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Relevant bibliographies by topics / Cell proliferation

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Academic literature on the topic 'Cell proliferation'

Author: Grafiati

Published: 4 June 2021

Last updated: 28 July 2024

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Journal articles on the topic "Cell proliferation"

1

M. Baghdadi, Houry. "Effect of stem cells on genetic mutations and proliferation in squamous cell carcinoma." International Journal of Academic Research 6, no. 1 (January 30, 2014): 192–97. http://dx.doi.org/10.7813/2075-4124.2014/6-1/a.25.

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Chung, Hyunju, and Seungjoon Park. "Ghrelin regulates cell cycle-related gene expression in cultured hippocampal neural stem cells." Journal of Endocrinology 230, no. 2 (August 2016): 239–50. http://dx.doi.org/10.1530/joe-16-0126.

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We have previously demonstrated that ghrelin stimulates the cellular proliferation of cultured adult rat hippocampal neural stem cells (NSCs). However, little is known about the molecular mechanisms by which ghrelin regulates cell cycle progression. The purpose of this study was to investigate the potential effects of ghrelin on cell cycle regulatory molecules in cultured hippocampal NSCs. Ghrelin treatment increased proliferation assessed by CCK-8 proliferation assay. The expression levels of proliferating cell nuclear antigen and cell division control 2, well-known cell-proliferating markers, were also increased by ghrelin. Fluorescence-activated cell sorting analysis revealed that ghrelin promoted progression of cell cycle from G0/G1 to S phase, whereas this progression was attenuated by the pretreatment with specific inhibitors of MEK/extracellular signal-regulated kinase 1/2, phosphoinositide 3-kinase/Akt, mammalian target of rapamycin, and janus kinase 2/signal transducer and activator of transcription 3. Ghrelin-induced proliferative effect was associated with increased expression of E2F1 transcription factor in the nucleus, as determined by Western blotting and immunofluorescence. We also found that ghrelin caused an increase in protein levels of positive regulators of cell cycle, such as cyclin A and cyclin-dependent kinase (CDK) 2. Moreover, p27KIP1 and p57KIP2 protein levels were reduced when cell were exposed to ghrelin, suggesting downregulation of CDK inhibitors may contribute to proliferative effect of ghrelin. Our data suggest that ghrelin targets both cell cycle positive and negative regulators to stimulate proliferation of cultured hippocampal NSCs.

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Fraser, Hamish M., Helen Wilson, Audrey Silvestri, Keith D. Morris, and Stanley J. Wiegand. "The Role of Vascular Endothelial Growth Factor and Estradiol in the Regulation of Endometrial Angiogenesis and Cell Proliferation in the Marmoset." Endocrinology 149, no. 9 (May 22, 2008): 4413–20. http://dx.doi.org/10.1210/en.2008-0325.

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The present studies explore the roles of vascular endothelial growth factor (VEGF) and estradiol on angiogenesis and stromal and epithelial cell proliferation in the marmoset endometrium during the proliferative phase of the ovulatory cycle. At the start of the proliferative phase, marmosets were 1) treated with vehicle, 2) treated with a VEGF inhibitor (VEGF Trap, aflibercept), 3) ovariectomized, 4) ovariectomized and given replacement estradiol, or 5) treated with VEGF Trap and given replacement estradiol. The uterus was examined 10 d later in the late proliferative phase. Changes in endothelial and epithelial cell proliferation were quantified using a volumetric density method after immunohistochemistry for bromodeoxyuridine to localize proliferating cells, CD31 to visualize endothelial cells, and dual staining to distinguish endothelial cell proliferation. Endothelial proliferation was elevated in late proliferative controls but virtually absent after VEGF Trap. Ovariectomy had a similar inhibitory effect, whereas angiogenesis was restored by estrogen replacement. Estradiol replacement in VEGF Trap-treated marmosets resulted in only a small increase in endothelial cell proliferation that remained significantly below control values. VEGF Trap treatment and ovariectomy also markedly reduced stromal cell proliferation but resulted in increased stromal cell density associated with a reduction in overall endometrial volume. Estrogen replacement in both ovariectomized and VEGF Trap-treated animals restored stromal proliferation rates and cell density. These results show that endometrial angiogenesis and stromal proliferation during the proliferative phase are driven by estradiol and that the effect of estrogen on angiogenesis is mediated largely by VEGF.

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Robey, H. L., P. S. Hiscott, and I. Grierson. "Cytokeratins and retinal epithelial cell behaviour." Journal of Cell Science 102, no. 2 (June 1, 1992): 329–40. http://dx.doi.org/10.1242/jcs.102.2.329.

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The expression of cytokeratins 18 and 19 by human retinal pigment epithelial cells (HRPE) has been suspected of being associated with HRPE proliferation. We have investigated the involvement of these cytokeratin subtypes in the proliferative and migratory behaviour of cultured HRPE. Cell proliferation markers (bromodeoxyuridine and proliferating cell nuclear antigen) and the cytokeratins were identified using immunohistochemical techniques. In vitro, cytokeratins 18 and 19, as detected by the monoclonal antibodies RGE 53 and K4.62, were expressed in a subset of HRPE and this subset was significantly less likely to be proliferating. Micro-chemotaxis chambers were used to study migrating cells and immunohistochemical staining for cytokeratins 18 and 19 revealed that actively migrating cells always expressed these two cytokeratins, whereas stationary cells did not label for these cytokeratin subtypes. It was apparent that cytokeratins 18 and 19 were not markers of proliferation, but were involved in the mobility of HRPE in vitro. Cytokeratins 18 and 19 may be useful indicators of simple epithelial cell migration in tissues.

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Kabraji, Sheheryar Kairas, Giorgio Gaglia, Danae Argyropoulou, Yang Dai, Shu Wang, Johann Bergholz, Shannon Coy, et al. "Temporal and spatial topography of cell proliferation in cancer." Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021): 3122. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.3122.

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3122 Background: Tumors are complex ecosystems where exogenous and endogenous cues are integrated to either stimulate or inhibit cancer cell proliferation. However, the nature of these complex cell cycle states, their spatial organization, response to perturbation, and implications for clinical outcomes, are poorly characterized in tumor tissues. Methods: We used multiplexed tissue imaging to develop a robust classifier of proliferation, the multivariate proliferation index (MPI), using 513 unique tumors across five cancer types. Next, we used dimensionality reduction analysis to assess how the patterns of cell cycle protein expression in tumors were altered in response to perturbation. Results: The MPI outperforms single markers, like Ki67, when classifying proliferative index across diverse tumor types and reveals the proliferative architecture of tumors in situ. We find that proliferative and non-proliferative cancer cells are organized across microscopic (cell-to-cell) and macroscopic (tissue-level) scales. Both domains are reshaped by therapy, and local clusters of proliferative and non-proliferative tumor cells preferentially neighbor distinct tumor-infiltrating immune cells. We further phenotyped non-proliferating cancer cells using markers of quiescent cancer cells, cancer stem cells, and dormant cancer cells. We found that these types of non-proliferating cancer cells can occupy distinct regions within the same primary tumor. In high-dimensional marker space, populations of proliferative cancer cells express canonical patterns of cell cycle protein markers, a property we refer to as “cell cycle coherence”. Untreated tumors exist in a continuum of coherence states, ranging from optimal coherence, akin to freely cycling cells in culture, to reduced coherence characterized by either cell cycle polarization or non-canonical marker expression. Coherence can be stereotypically altered by induction and abrogation of mitogen signaling in a HER2-driven model of breast cancer. Cell cycle coherence is modulated by neoadjuvant therapy in patients with localized breast cancer, and coherence is associated with disease-free survival after adjuvant therapy in patients with colorectal cancer, mesothelioma and glioblastoma. Conclusions: The MPI robustly defines proliferating and non-proliferating cells in tissues, with immediate implications for clinical practice and research. The coherence metrics capture the diversity of post-treatment cell cycle states directly in clinical samples, a fundamental step in advancing precision medicine. More broadly, replacing binary metrics with multivariate traits provides a quantitative framework to study temporal processes from fixed static images and to investigate the rich spatial biology of human cancers.

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Chan, Ming Liang, Janka Petravic, Alexandra M. Ortiz, Jessica Engram, Mirko Paiardini, Deborah Cromer, Guido Silvestri, and Miles P. Davenport. "Limited CD4+ T cell proliferation leads to preservation of CD4+ T cell counts in SIV-infected sooty mangabeys." Proceedings of the Royal Society B: Biological Sciences 277, no. 1701 (June 30, 2010): 3773–81. http://dx.doi.org/10.1098/rspb.2010.0972.

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Human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) infections result in chronic virus replication and progressive depletion of CD4+ T cells, leading to immunodeficiency and death. In contrast, ‘natural hosts’ of SIV experience persistent infection with high virus replication but no severe CD4+ T cell depletion, and remain AIDS-free. One important difference between pathogenic and non-pathogenic infections is the level of activation and proliferation of CD4+ T cells. We analysed the relationship between CD4+ T cell number and proliferation in HIV, pathogenic SIV in macaques, and non-pathogenic SIV in sooty mangabeys (SMs) and mandrills. We found that CD4+ T cell proliferation was negatively correlated with CD4+ T cell number, suggesting that animals respond to the loss of CD4+ T cells by increasing the proliferation of remaining cells. However, the level of proliferation seen in pathogenic infections (SIV in rhesus macaques and HIV) was much greater than in non-pathogenic infections (SMs and mandrills). We then used a modelling approach to understand how the host proliferative response to CD4+ T cell depletion may impact the outcome of infection. This modelling demonstrates that the rapid proliferation of CD4+ T cells in humans and macaques associated with low CD4+ T cell levels can act to ‘fuel the fire’ of infection by providing more proliferating cells for infection. Natural host species, on the other hand, have limited proliferation of CD4+ T cells at low CD4+ T cell levels, which allows them to restrict the number of proliferating cells susceptible to infection.

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Tsunoda, Mikiya, Hiroyasu Aoki, Munetomo Takahashi, Haruka Shimizu, Haru Ogiwara, Shigeyuki Shichino, Kouji Matsushima, and Satoshi Ueha. "Abstract 5180: T cell receptor repertoire analysis revealed tissue tropism of tumor-reactive T-cell clones in cell cycle reporter mice." Cancer Research 83, no. 7_Supplement (April 4, 2023): 5180. http://dx.doi.org/10.1158/1538-7445.am2023-5180.

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Abstract Tumor-reactive T cells are composed of clones with various TCRs, and each clone has different in vivo kinetics. By analyzing TCR repertoire of tumor and tumor-draining lymph node (dLN), we have demonstrated that Tumor-reactive CD8+ T cells can be classified into “dLN Major”, “Tumor Major”, and “Double Major” clones, which exhibited high frequency in the dLN, tumor, or both tissues. To investigate whether this classification was related to the tissue tropism in the proliferation of each clone, we here employed tumor-bearing Fucci transgenic mice expressing a fluorescent cell-cycle indicator to identify the proliferation of T-cell clones in each tissue. We purified proliferating- and resting-CD8+ T cells from the tumors and dLN and analyzed their TCR repertoire in an LLC subcutaneous tumor model. All Tumor Major clones were proliferated in the tumor, while nearly 0% for dLN Major, indicated their different proliferative capacity in the tumor. The percentage of proliferating clones in the dLN was 20% for Tumor Major and 15% for dLN Major, indicating that these clones had equivalent proliferative capacity in the dLN. These proliferating dLN major clones overlapped more with the tumor than the non-proliferating dLN major clones, suggesting that proliferating dLN Major clones had higher tumor migration capacity. Furthermore, these proliferating dLN major clones were more proliferative in the tumor. These results suggested that dLN Major responded to antigen presentation in the dLN but not in the tumor, whereas Tumor Major responded to those in the dLN and tumor. In addition, there are two types of dLN major, “clones that are proliferating in dLN” and “clones that are not proliferating in dLN” indicating that the former may contribute to the anti-tumor response. Immune checkpoint inhibitor (ICI) treatment not only reactivates clones in the tumor but also activates tumor-reactive clones in the dLN. In conformity with these previous studies, the percentage of proliferating clones among dLN Major increased to about 50% and 80% in the dLN in mice with anti-PD-L1 and anti-CD4 treatment, respectively. This result suggests ICI treatment enhances anti-tumor responses mainly by promoting the activation and proliferation of dLN Major clones. This study shows new findings that tumor-reactive T cells differ in the tissue tropism of their proliferation of each clone. In the future, a quantitative understanding of the contribution of each class of clones to the anti-tumor response will hopefully lead to the development of new combined immunotherapies that optimize the anti-tumor T-cell response. Citation Format: Mikiya Tsunoda, Hiroyasu Aoki, Munetomo Takahashi, Haruka Shimizu, Haru Ogiwara, Shigeyuki Shichino, Kouji Matsushima, Satoshi Ueha. T cell receptor repertoire analysis revealed tissue tropism of tumor-reactive T-cell clones in cell cycle reporter mice. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 5180.

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Hall, Peter A. "Cell proliferation." Journal of Pathology 165, no. 4 (December 1991): 349–54. http://dx.doi.org/10.1002/path.1711650412.

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Deniz, Özdemir. "KAN0438757: A NOVEL PFKFB3 INHIBITOR THAT INDUCES PROGRAMMED CELL DEATH AND SUPPRESSES CELL MIGRATION IN NON-SMALL CELL LUNG CARCINOMA CELLS." Biotechnologia Acta 16, no. 5 (October 31, 2023): 34–44. http://dx.doi.org/10.15407/biotech16.05.034.

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Aim. PFKFB3 is glycolytic activators that is overexpressed in human lung cancer and plays a crucial role in multiple cellular functions including programmed cell death. Despite the many small molecules described as PFKFB3 inhibitors, some of them have shown disappointing results in vitro and in vivo. On the other hand KAN0438757, selective and potent, small molecule inhibitor has been developed. However, the effects of KAN0438757, in non-small cell lung carcinoma cells remain unknown. Herein, we sought to decipher the effect of KAN0438757 on proliferation, migration, DNA damage, and programmed cell death in non-small cell lung carcinoma cells. Methods. The effects of KAN0438757 on cell viability, proliferation, DNA damage, migration, apoptosis, and autophagy in in non-small cell lung carcinoma cells was tested by WST-1, real-time cell analysis, comet assay, wound-healing migration test, and MMP/JC-1 and AO/ER dual staining assays as well as western blot analysis. Results. Our results revealed that KAN0438757 significantly suppressed the viability and proliferation of A549 and H1299 cells and inhibited migration of A549 cells. More importantly, KAN0438757 caused DNA damage and triggered apoptosis and this was accompanied by the up-regulation of cleaved PARP in A549 cells. Furthermore, treatment with KAN0438757 resulted in increased LC3 II and Beclin1, which indicated that KAN0438757 stimulated autophagy. Conclusions. Overall, targeting PFKFB3 with KAN0438757 may be a promising effective treatment approach, requiring further in vitro and in vivo evaluation of KAN0438757 as a therapy in non-small cell lung carcinoma cells.

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Levine, Richard, Magnus S. Agren, and Patricia M. Mertz. "Effect of Occlusion on Cell Proliferation during Epidermal Healing." Journal of Cutaneous Medicine and Surgery 2, no. 4 (April 1998): 193–98. http://dx.doi.org/10.1177/120347549800200403.

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Background: Occlusive dressings influence epithelization of superficial wounds by some unknown mechanism(s). Objective: The effects of occlusion on epidermal cell proliferation in two types of wounds were examined. Methods: Partial-thickness wounds and tape-stripped skin wounds were compared. An immunohistochemical technique, employing PC10 — a monoclonal antibody against proliferating cell nuclear antigen (PCNA) — was applied to formalin-fixed, paraffin-embedded porcine tissue sections. Results: The number of PC10-positive cells was low during the migratory phase, then increased to a peak of proliferation 2 to 3 days after resurfacing. An overall increased proliferative response (mean = 21%) was seen in occluded compared to control partial-thickness wounds (day 10 postoperatively); an opposite effect of occlusion on epidermal proliferation was seen in tape-stripped skin. Occlusion decreased the proliferative response (mean = 42%) compared to air-exposure. Conclusion: Occlusion increased epidermal cell proliferation in wounds (where the entire surface epithelium and papillary dermis was removed), whereas an opposite effect was seen in tape-stripped skin from which only the stratum corneum had been removed.

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Dissertations / Theses on the topic "Cell proliferation"

1

Falk, Anna. "Stem cells : proliferation, differentiation, migration /." Stockholm, 2005. http://diss.kib.ki.se/2006/91-7140-497-X/.

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Cheng, Wai. "The relationship between peroxisome proliferator-activated receptors (PPARs) and cell proliferation /." View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36433937.

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Cheng, Wai, and 鄭蔚. "The relationship between peroxisome proliferator-activated receptors (PPARs) and cell proliferation." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B45010614.

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Ashagbley, Anthony J. "Ethanolamine requirement and cell proliferation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq23203.pdf.

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Hooper, Nigel I. "Methylglyoxal, glyoxalases and cell proliferation." Thesis, Aston University, 1987. http://publications.aston.ac.uk/12548/.

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The metabolic function of the glyoxalase system was investigated in (a) the differentiation and proliferation of human tumour cells in vitro, (b) the cell-free assembly of microtubules and (c) in the red blood cells during hyperglycaemia associated with Diabetes Mellitus. Chemically-induced differentiation of human promyelocytic HL60 leukaemia cells to neutrophils, and K562 erythroleukaemia cells, was accompanied by a decrease and an increase in the activity of glyoxalase I, respectively. Growth-arrest of Burkitt's lymphoma Raji cells and GM892 lymphoblastoid cells was accompanied by an increase and a decrease in the activity of glyoxalase I respectively. However, differentiation and growth arrest generally proceeded with an increase in the activity of glyoxalase II. Glyoxalase I activity did not consistently correlate with cell differentiation or proliferation status; hence, it is unlikely that glyoxalase I activity is either an indicator or a regulator of cell differentiation or proliferation. Conversely, glyoxalase II activity consistently increased during cell differentiation and growth-arrest and may be both an indicator and regulator of cell differentiation or proliferation. This may be related to the control of cellular microtubule assembly. S-D-Lactoylglutathione potentiated the cell-free, GTP-promoted assembly of microtubules. The effect was dose-related and was inhibited by glyoxalase II. During assembly, S-D-lactoylglutathione was consumed. This suggests that the glyoxalase system, through the influence of S-D-lactoylglutathione, may regulate the assembly of microtubules in cellular systems The whole blood concentrations of methylglyoxal and S-D-lactoylglutathione were increased in Diabetes Mellitus. There was no significant difference between red blood cell glyoxalase activities in diabetics, compared to healthy controls. However, insulin-dependent diabetic patients with retinopathy had a significantly higher glyoxalase I activity and a lower glyoxalase II activity, than patients without retinopathy. Diabetic retinopathy correlated with high glyoxalase I activity and low glyoxalase II activity and suggests the glyoxalase system may be involved in the development of diabetic complications.

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Ellison, David William. "Cell proliferation, cell death, and differentiation in gliomas." Thesis, University of Southampton, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295912.

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Petersen, Cecilia. "Paracrine regulation of Sertoli cell proliferation /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-443-7/.

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Zhang, Jiao, and 张姣. "Regulation of cell proliferation and modulation of differentiation in human induced pluripotent stem cell-derived mesenchumal stem cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B49617503.

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Functional mesenchymal stem cells (MSCs) derived from human induced pluripotent stem cells (iPSCs) may represent an unlimited cell source with superior therapeutic benefits for tissue regeneration to somatic tissue, such as bone marrow (BM)-derived MSC. In the first part of this project, I investigated whether the differential expression of ion channels in iPSC-MSCs was responsible for their higher proliferation capacity than that of BM-MSCs. The expression of ion channels for K+, Na+, Ca2+ and Cl- currents was assessed by reverse transcription-polymerase chain reaction (RT-PCR). The functional role of these ion channels were then verified by patch clamp experiments to compare the electrophysiological properties of iPSC-MSCs versus BM-MSCs. I detected significant mRNA expression of ion channel genes including KCa1.1, KCa3.1, KCNH1, Kir2.1, SCN9A, CACNA1C and Clcn3 in both human iPSC-MSCs and BM-MSCs; while Kir2.2 and Kir2.3 were only observed in human iPSC-MSCs. Furthermore, I identified five types of currents (BKCa, IKDR, IKir, IKCa and ICl) in iPSC-MSCs, while only four of them (BKCa, IKDR, IKir and IKCa) were observed in BM-MSCs. The rate of cell proliferation was 1.4 fold faster in iPSC-MSCs as compared to BM-MSCs. Interestingly, the proliferation rate of human iPSCMSCs was significantly reduced when inhibiting IKDR with shRNA and hEAG1 channel blockers, 4-AP and astemizole. Though to a lesser extent, the proliferation rate of human BM-MSCs also decreased by IKDR blockage. These results demonstrated that hEAG1 channel plays a crucial role in controlling the proliferation rate of human iPSC-MSCs but to a lesser extent in BM-MSCs. Next, I examined whether forced expression of a transcription factor- myocardin in iPSC-MSC using viral vectors (adenovirus or lentivirus) can further enhance their trans-differentiation to cardiomyocytes and improve their electrophysiological properties for cardiac regeneration. My results on RT-PCR and immunofluorescent staining revealed that myocardin induced the expression of several cardiac and smooth muscle cell markers, including α-MHC, cTnT, GATA4, α-actinin, and cardiac MHC, smooth muscle cell markers MYH11, calponin, and SM α-actin, but not the more mature cardiac markers such as β-MHC and MLC2v in iPSC-MSCs. These findings indicate that forced expression of myocardin in iPSC-MSC resulted in partial trans-differentiation into cardiomyocytes phenotype. Furthermore, I also discovered that myocardin altered the electrophysiological properties of iPSC-MSCs when examined by RT-PCR and patch clamp experiments. Forced expression of myocardin in iPSC-MSC enhanced the expression of Kv4.3, SCN9A and CACNA1C, but reduced that of KCa3.1 and Kir 2.2 in iPSC-MSCs. Moreover, BKCa, IKir, ICl, Ito and INa.TTX were detected in iPSC-MSC with ectopic expression of myocardin; while only BKCa, IKir, ICl, IKDR and IKCa were noted in iPSC-MSC transfected with green florescence protein. Furthermore, as measured by multi-electrode arrays recording plate, the conduction velocity of the neonatal rat ventricular cardiomyocytes cocultured iPSC-MSC monolayer was significantly increased after ectopic expression of myocardin. Taken together, I have demonstrated that hEAG1 channel is important in the regulation of iPSC-MSC proliferation and forced expression of myocardin in iPSC-MSC resulted in their partial transdifferentiation into cardiomyocytes phenotype and improved the electrical conduction during integration with mature cardiomyocytes.
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Medicine
Doctoral
Doctor of Philosophy

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Yamak, Fatimah Abir. "GATA4 Partners in Cardiac Cell Proliferation." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/23802.

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Cardiovascular diseases are the leading cause of death in humans throughout the world and “congenital heart defects” (CHDs) are the major cause of infant mortality and morbidity. GATA4 is one of the most critical and intensely studied cardiac transcription factor. It is important for proliferation of cardiomyocytes as well as their survival and adaptive response. The focus of the following thesis was to identify GATA4 mediators and cofactors in cardiac growth. The first part focused on cyclin D2 (CycD2), a growth inducible cell cycle protein. We identified Ccnd2 (gene encoding CycD2) as a direct transcriptional target of GATA4 in postnatal cardiomyocytes and Ccnd2 cardiomyocyte specific overexpression in Gata4 heterozygote mice was able to rescue their heart size and function. We further uncovered a novel regulatory loop between GATA4 and CycD2. CycD2 enhanced GATA4 activation of its target promoters. GATA4 was able to physically interact with CycD2 and its cyclin dependent kinase CDK4 suggesting that GATA4 recruits CycD2/CDK4 to its target promoters. Together, our data uncover a role of CycD2 in the developing and postnatal heart and provide novel insight for the potential of targeting the cell cycle in cardiac therapy. The second part of the project focused on KLF13, a cell specific cofactor of GATA4. KLF13 is a member of the Krϋppel-like transcription factors that are important regulators of cell proliferation and differentiation. Klf13 is highly enriched in the developing heart where it is found in both myocardial and endocardial cells. To determine its role in the mammalian heart, we deleted the Klf13 gene in transgenic mice. Klf13-/- mice were born at 50% reduced frequency and presented with variable cardiac phenotypes. Epithelial-mesenchymal transformation (EMT) was affected in these mice and reduced cell proliferation was evident in the AV cushion. These data uncover a role for a new class of transcription factors in heart formation and point to KLF13 as a regulator of endocardial cell proliferation and a potential CHD causing gene. Future discovery of more cardiac regulators and understanding the molecular basis of CHDs is essential for preventions of these defects and possible development of therapeutic approaches for myocardial repair.

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Cheung, Man-keung, and 張文強. "FBI-1 and choriocarcinoma cell proliferation." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193565.

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Gestational trophoblastic disease (GTD) includes a spectrum of diseases that involve abnormal growth of trophoblastic cells inside the uterus. It can range from benign hydatidiform moles (HM) to frankly malignant choriocarcinoma, placental site trophoblastic tumor (PSTT) or epithelioid trophoblastic tumour (ETT).GTD are considered curable if the patient is correctly diagnosed and receive appropriate treatment during the early stage of the disease. About 15% -30% of hydatidiform moles will develop persistent GTD, but majority of them can usually resolved by surgical intervention and post-operation weekly serial serum β-hCG level monitoring. In contrast, choriocarcinoma is a frankly malignant gestational trophoblastic neoplasm (GTN). Most choriocarcinoma arise from HM but can develop from any pregnancy related events such as ectopic pregnancy, live-birth or stillbirth. Being the most aggressive neoplasm in GTD, choriocarcinoma can develop widespread metastasis and can be fatal. FBI-1 (Pokemon) is a transcription factor that is often overexpressed in various types of human cancer. We have reported overexpression of FBI-1 in ovarian cancer in association with cell proliferation and invasiveness. Our recent study also suggested that overexpression of FBI-1 in HM was related to subsequent development of gestational trophoblastic neoplasms(GTN). In this study, we evaluated the role of FBI-1 inchoriocarcinoma cell proliferation. By MTT assay, the proliferation rates of two choriocarcinoma cell lines (JAR and JEG-3) was found to decrease when FBI-1 was downregulated by shRNA approach with statistical significance reached in JEG-3 (p < 0.05). By quantitative real time PCR, the relative levels of a panel of hedgehog pathway related genes, including SHH, SMO, GLI1, GLI2, GLI3, and KIF7 were assessed after knockdown of FBI-1 gene. Sonic hedgehog (SHH) was found to be consistently downregulated in JEG-3 and JAR transfected with FBI-1 shRNA constructs. In conclusion, FBI-1 may play a role in choriocarcinoma cell proliferation and FBI-1 may be explored as a potential therapeutic target for GTD in the future.
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Pathology
Master
Master of Medical Sciences

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Books on the topic "Cell proliferation"

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1950-, Hughes David, and Mehmet H, eds. Cell proliferation & apoptosis. Oxford, UK: BIOS Scientific, 2003.

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P, Briggs Andre, and Coburn Jacob A, eds. Handbook of cell proliferation. Hauppauge, NY: Nova Science Publishers, 2009.

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Enders, Greg H. Cell cycle deregulation in cancer. New York: Springer, 2010.

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L, Boynton Alton, and Leffert H. L, eds. Control of animal cell proliferation. Orlando: Academic Press, 1985.

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John, Crocker, ed. Cell Proliferation in Lymphomas. Oxford: Blackwell Scientific Publications, 1993.

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Heath, John K., ed. Principles of Cell Proliferation. Oxford, UK: Blackwell Publishing Ltd, 2001. http://dx.doi.org/10.1002/9780470757086.

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Principles of cell proliferation. Malden, MA: Blackwell Science, 2001.

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Heath, John K. Principles of Cell Proliferation. New York: John Wiley & Sons, Ltd., 2008.

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M, Soto A., ed. The society of cells: Cancer control of cell proliferation. Oxford: Bios Scientific Publishers, 1999.

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Sonnenschein, C. The society of cells: Cancer and control of cell proliferation. Oxford: Bios Scientific Publishers, 1999.

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Book chapters on the topic "Cell proliferation"

1

Wardle, E. Nigel. "Cell Proliferation." In Guide to Signal Pathways in Immune Cells, 77–90. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-538-5_5.

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Roy, Priti Kumar. "T Cell Proliferation." In Mathematical Models for Therapeutic Approaches to Control HIV Disease Transmission, 43–58. Singapore: Springer Singapore, 2015. http://dx.doi.org/10.1007/978-981-287-852-6_3.

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Lovicu, F. J., L. Iyengar, L. J. Dawes, and J. W. McAvoy. "Lens Epithelial Cell Proliferation." In Lens Epithelium and Posterior Capsular Opacification, 59–80. Tokyo: Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-54300-8_4.

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Kuwayama, Hajime. "Sucralfate and Cell Proliferation." In Sucralfate, 141–49. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-0-585-32154-7_14.

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Serrano, Manuel. "Proliferation: the Cell Cycle." In Advances in Experimental Medicine and Biology, 13–17. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0081-0_2.

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Schwarz, Michael, Albrecht Buchmann, Larry W. Robertson, and Werner Kunz. "Cell Proliferation and Hepatocarcinogenesis." In Scientific Issues in Quantitative Cancer Risk Assessment, 96–115. Boston, MA: Birkhäuser Boston, 1990. http://dx.doi.org/10.1007/978-1-4684-9218-7_6.

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Lee, Sun-Hwa, Stacy Lee, and Jae Ung Jung. "Virus-Mediated Cell Proliferation." In Cancer Associated Viruses, 45–80. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4614-0016-5_3.

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Thiriet, Marc. "Cell Growth and Proliferation." In Control of Cell Fate in the Circulatory and Ventilatory Systems, 85–176. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-0329-6_2.

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Wang, Zhihui, and Thomas S. Deisboeck. "Multilevel Modeling, Cell Proliferation." In Encyclopedia of Systems Biology, 1464–67. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_50.

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Watanabe, Nobumoto, and Hiroyuki Osada. "Cell Proliferation and Differentiation." In Bioprobes, 11–35. Tokyo: Springer Japan, 2017. http://dx.doi.org/10.1007/978-4-431-56529-1_2.

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Conference papers on the topic "Cell proliferation"

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Previtera, Michelle L., Mason Hui, Malav Desai, Devendra Verma, Rene Schloss, and Noshir A. Langrana. "Neuronal Precursor Cell Proliferation on Elastic Substrates." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53246.

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Numerous stem cells therapies have been studied for the replacement of damaged neurons due to spinal cord injury. Our laboratory’s goal is to design an implantable platform for spinal cord neuron (SCN) proliferation and differentiation in order to replace damaged neurons in the injured spinal cord. Based on previous literature, we suspect we can promote neuronal precursor cell (NPC) proliferation and differentiation utilizing elastic matrices.

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Xu, F., A. E. Emre, E. S. Turali, S. K. Hasan, S. Moon, J. Nagatomi, A. Khademhosseini, and U. Demirci. "Cell proliferation in bioprinted cell-laden collagen droplets." In 2009 IEEE 35th Annual Northeast Bioengineering Conference. IEEE, 2009. http://dx.doi.org/10.1109/nebc.2009.4967727.

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"Does Progesterone Influence Hela Cell Proliferation?" In 2016 International Conference on Biological and Environmental Science. Universal Researchers, 2016. http://dx.doi.org/10.17758/ur.u0616232.

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Gu, Ying, Shanxiang Jiang, Elahe Mahdavian, and Shile Huang. "Abstract 4566: Fusarochromanone inhibits cell proliferation and induces cell death in COS7 cells." 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.am2014-4566.

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Ghaffari, A., S. Ghanizadeh Chenarbon, and P. Rahmani Vahid. "Mathematical and Optimization for a Non-Linear Yeast Cell Proliferation Problem Using Genetic Algorithm." In ASME 2008 International Mechanical Engineering Congress and Exposition. ASMEDC, 2008. http://dx.doi.org/10.1115/imece2008-68480.

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We consider an age-maturity structured model arising from a yeast cell proliferation problem. This model is a new study in the filed of analysis of cell kinetics and cell division using mathematical modeling and optimized by Genetic Algorithm. We use our mathematical analysis in conjunction with experimental data from the division analysis of primitive cells to characterize the maturation/proliferation process.

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Liote, F., M. P. Wautier, E. Savariau, H. Setiadi, and J. L. Wautier. "INHIBITION OF ENDOTHELIAL CELL PROLIFERATION BY NORMAL HUMAN MONOCYTES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643170.

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Human peripheral blood monocytes and macrophages possess factors which are capable of inhibiting or stimulating endothelial cell proliferation. We have further explored if such activity is due to cytotoxic effects of monocytes. Normal mononuclear cells were isolated first by density gradient. Monocytes were then purified by three different techniques: 1) counter centrifugation elutriation (CCE) (Beckman) 2) selective adhesion to gelatin-plasma (GPI) 3) selective adhesion to fibronectin (Fn). Cytotoxicity was estimated by counting the release of 51cr used to label the human umbilical vein endothelial cells (HUVE) prior to the addition of monocytes. Whilst [3H] thymidine incorporation by HUVE permitted us to measure the effect of monocytes on the growth of the endothelial cells. Monocytes were incubated with HUVE (12×103) for 24 to 36h at various concentrations '(1.5-12×103). No cytotoxic effect could be demonstrated but an inhibition of [3h] thymidine uptake was observed and was dependent upon monocytes concentration. Monocytes isolated on GP1 exhibited a significantly higher inhibitory effect (p<0.05) compared to those purified on Fn or by CCE.(GP1: 85±6%, Fn:58±6%, CCE:67±5%). These results indicated t*hat normal monocytes can inhibit endothelial cell proliferation. This activity appeared to be higher when monocytes were isolated on GP1 which suggest that the adhesion on this surface could stimulate monocytes not only by its fibronectin receptor. This inhibitory activity of monocyte on endothelial cells proliferation could be different in patients with vascular disorders.

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Nobile, Marco S., Thalia Vlachou, Simone Spolaor, Paolo Cazzaniga, Giancarlo Mauri, Pier Giuseppe Pelicci, and Daniela Besozzi. "ProCell: Investigating cell proliferation with Swarm Intelligence." In 2019 IEEE Conference on Computational Intelligence in Bioinformatics and Computational Biology (CIBCB). IEEE, 2019. http://dx.doi.org/10.1109/cibcb.2019.8791468.

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Vinjimore Kesavan, S., C. P. Allier, F. Navarro, F. Mittler, B. Chalmond, and J. M. Dinten. "Lensless imaging system to quantify cell proliferation." In SPIE BiOS, edited by Daniel L. Farkas, Dan V. Nicolau, and Robert C. Leif. SPIE, 2013. http://dx.doi.org/10.1117/12.2001826.

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Wang, Hao, Xiaoyi Lv, Guohua Wu, Guodong Lv, and Xiangxiang Zheng. "Cell proliferation detection based on deep learning." In 2020 2nd International Conference on Information Technology and Computer Application (ITCA). IEEE, 2020. http://dx.doi.org/10.1109/itca52113.2020.00051.

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Vander Heiden, Matthew G. "Abstract IA10: Metabolic regulation of cell proliferation." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 27-30, 2018; Miami Beach, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm18-ia10.

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Reports on the topic "Cell proliferation"

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Baker, Nicholas E. Cell Proliferation, Cell Death, and Size Regulation. Fort Belvoir, VA: Defense Technical Information Center, October 1998. http://dx.doi.org/10.21236/adb248354.

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Band, Hamid. Compartmentalized Signaling and Breast Cancer Cell Proliferation. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada400191.

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Band, Hamid. Compartmentalized Signaling and Breast Cancer Cell Proliferation. Fort Belvoir, VA: Defense Technical Information Center, July 2003. http://dx.doi.org/10.21236/ada431079.

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DeVries, George H. Molecular Mechanisms of Schwann Cell Proliferation in NF1. Fort Belvoir, VA: Defense Technical Information Center, September 2001. http://dx.doi.org/10.21236/ada407274.

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DeVries, George H. Molecular Mechanisms of Schwann Cell Proliferation in NF1. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada390950.

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DeVries, George H. Molecular Mechanisms of Schwann Cell Proliferation in NF1. Fort Belvoir, VA: Defense Technical Information Center, September 2000. http://dx.doi.org/10.21236/ada392306.

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Eckert, Richard L. TIG3-A Novel Inhibitor of Breast Cancer Cell Proliferation. Fort Belvoir, VA: Defense Technical Information Center, September 2003. http://dx.doi.org/10.21236/ada420065.

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Eckert, Richard L. TIG3 - A Novel Inhibitor of Breast Cancer Cell Proliferation. Fort Belvoir, VA: Defense Technical Information Center, September 2000. http://dx.doi.org/10.21236/ada391127.

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Fletterick, Robert J. Inhibition of Pancreatic Cancer Cell Proliferation by LRH-1 Inhibitors. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada599687.

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Balatoni, Julius A. New Positron-Emitting Probe for Imaging Cell Proliferation in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2005. http://dx.doi.org/10.21236/ada446271.

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