lynch Henry, i Fusaro Ramon M, red. Hereditary malignant melanoma. Boca Raton: CRC Press, 1991.

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Lynch, Henry T., i Ramon M. Fusaro. Hereditary Malignant Melanoma. Taylor & Francis Group, 2019.

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Lynch, Henry T., i Ramon M. Fusaro. Hereditary Malignant Melanoma. Taylor & Francis Group, 2019.

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Lynch, Henry T., i Ramon M. Fusaro. Hereditary Malignant Melanoma. Taylor & Francis Group, 2019.

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Lynch, Henry T., i Ramon M. Fusaro. Hereditary Malignant Melanoma. Taylor & Francis Group, 2019.

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Części książek na temat "Malignant Cells - Molecular Characetrization"

Hess, David A., i Alison L. Allan. "Migratory Strategies of Normal and Malignant Stem Cells". W Methods in Molecular Biology, 25–44. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-145-1_2.

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Pilarski, Linda M., Tony Reiman, Patrick M. Pilarski, F. William Orr i Andrew R. Belch. "The Malignant Hierarchy in Multiple Myeloma: Relationships between Malignant Cells and Bone Disease". W Bone Metastasis and Molecular Mechanisms, 109–38. Dordrecht: Springer Netherlands, 2004. http://dx.doi.org/10.1007/978-1-4020-2036-0_7.

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Kizhakeyil, Atish, Mobashar Hussain Urf Turabe Fazil i Navin Kumar Verma. "Targeted Gene Silencing in Malignant Hematolymphoid Cells Using GapmeR". W Methods in Molecular Biology, 209–19. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0771-8_15.

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Jalili-Nik, Mohammad, Amir R. Afshari, Khadijeh Mahboobnia, Paul C. Guest, Tannaz Jamialahmadi i Amirhossein Sahebkar. "Analysis of Cytotoxic Effects of in Malignant Glioblastoma Cells". W Methods in Molecular Biology, 361–69. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1558-4_26.

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Milosevic, Vladan, Reidunn J. Edelmann, Johanna Hol Fosse, Arne Östman i Lars A. Akslen. "Molecular Phenotypes of Endothelial Cells in Malignant Tumors". W Biomarkers of the Tumor Microenvironment, 31–52. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-98950-7_3.

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Cherukuri, Paul, i Steven A. Curley. "Use of Nanoparticles for Targeted, Noninvasive Thermal Destruction of Malignant Cells". W Methods in Molecular Biology, 359–73. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-609-2_24.

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Neschadim, Anton, i Jeffrey A. Medin. "Engineered Thymidine-Active Deoxycytidine Kinase for Bystander Killing of Malignant Cells". W Methods in Molecular Biology, 149–63. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8922-5_12.

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Wang, Yue J., Jennifer M. Bailey, Meritxell Rovira i Steven D. Leach. "Sphere-Forming Assays for Assessment of Benign and Malignant Pancreatic Stem Cells". W Methods in Molecular Biology, 281–90. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-287-2_15.

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Mimeault, Murielle, i Surinder K. Batra. "Characterization of Nonmalignant and Malignant Prostatic Stem/Progenitor Cells by Hoechst Side Population Method". W Methods in Molecular Biology, 139–49. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-280-9_8.

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Küppers, Ralf, Markus Schneider i Martin-Leo Hansmann. "Laser-Based Microdissection of Single Cells from Tissue Sections and PCR Analysis of Rearranged Immunoglobulin Genes from Isolated Normal and Malignant Human B Cells". W Methods in Molecular Biology, 61–75. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9151-8_3.

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Streszczenia konferencji na temat "Malignant Cells - Molecular Characetrization"

Jeffress, Mara, Alain Beliveau, Eric Campeau, Joe Gray i Paul Yaswen. "Abstract B91: RNAi knockdown of Mek2, but not Mek1, increases proliferation of malignant and non‐malignant human breast cells". W Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-b91.

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Deeb, Kristin K., Song Liu, Wei Luo, Adam R. Karpf, Carl Morrison, Candace S. Johnson i Donald L. Trump. "Abstract 1288: Molecular features of endothelial cells isolated from benign and malignant prostatic tissues". W 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.am10-1288.

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Kaza, Niroop, i Kevin A. Roth. "Abstract A34: Analysis of gossypol-induced cytotoxicity in malignant peripheral nerve sheath tumor cells." W Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-a34.

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Wang, Wei-Ting, James Catto i Mark Meuth. "Abstract B61: Differential response of normal and malignant urothelial cells to CHK1 and ATM inhibitors." W Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-b61.

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King, Trey, Mickeal Key, John Clifford, Jennifer Roberts Gill, Yoonjee Kim, Elahe Mahdavian, Urska Cvek i in. "Abstract A35: DNA microarray analysis of the effect of fusarochromanone on human malignant bladder cancer cells." W Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-a35.

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Dupéré‐Richer, Daphné, Luca Petruccelli, Hélène Retrouvey, Monica Dobocan, Miranda Tomenson, Filippa Pettersson i Wilson H. Miller. "Abstract A188: Proapoptoticversusprosurvival function of the MAP kinase p38 induced by HDAC inhibitor in hematological malignant cells". W Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-a188.

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Kohli, Latika, Steven L. Carroll i Kevin A. Roth. "Abstract A33: Pan erbB inhibition enhances lysosomal dysfunction-induced death in malignant peripheral nerve sheath tumor cells." W Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-a33.

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The Van, Trung, Takuya Kuramoto, Hisatsugu Goto, Soji Kakiuchi, Tetsuo Taniguchi, Yoshitaka Sekido, Yasuhiko Nishioka i Saburo Sone. "Abstract B7: TSU‐68 suppresses the progression of malignant pleural mesothelioma cells in SCID mice by inhibiting angiogenesis". W Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-b7.

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Welte, Yvonne, Hella Kohlhof, Johann Leban i Christian RA Regenbrecht. "Abstract A59: Wnt, Notch, and Hedgehog pathways as potential therapeutic targets in OCT4A expressing cancer stem cells of malignant melanoma." W Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-a59.

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Vatansever, D., G. Bildik, C. Taskiran i O. Oktem. "EP1132 A comperative molecular analysis of DNA damage response and apoptosis of malignant granulosa cells after exposure to gemcitabine and cisplatin". W ESGO Annual Meeting Abstracts. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/ijgc-2019-esgo.1174.

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Raporty organizacyjne na temat "Malignant Cells - Molecular Characetrization"

Xu, Xiangxi M. A Molecular Basis Accounted for the Malignant Features of Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, kwiecień 2012. http://dx.doi.org/10.21236/ada589287.

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Xu, Xiangxi. A Molecular Basis Accounted for the Malignant Features of Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, październik 2011. http://dx.doi.org/10.21236/ada555893.

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