Relevant bibliographies by topics / Cancer cells – Proliferation

Academic literature on the topic 'Cancer cells – Proliferation'

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Published: 4 June 2021
Last updated: 11 February 2022

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Journal articles on the topic "Cancer cells – Proliferation"

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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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Cho, Min Soon, Justin Bottsford-Miller, Hernan G. Vasquez, Rebecca Stone, Behrouz Zand, Michael H. Kroll, Anil K. Sood, and Vahid Afshar-Kharghan. "Platelets increase the proliferation of ovarian cancer cells." Blood 120, no. 24 (December 6, 2012): 4869–72. http://dx.doi.org/10.1182/blood-2012-06-438598.

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Abstract Platelets promote metastasis and angiogenesis, but their effect on tumor cell growth is uncertain. Here we report a direct proliferative effect of platelets on cancer cells both in vitro and in vivo. Incubation of platelets with ovarian cancer cells from murine (ID8 and 2C6) or human (SKOV3 and OVCAR5) origin increased cell proliferation. The proliferative effect of platelets was not dependent on direct contact with cancer cells, and preincubation of platelets with blocking antibodies against platelet adhesion molecules did not alter their effect on cancer cells. The proliferative effect of platelets was reduced by fixing platelets with paraformaldehyde, preincubating platelets with a TGF-β1–blocking antibody, or reducing expression of TGF-βR1 receptor on cancer cells with siRNA. Infusing platelets into mice with orthotopic ovarian tumors significantly increased the proliferation indices in these tumors. Ovarian cancer patients with thrombocytosis had higher tumor proliferation indices compared with patients with normal platelet counts.
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Cho, Minsoon, Justin Bottsford-Miller, Behrouz Zand, Hernan G. Vasquez, Rebecca L. Stone, Michael H. Kroll, Anil K. Sood, and Vahid Afshar-Kharghan. "Platelets Promote Ovarian Cancer Growth: New Insights On Proliferation." Blood 120, no. 21 (November 16, 2012): 96. http://dx.doi.org/10.1182/blood.v120.21.96.96.

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Abstract Abstract 96 Introduction. Platelets can promote metastasis by a multitude of effects. We have recently shown that reducing platelet counts decreased the size and number of tumor nodules in a murine model of orthotopic ovarian cancer. Here, we report a previously unrecognized pro-proliferative effects of platelets on ovarian cancer cells, using in vivo and in vitro assays. Methods and Results. The proliferation rate of human and murine ovarian cancer cells increased significantly after coincubation with platelets (Figure 1A). This effect was platelet-specific, as red blood cells did not alter the proliferation rate. Direct contact between platelets and cancer cells or intact platelets was not required for the proliferative response. Furthermore, platelets isolated from tumor-bearing mice were similar to platelets from control mice in their proliferative effect (Figure 1B). Blocking platelet adhesive surface proteins (GPIba, GPIIbb3, and P-selectin) did not diminish the proliferative effect of platelets (Figure 1C) and aspirin only partially inhibited it (Figure 1D). Fixation of platelets with paraformaldehye (2%) completely eliminated the effect of platelets on proliferation of cancer cells (Figure 1D). To determine mechanism, we examined the effect of blocking antibody to TGFb1 and identified a dose-dependent inhibition of the proliferative effect of platelets on ovarian cancer cells by the anti-TGF b1 antibody. To confirm results obtained with the TGF b1-blocking antibody, we reduced expression of TGFbR1 receptors on ovarian cancer cells with siRNA prior to their incubation with platelets (Figure 1E). Consistent with results observed following treatment with the TGFb1-blocking antibody, TGFbR1 siRNA reduced proliferation of ovarian cancer cells (Figure 1F). To study the effect of platelets in vivo, we injected syngeneic platelets into mice with orthotopic ovarian cancer on a weekly basis for four weeks, and measured the proliferation index in the resected tumors using Ki67 staining. We found that mice receiving platelet infusions had a significantly higher percentage of Ki67 positivity compared to control tumor-bearing mice (83.5% vs 66.3%, respectively; p<0.0005). To extend these findings to human disease, we next measured proliferation indices in 20 tumor specimens collected from patients with ovarian cancer. Ten of these patients had thrombocytosis (> 450,000/ml) and 10 had normal platelet counts with an average of 284,000/ml. Thrombocytosis was associated with a higher percentage of Ki67 positivity in tumors (68% vs, 57%, respectively; p=0.03). Summary and conclusion. In summary, platelets significantly increase the proliferation of ovarian cancer cells. These results provide a new understanding of mechanisms by which platelets contribute to tumor progression. Disclosures: Kroll: Aplagon: Membership on an entity's Board of Directors or advisory committees; Optimer: Consultancy; Leo: Honoraria, Travel Expenses, Travel Expenses Other.
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Hubbard, Joleen M., and Axel Grothey. "Cancer Stem Cells and Cancer Stem Cell Inhibitors in Gastrointestinal Cancers." Oncology & Hematology Review (US) 12, no. 01 (2016): 41. http://dx.doi.org/10.17925/ohr.2016.12.01.41.

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Cancer stem cells (CSCs) are a subpopulation of phenotypically distinct cancer cells that may play an important role in tumor pathogenesis. The gastrointestinal (GI) system provides a good example for investigation of the role of CSCs in tumor proliferation; GI CSCs are suitable for study due to their abundance, proliferative potential, and consistent structural arrangement that is maintained under tightly controlled signaling pathways. GI stem cells have a long lifespan and this, combined with their rapid turnover, may predispose them to forming CSCs. Alternative possible sources of GI CSCs include differentiated intestinal cells, bone marrow, and cancer cells. Therapies that specifically target CSCs present an exciting opportunity to treat patients with cancer. Enhanced understanding of CSC markers, such as CD133, CD44, and epithelial cell adhesion molecule (EpCAM), may facilitate development of therapies that target them. Among the stemness pathways that have been targeted are Wnt/β-catenin, STAT, Notch, and Nanog.
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Harris, George, Raed Abu Ghazallah, David Nascene, Beverly Wuertz, and Frank G. Ondrey. "PPAR Activation and Decreased Proliferation in Oral Carcinoma Cells With 4-HPR." Otolaryngology–Head and Neck Surgery 133, no. 5 (November 2005): 695–701. http://dx.doi.org/10.1016/j.otohns.2005.07.019.

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OBJECTIVE: To explore whether the mechanism of action of 4-hydroxyphenylretinamide (4-HPR, fenretidine), a synthetic retinoid, involves the functional activation of the nuclear hormone receptor class known as PPARs (peroxisome proliferator-activated receptors). Also, to examine whether anti-proliferative effects of this agent in head and neck cancer cells occur at biologically relevant concentrations. STUDY DESIGN/METHODS: CA 9–22, NA, and UM SCC 11B cells were treated with 4-HPR during their log phase growth and functional activation of PPAR γ was evaluated by plate luminometry. Cellular proliferation was analyzed by standard MTT cell proliferation assays and cell counting. Student's t tests were performed for all experiments. RESULTS: Significant dose-dependent increases in PPAR γ activation occurred in response to 4-HPR treatment. Proliferation was significantly inhibited by 4-HPR in a dose-dependent manner as judged by MTT and cell counting assays. These effects occurred at equimolar concentrations in both types of experiments within a range of clinically achievable doses (1–4 μM) of 4-HPR. CONCLUSIONS: 4-HPR can functionally activate PPAR γ at clinically achievable doses. Decreased cancer cell proliferation secondary to PPAR γ activation has been observed in other malignancies as well as upper aerodigestive cancer. PPAR γ activation by 4-HPR represents another potential anti-cancer mechanism of action for this drug. CLINICAL SIGNIFICANCE: PPAR γ activation represents a novel target for anti-cancer therapy for head and neck cancer and the current level of clinical toxicity of 4-HPR would be judged acceptable to utilize this agent alone or in combination chemotherapy.
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Isazadeh, Alireza, Saba Hajazimian, Behrouz Shadman, Sahar Safaei, Ahmad Babazadeh Bedoustani, Reza Chavoshi, Dariush Shanehbandi, Mohammadreza Mashayekhi, Mohammadreza Nahaei, and Behzad Baradaran. "Anti-Cancer Effects of Probiotic Lactobacillus acidophilus for Colorectal Cancer Cell Line Caco-2 through Apoptosis Induction." Pharmaceutical Sciences 27, no. 2 (October 2, 2020): 262–67. http://dx.doi.org/10.34172/ps.2020.52.

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Background: Colorectal cancer is one of the most common cancers worldwide. Probiotics are useful and non-pathogenic microorganisms in the gastrointestinal tract, which can show anticancer activity through the induction of apoptosis. This study aimed to evaluate the antiproliferative effects of Lactobacillus acidophilus probiotic on the Caco-2 colorectal cancer cell line. Methods: The supernatant (secreted metabolites) and bacterial extract of L. acidophilus probiotics were prepared and used as an anti-proliferative agent on the colorectal cancer cell line, Caco-2 in vitro. The effects of supernatant and extract of L. acidophilus were evaluated on the viability and proliferation of cancer cells using MTT assay. Moreover, morphological alterations of cancer cells treated with supernatant and extract of L. acidophilus were evaluated by an inverted phase contrast microscope. The mRNA expression levels of apoptosis-related genes (SURVIVIN and SMAC) in treated cancer cells and untreated controls were evaluated using the Real-Time PCR method. Results: The results showed that the supernatant and extract of L. acidophilus inhibited the viability and proliferation of cancer cells in a dose and time-dependent manner. Moreover, various morphological alterations were observed in the treated cancer cells, which are indicators of apoptosis induction. The mRNA expression of SURVIVIN and SMAC genes were significantly up-regulated and downregulated in the treated cancer cells, respectively. Conclusion: The results of the present study suggested that the supernatant and extract of L.acidophilus could inhibit the viability and proliferation of colorectal cancer cell line, Caco-2through induction of apoptosis, increase the survival rate of colon cancer patients.
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Chen, Qi, Victoria Rutten, Wei-Tzu Cheng, Mancy Tong, Jia Wei, Peter Stone, Lai-Ming Ching, and Lawrence W. Chamley. "Phagocytosis of Extracellular Vesicles Extruded From the Placenta by Ovarian Cancer Cells Inhibits Growth of the Cancer Cells." International Journal of Gynecologic Cancer 28, no. 3 (March 2018): 545–52. http://dx.doi.org/10.1097/igc.0000000000001140.

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ObjectiveOvarian cancer is a common gynecological cancer, and parity is negatively associated with the incidence of this disease. This negative association is hypothesized to be due in part to shifting the balance of estrogen and progesterone toward more progesterone and reduced ovulation during pregnancy. However, studies suggested that parity is also associated with estrogen-independent gynecological cancers suggesting balance of hormones may not be the only protective factor. Extracellular vesicles (EVs) play an important role in cell-to-cell communication in physiological and pathological conditions. During pregnancy, large amounts of EVs are extruded from the placenta, and they seem to be involved in the remarkable adaptation of a woman's body to normal pregnancy. We hypothesized that EVs extruded from the placenta play a role in this protective effect.MethodsPlacental EVs were collected from first-trimester placentae, and cancer cell EVs were isolated from ovarian cancer cells. The EVs were exposed to ovarian cancer cells for 48 hours. The proliferation of cancer cells and the cell cycle were measured. In addition, phagocytosis of deported placental EVs by cancer cells was also measured.ResultsThe proliferation of cancer cells was significantly reduced by treatment with placental EVs (P = 0.001, analysis of variance), but not EVs from monocytes (P = 0.195), compared with untreated cancer cells. Furthermore, placental EVs also prevented the proliferation of cancer cells induced by cancer cell–derived EVs (P = 0.001). This inhibition of proliferation of ovarian cancer cells was partially due to phagocytosis of placental EVs by cancer cells. Phagocytosis of placental EVs delayed progression through the cell cycle. Calreticulin, a phagocytic “eat me” signal carried by placental EVs significantly inhibited ovarian cancer growth (P = 0.001).ConclusionsOur data demonstrated that EVs extruded from the placenta prevented ovarian cancer cell growth by a mechanism that involved delaying progression of the cell cycle after phagocytosis of the EVs.
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Subramaniam, Kavita S., Seng Tian Tham, Zahurin Mohamed, Yin Ling Woo, Noor Azmi Mat Adenan, and Ivy Chung. "Cancer-Associated Fibroblasts Promote Proliferation of Endometrial Cancer Cells." PLoS ONE 8, no. 7 (July 26, 2013): e68923. http://dx.doi.org/10.1371/journal.pone.0068923.

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Paiboon, Nitchapon, Witchayaporn Kamprom, Sirikul Manochantr, Chairat Tantrawatpan, Duangrat Tantikanlayaporn, Sittiruk Roytrakul, and Pakpoom Kheolamai. "Gestational Tissue-Derived Human Mesenchymal Stem Cells Use Distinct Combinations of Bioactive Molecules to Suppress the Proliferation of Human Hepatoblastoma and Colorectal Cancer Cells." Stem Cells International 2019 (July 4, 2019): 1–15. http://dx.doi.org/10.1155/2019/9748795.

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Background. Cancer has been considered a serious global health problem and a leading cause of morbidity and mortality worldwide. Despite recent advances in cancer therapy, treatments of advance stage cancers are mostly ineffective resulting in poor survival of patients. Recent evidences suggest that multipotent human mesenchymal stem cells (hMSCs) play important roles in growth and metastasis of several cancers by enhancing their engraftment and inducing tumor neovascularization. However, the effect of hMSCs on cancer cells is still controversial because there are also evidences demonstrating that hMSCs inhibited growth and metastasis of some cancers. Methods. In this study, we investigated the effects of bioactive molecules released from bone marrow and gestational tissue-derived hMSCs on the proliferation of various human cancer cells, including C3A, HT29, A549, Saos-2, and U251. We also characterized the hMSC-derived factors that inhibit cancer cell proliferation by protein fractionation and mass spectrometry analysis. Results. We herein make a direct comparison and show that the effects of hMSCs on cancer cell proliferation and migration depend on both hMSC sources and cancer cell types and cancer-derived bioactive molecules did not affect the cancer suppressive capacity of hMSCs. Moreover, hMSCs use distinct combination of bioactive molecules to suppress the proliferation of human hepatoblastoma and colorectal cancer cells. Using protein fractionation and mass spectrometry analysis, we have identified several novel hMSC-derived factors that might be able to suppress cancer cell proliferation. Conclusion. We believe that the procedure developed in this study could be used to discover other therapeutically useful molecules released by various hMSC sources for a future in vivo study.
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Futakuchi, Mitsuru, Kris Lami, Yuri Tachibana, Yukari Yamamoto, Masahiro Furukawa, and Junya Fukuoka. "The Effects of TGF-β Signaling on Cancer Cells and Cancer Stem Cells in the Bone Microenvironment." International Journal of Molecular Sciences 20, no. 20 (October 15, 2019): 5117. http://dx.doi.org/10.3390/ijms20205117.

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Background: Transforming growth factor-β (TGF-β) plays a key role in bone metastasis formation; we hypothesized the possible involvement of TGF-β in the induction of cancer stem cells (CSCs) in the bone microenvironment (micro-E), which may be responsible for chemo-resistance. Methods: Mouse mammary tumor cells were implanted under the dorsal skin flap over the calvaria and into a subcutaneous (subQ) lesions in female mice, generating tumors in the bone and subQ micro-Es. After implantation of the tumor cells, mice were treated with a TGF-β R1 kinase inhibitor (R1-Ki). Results: Treatment with R1-Ki decreased tumor volume and cell proliferation in the bone micro-E, but not in the subQ micro-E. R1-Ki treatment did not affect the induction of necrosis or apoptosis in either bone or subQ micro-E. The number of cells positive for the CSC markers, SOX2, and CD166 in the bone micro-E, were significantly higher than those in the subQ micro-E. R1-Ki treatment significantly decreased the number of CSC marker positive cells in the bone micro-E but not in the subQ micro-E. TGF-β activation of the MAPK/ERK and AKT pathways was the underlying mechanism of cell proliferation in the bone micro-E. BMP signaling did not play a role in cell proliferation in either micro-E. Conclusion: Our results indicated that the bone micro-E is a key niche for CSC generation, and TGF-β signaling has important roles in generating CSCs and tumor cell proliferation in the bone micro-E. Therefore, it is critically important to evaluate responses to chemotherapeutic agents on both cancer stem cells and proliferating tumor cells in different tumor microenvironments in vivo.
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Dissertations / Theses on the topic "Cancer cells – Proliferation"

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Harnagea, Theophilus Eugenia. "Acetaminophen stimulates proliferation of breast cancer cells." Morgantown, W. Va. : [West Virginia University Libraries], 1999. http://etd.wvu.edu/templates/showETD.cfm?recnum=773.

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Thesis (Ph. D.)--West Virginia University, 1999.
Title from document title page. Document formatted into pages; contains ix, 137 p. : ill. Vita. Includes abstract. Includes bibliographical references (p. 115-134).
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Liu, Po-shiu Jackie. "Effects of flavonoids on proliferation of breast cancer cells and vascular smooth muscle cells /." View the Table of Contents & Abstract, 2007. http://sunzi.lib.hku.hk/hkuto/record/B38480189.

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廖寶韶 and Po-shiu Jackie Liu. "Effects of flavonoids on proliferation of breast cancer cells and vascular smooth muscle cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B45011394.

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Pfeiffer, Thomas J. "Phytoestrogens may inhibit proliferation of MCF-7 cells, an estrogen-responsive breast adenocarcinoma cell line." Link to electronic thesis, 2004. http://www.wpi.edu/Pubs/ETD/Available/etd-0430104-132238.

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Ng, Wai Yee. "Ginsenosides on the growth and proliferation of glial tumor cells." HKBU Institutional Repository, 2008. http://repository.hkbu.edu.hk/etd_ra/998.

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Fancher, Karen. "Transcriptional Alterations during Mammary Tumor Progression in Mice and Humans." Fogler Library, University of Maine, 2008. http://www.library.umaine.edu/theses/pdf/FancherK2008.pdf.

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SIPES, NANCY JO. "GROWTH REGULATION OF HUMAN MELANOMA: FACTORS INVOLVED IN THE EXPRESSION OF THE TRANSFORMED PHENOTYPE (SOFT AGAR, GROWTH FACTORS, PLATELETS, ENDOTHELIAL CELLS, PARACRINE)." Diss., The University of Arizona, 1986. http://hdl.handle.net/10150/183788.

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Cellular transformation is accomplished in vitro through the concerted action of growth factors and oncogenes. This association has demonstrated that malignant growth results from aberrations in pathways that normally operate to control proliferation. Activation of genes that code for growth factors, their receptors, and/or molecules essential in the transduction of signals from the cell surface to the nucleus are all potential mechanisms by which tumor cells could establish a selective growth advantage over normal cells. This dissertation addresses the question of what oncogenic mechanisms are important in the development and progression of human melanoma. These studies show that melanoma growth is regulated by endogenous substances produced by the melanoma cells themselves (autocrine stimulation), as well as by exogenous substances supplied by neighboring cells and platelets (paracrine stimulation). These factors work to drive the expression of the transformed phenotype for melanoma as evidenced by induction of serum-free soft agar growth. Human platelets were found to the the richest source of paracrine growth promoters. The factor from human platelets was characterized and partially purified. Melanoma cells respond to this 60,000 molecular weight, disulfide-bond-containing protein in colony formation assays. In addition, the protein has endothelial cell growth factor activity. Purified fractions which promoted optimal colony formation for human melanoma cells also maximally stimulated monolayer growth of bovine aortic endothelial cells, while melanocytes were nonresponsive. This implies that melanoma cells are expressing receptors for a protein which plays no known or apparent role in the normal growth of melanocytes. Melanoma cells are sensitive to growth regulatory molecules of autocrine and paracrine nature. This dissertation provides clues to the genetic lesions which have occurred in these melanoma cells to influence their proliferation. The aberrations appear to reside in those genes important in growth factor pathways at the level of endogenous production and misguided response to exogenous factors through receptor expression. We can not hope to fully inhibit the proliferation of tumor cells until we identify and understand those forces which drive their growth. These studies have increased our knowledge of those signals which stimulate melanoma cellular proliferation, and thus provide insight into important therapeutic targets.
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Fettig, Amy E. "Identification of cellular targets influenced by ectopic expression of TAL1 and LMO1 genes." Virtual Press, 2001. http://liblink.bsu.edu/uhtbin/catkey/1222830.

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Cancer has been a disease, which has generated intense research interest for many years. Misexpression of two oncoproteins, TAL 1 and LMO 1, has been found to help induce a particular type of leukemia, called T-cell acute lymphoblastic leukemia (T-ALL). Presently, it is not completely understood how these proteins induce leukemogenesis or what other cellular proteins they interact with to drive this progression. In this study, a series of experiments were conducted to identify downstream targets of TALI and LMO1. Using retroviral gene transfer, both genes were introduced, either singly or in combination, into a murine T-cell line called AKR-DP-603. Empty vectors were introduced as controls. In order to assay the effects of TALI and LMO I expression on expression of other proteins, a series of Western blots were completed on all populations of engineered cells. It was determined that there were differences in expression of Bcl-2 and p16 as indicated by differences in band intensities on the blots. This is important because it implies an effect on protein levels by TAL 1 and LMO 1. However, there were no differences in protein expression levels for Bax or cyclin D1. This suggests that TAL1 and LMOI do not have any regulatory effects on these proteins. In addition, apoptotic assays were completed on all populations of cells. The results of both a TUNEL assay and ethidium bromide/acridine orange staining protocol showed TAL1- and LMO1expressing cells to have an increase in cell survival under starvation conditions and a lower frequency of apoptosis. Statistical analysis verified significant difference in the apoptosis assays. The data suggests an up-regulation of anti-apoptotic proteins. The finding of this research allow a clearer understanding of the process of leukemogenesis and may lead to a development of better cancer treatments.
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Wang, Haizhen. "The C-Phycocyanin/Beta Protein Inhibits Cancer Cell Proliferation." unrestricted, 2008. http://etd.gsu.edu/theses/available/etd-04212008-155113/.

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Thesis (M.S.)--Georgia State University, 2008.
Title from file title page. Zhi-Ren Liu, committee chair; Delon W. Barfuss, Jenny J. Yang, committee members. Electronic text (69 p. : ill. (some col.)) : digital, PDF file. Description based on contents viewed June 11, 2008. Includes bibliographical references (p. 61-67).
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Hui, Cheuk-man, and 許卓文. "Role of Id-1 in proliferation and survival of esophageal carcinoma cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B29947492.

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Books on the topic "Cancer cells – Proliferation"

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

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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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Ito, Takaaki. Differentiation and proliferation of pulmonary neuroendocrine cells. Jena, Germany: Urban & Fischer, 1999.

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Cancer Stem Cell Workshop (2007? Berlin-Brandenburg Academy of Sciences and Humanities). Cancer stem cells: Novel concepts and prospects for tumor therapy. Edited by Wiestler O. D. 1956-, Haendler B, and Mumberg D. Berlin: Springer, 2007.

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Cancer Stem Cell Workshop (2007? Berlin-Brandenburg Academy of Sciences and Humanities). Cancer stem cells: Novel concepts and prospects for tumor therapy. Edited by Wiestler O. D. 1956-, Haendler B, and Mumberg D. Berlin: Springer, 2007.

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Meridith, Alan T. Handbook of prostate cancer cell research: Growth, signalling, and survival. New York: Nova Biomedical Books, 2009.

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Handbook of prostate cancer cell research: Growth, signalling, and survival. New York: Nova Biomedical Books, 2009.

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V, Pavlova Lyudmila, and Yakovlev Andrej Yu 1944-, eds. Biomathematical problems in optimization of cancer radiotherapy. Boca Raton: CRC Press, 1994.

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Ludlow, John W. Tumor suppressors: Involvement in human diseases, viral protein interactions, and growth regulation. Austin: R.G. Landes, 1994.

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Book chapters on the topic "Cancer cells – Proliferation"

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Antonio, Marjorie Justine, Cissy Zhang, and Anne Le. "Different Tumor Microenvironments Lead to Different Metabolic Phenotypes." In The Heterogeneity of Cancer Metabolism, 137–47. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65768-0_10.

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AbstractThe beginning of the twenty-first century offered new advances in cancer research, including new knowledge about the tumor microenvironment (TME). Because TMEs provide the niches in which cancer cells, fibroblasts, lymphocytes, and immune cells reside, they play a crucial role in cancer cell development, differentiation, survival, and proliferation. Throughout cancer progression, the TME constantly evolves, causing cancer cells to adapt to the new conditions. The heterogeneity of cancer, evidenced by diverse proliferation rates, cellular structures, metabolisms, and gene expressions, presents challenges for cancer treatment despite the advances in research. This chapter discusses how different TMEs lead to specific metabolic adaptations that drive cancer progression.
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Van Pham, Phuc. "Breast Cancer Stem Cell Culture and Proliferation." In SpringerBriefs in Stem Cells, 41–55. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-22020-8_4.

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Li, Ting, Christopher Copeland, and Anne Le. "Glutamine Metabolism in Cancer." In The Heterogeneity of Cancer Metabolism, 17–38. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65768-0_2.

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AbstractMetabolism is a fundamental process for all cellular functions. For decades, there has been growing evidence of a relationship between metabolism and malignant cell proliferation. Unlike normal differentiated cells, cancer cells have reprogrammed metabolism in order to fulfill their energy requirements. These cells display crucial modifications in many metabolic pathways, such as glycolysis and glutaminolysis, which include the tricarboxylic acid (TCA) cycle, the electron transport chain (ETC), and the pentose phosphate pathway (PPP) [1]. Since the discovery of the Warburg effect, it has been shown that the metabolism of cancer cells plays a critical role in cancer survival and growth. More recent research suggests that the involvement of glutamine in cancer metabolism is more significant than previously thought. Glutamine, a nonessential amino acid with both amine and amide functional groups, is the most abundant amino acid circulating in the bloodstream [2]. This chapter discusses the characteristic features of glutamine metabolism in cancers and the therapeutic options to target glutamine metabolism for cancer treatment.
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Zipori, Dov. "Self-Renewal, Induced Proliferation, and Autonomous Cell Growth Represent Distinct Modes of Cell Multiplication." In Cancer Stem Cells, 39–47. Hoboken, NJ: John Wiley & Sons, 2014. http://dx.doi.org/10.1002/9781118356203.ch3.

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Munoz, Jessian L., Jacqueline M. Park, Sarah A. Bliss, and Pranela Rameshwar. "Cancer Cell Dormancy: Potential Therapeutic Targets To Eradicate Cancer Cells Within the Niche." In Trends in Stem Cell Proliferation and Cancer Research, 559–71. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6211-4_21.

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Gires, Olivier. "Markers of Cancer Stem Cells and Their Functions." In Trends in Stem Cell Proliferation and Cancer Research, 533–58. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6211-4_20.

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Koeffler, H. Phillip. "Study of Differentiation and Proliferation of Leukemic Cells Using Myeloid Leukemia Cell Lines." In Cancer Treatment and Research, 27–68. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2581-9_2.

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Kahn, Suzana A., Ema Torrado, Dora Brites, and Vivaldo Moura-Neto. "Implications of Glioblastoma Stem Cells in Chemoresistance." In Trends in Stem Cell Proliferation and Cancer Research, 435–62. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6211-4_16.

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Tanimoto, Kotaro, Yu-Ching Huang, and Kazuo Tanne. "Proliferation of Bone Marrow-Derived Human Mesenchymal Stem Cells: Role of Enamel Matrix Proteins." In Stem Cells and Cancer Stem Cells, Volume 4, 139–45. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-2828-8_13.

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Liu, Yong, Haixia Lu, and Xinlin Chen. "Rat Embryonic Cortical Neural Stem Cells: Role of Hypoxia on Cell Proliferation and Differentiation." In Stem Cells and Cancer Stem Cells,Volume 3, 49–61. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-2415-0_6.

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Conference papers on the topic "Cancer cells – Proliferation"

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Said, Asaad, Lina Karam, Michael Berens, Zoe Lacroix, and Rosemary Renaut. "MIGRATION AND PROLIFERATION ANALYSIS FOR BLADDER CANCER CELLS." In 2007 4th IEEE International Symposium on Biomedical Imaging: From Nano to Macro. IEEE, 2007. http://dx.doi.org/10.1109/isbi.2007.356853.

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MacEwan, Melanie Elizabeth, Timmy O'Connell, Hong Zhao, Codrin Iacob, Nina Suslina, Augustine Moscatello, Edward Shin, Raj Tiwari, Zbigniew Darzynkiewicz, and Jan Geliebter. "Abstract 2122: Androgen decreases proliferation of thyroid cancer 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.am2014-2122.

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Taheri, Arash, Meisam Mohammadi-Amin, and Ali Habibpour-Ledari. "An Optimization Methodology for Cancer Growth Control Base on Breeder Genetic Algorithm-Finite Volume Coupling." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-203638.

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Cancer is a genetic disease caused by mutations in somatic cells. It appears to arise by a process in which an initial population of altered cells begins to proliferate abnormally. At each step, one cancerous cell acquires an additional mutation that gives it a selective advantage over its neighbors, such as more rapid growth, and the descendants of this cell become dominant within the cancer population. In culture, the proliferation of the most cancerous cells is not sensitive to density-dependent inhibition; therefore, cancerous cells usually continue growing to high cell densities.
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Kwong Soon, Thomas Tiong, Naohiro Hozumi, Rahma Rahavu Hutami, Sachiko Yoshida, Kyouichi Takanashi, and Kazuto Kobayashi. "Non-Invasive Intracellular Observation of Cancer Cells Associated with Proliferation." In 2018 IEEE International Ultrasonics Symposium (IUS). IEEE, 2018. http://dx.doi.org/10.1109/ultsym.2018.8580044.

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Sree, V. Gowri, C. Muthuraman, and Raji Sundararajan. "Anti-proliferation control of breast cancer cells using electric pulses." In 2015 IEEE 11th International Conference on the Properties and Applications of Dielectric Materials (ICPADM). IEEE, 2015. http://dx.doi.org/10.1109/icpadm.2015.7295233.

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Le Calvé, B., M. Bury, J. Saliba, T. Dal Maso, F. Lessard, C. Michiels, and V. Blank. "PO-117 Role of NFE2L3 in colon cancer by regulating cancer cells proliferation." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.158.

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Yamamura, Soichiro, Takeshi Chiyomaru, Shinichiro Fukuhara, Sharanjot Saini, Shahana Majid, Guoren Deng, Vary Shahryary, et al. "Abstract 5340: MicroRNA-720 promotes cell proliferation and invasion in prostate cancer cells." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5340.

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(Elliott), Bethtrice Thompson, Ana Cecilia Millena, Lilya Matyunina, Mengnan Zhang, Jin Zou, Guangdi Wang, Qiang Zhang, et al. "Abstract 4306: JunD-induced cell proliferation requires MYC signaling in prostate cancer cells." 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.sabcs18-4306.

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(Elliott), Bethtrice Thompson, Ana Cecilia Millena, Lilya Matyunina, Mengnan Zhang, Jin Zou, Guangdi Wang, Qiang Zhang, et al. "Abstract 4306: JunD-induced cell proliferation requires MYC signaling in prostate cancer cells." 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.am2019-4306.

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Patel, Sagar S., Ramesh Natarajan, and Rebecca L. Heise. "Mechanotransduction of Primary Cilia in Lung Adenocarcinoma." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80435.

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Lung cancer causes more than 1 million deaths worldwide annually [1]. In a recent study by the American Cancer Society in 2011, more than 221,000 new cases of lung cancers were reported [2]. Out of these, the mortality rate was found in roughly 70% of the cases [2]. Lung cancer is divided into two major categories: small cell and non-small cell. In the United States, non-small cell lung cancer accounts for 85% of all lung cancers and is considered the most common type of lung cancer [2]. It is usually resistant to chemotherapy, therefore making it extremely difficult to treat [3]. Furthermore adenocarcinomas, a type of non-small cell lung cancer, occur towards the periphery of the lungs and are the most common type accounting for 40–45% of all lung cancer cases [3]. Epithelial cells in the healthy lungs undergo stresses during inhalation and expiration of normal breathing. In addition to the forces of normal breathing, lung cancer cells may also experience abnormal mechanical forces due to pre-existing lung diseases such as asthma, bronchitis and chronic obstructive pulmonary disease or other tumor associated structural changes. These conditions can significantly alter the structure of the lungs and cell phenotype [4]. The change in the structure of the lungs affects the mechanical environment of the cells. Changes in extracellular (ECM) stiffness, cell stretch, and shear stress influence tumorigenesis and metastasis [5]. One mechanism through which the cells sense and respond to the cellular mechanical environment is through the primary cilia [6–7]. Primary cilia are non-motile, solitary structures formed from the cellular microtubules and protrude out of each cell. They have also been shown to play an important role in facilitating common cancer signaling pathways such as Sonic Hedgehog and Wnt/β-catenin signaling [8–9]. The objective of this study was to test the hypothesis that lung cancer cells respond to mechanical stimuli with the formation of primary cilia that are necessary for 3 hallmarks of tumor progression: proliferation, epithelial mesenchymal-transition, and migration.
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Reports on the topic "Cancer cells – Proliferation"

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Zhu, LIang. P16 Axie in Androgen-Dependent Proliferation of Prostate Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2001. http://dx.doi.org/10.21236/ada397994.

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Zhu, Liang. P16 Axis in Androgen-Dependent Proliferation of Prostate Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2003. http://dx.doi.org/10.21236/ada416499.

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Zhu, Liang. P16 Axis in Androgen-Dependent Proliferation of Prostate Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2002. http://dx.doi.org/10.21236/ada406854.

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Zhu, Liang. P16 Axis in Androgen-Dependent Proliferation of Prostate Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2004. http://dx.doi.org/10.21236/ada427114.

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Tan, Huaming, and John Koland. Regulatory Pathways Involved in Heregulin-Induced Proliferation and Differentiation of Human Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, May 2000. http://dx.doi.org/10.21236/ada391701.

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Guo, Xuning E. Pilot Study on Factors Secreted by Differentiating Mammary Epithelial Cells (MECs) That Can Suppress Proliferation of Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, October 2007. http://dx.doi.org/10.21236/ada492688.

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Li, Jing. Effects of oxymatrine on the proliferation of human liver cancer Bel-7404 cells: a protocol of systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review Protocols, April 2020. http://dx.doi.org/10.37766/inplasy2020.4.0026.

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Li, Jing. Effects of artemisinin on proliferation and apoptosis of human liver cancer HepG2 cells: a protocol of systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2020. http://dx.doi.org/10.37766/inplasy2020.4.0075.

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Weiser, Douglas C. The Role of GADD34 (Growth Arrest and DNA Damage-Inducible Protein) in Regulating Apoptosis, Proliferation, and Protein Synthesis in Human Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, July 2003. http://dx.doi.org/10.21236/ada418759.

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Weiser, Douglas C. The Role of GADD34 (Growth Arrest and DNA Damage-Inducible Protein) in Regulating Apoptosis, Proliferation, and Protein Synthesis in Human Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada427916.

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