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Journal articles on the topic 'Cellular Proliferation'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Yao, Guang. "Modelling mammalian cellular quiescence." Interface Focus 4, no. 3 (2014): 20130074. http://dx.doi.org/10.1098/rsfs.2013.0074.

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Cellular quiescence is a reversible non-proliferating state. The reactivation of ‘sleep-like’ quiescent cells (e.g. fibroblasts, lymphocytes and stem cells) into proliferation is crucial for tissue repair and regeneration and a key to the growth, development and health of higher multicellular organisms, such as mammals. Quiescence has been a primarily phenotypic description (i.e. non-permanent cell cycle arrest) and poorly studied. However, contrary to the earlier thinking that quiescence is simply a passive and dormant state lacking proliferating activities, recent studies have revealed that

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2

Hatchell, D. L., T. McAdoo, S. Sheta, R. T. King, and J. V. Bartolome. "Quantification of Cellular Proliferation in Experimental Proliferative Vitreoretinopathy." Archives of Ophthalmology 106, no. 5 (1988): 669–72. http://dx.doi.org/10.1001/archopht.1988.01060130731033.

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3

Rubtsova, Maria P., Denis A. Nikishin, Mikhail Y. Vyssokikh, Maria S. Koriagina, Andrey V. Vasiliev, and Olga A. Dontsova. "Telomere Reprogramming and Cellular Metabolism: Is There a Link?" International Journal of Molecular Sciences 25, no. 19 (2024): 10500. http://dx.doi.org/10.3390/ijms251910500.

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Telomeres—special DNA–protein structures at the ends of linear eukaryotic chromosomes—define the proliferation potential of cells. Extremely short telomeres promote a DNA damage response and cell death to eliminate cells that may have accumulated mutations after multiple divisions. However, telomere elongation is associated with the increased proliferative potential of specific cell types, such as stem and germ cells. This elongation can be permanent in these cells and is activated temporally during immune response activation and regeneration processes. The activation of telomere lengthening m

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4

Zhang, Jian Chun, Howard E. Savage, Peter G. Sacks, et al. "Innate cellular fluorescence reflects alterations in cellular proliferation." Lasers in Surgery and Medicine 20, no. 3 (1997): 319–31. http://dx.doi.org/10.1002/(sici)1096-9101(1997)20:3<319::aid-lsm11>3.0.co;2-8.

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5

Calderón, Christian G., and Francisco Arvelo. "Kca3.1-Related Cellular Signalling Involved in Cancer Proliferation." Cellular Physiology and Biochemistry 58, no. 1 (2024): 107–27. http://dx.doi.org/10.33594/000000688.

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Anomalous expression of potassium channels in cancer tissues is associated with several cancer hallmarks that support deregulated proliferation and tumor progression. Ion channels seem to influence cell proliferation; however, the crucial molecular mechanisms involved remain elusive. Some results show how extracellular mitogenic signals modulate ion channel activity through intracellular secondary messengers. It is relevant because we are beginning to understand how potassium channels can affect the proliferative capacity of cells, either in normal mitogen-dependent proliferation or in mitogen

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6

CLARKE, CHRISTINE L., and ROBERT L. SUTHERLAND. "Progestin Regulation of Cellular Proliferation*." Endocrine Reviews 11, no. 2 (1990): 266–301. http://dx.doi.org/10.1210/edrv-11-2-266.

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7

Lenkala, Divya, Eric R. Gamazon, Bonnie LaCroix, Hae Kyung Im, and R. Stephanie Huang. "MicroRNA biogenesis and cellular proliferation." Translational Research 166, no. 2 (2015): 145–51. http://dx.doi.org/10.1016/j.trsl.2015.01.012.

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8

Mankoff, David A., Anthony F. Shields, and Kenneth A. Krohn. "PET imaging of cellular proliferation." Radiologic Clinics of North America 43, no. 1 (2005): 153–67. http://dx.doi.org/10.1016/j.rcl.2004.09.005.

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9

VINCENT, P. C. "Leukemic Cellular Proliferation: A Perspective." Annals of the New York Academy of Sciences 459, no. 1 Hematopoietic (1985): 308–27. http://dx.doi.org/10.1111/j.1749-6632.1985.tb20839.x.

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10

Zlotorynski, Eitan, and Reuven Agami. "A PASport to Cellular Proliferation." Cell 134, no. 2 (2008): 208–10. http://dx.doi.org/10.1016/j.cell.2008.07.003.

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11

Verdoorn, Cornelis. "Cellular Migration, Proliferation, and Contraction." Archives of Ophthalmology 104, no. 8 (1986): 1216. http://dx.doi.org/10.1001/archopht.1986.01050200122064.

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12

Abrisqueta, Pau, Neus Villamor, Ana Muntañola, et al. "Biological Analysis and Prognostic Significance of Proliferative Cellular Compartment in Chronic Lymphocytic Leukemia (CLL)." Blood 114, no. 22 (2009): 667. http://dx.doi.org/10.1182/blood.v114.22.667.667.

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Abstract Abstract 667 Historically CLL has been considered a non-proliferative disease characterized by accumulation of leukemic cells. However, recent clinical and biological observations are questioning this concept. From the clinical standpoint, although some patients have lymphocyte counts stable during the course of the disease, others exhibit a short lymphocyte doubling time, suggesting the existence of a significant cell proliferation. Some specific anatomic locations (bone marrow (BM) and lymph nodes) seem to be more prone to proliferation than peripheral blood (PB). The amount of cell

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13

Chevalier, Robert L., Barbara A. Thornhill, and Jennifer T. Wolstenholme. "Renal cellular response to ureteral obstruction: role of maturation and angiotensin II." American Journal of Physiology-Renal Physiology 277, no. 1 (1999): F41—F47. http://dx.doi.org/10.1152/ajprenal.1999.277.1.f41.

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Renal angiotensin II (ANG II) is increased as a result of unilateral ureteral obstruction (UUO), and angiotensin AT2 receptors predominate over AT1 receptors in the early postnatal period. To examine the renal cellular response to 3-day UUO in the neonatal and adult rat, AT1and AT2 receptors were inhibited by losartan and PD-123319, respectively. Additional rats received exogenous ANG II, 0.5 mg ⋅ kg−1 ⋅ day−1. Renal cellular proliferation and apoptosis were quantitated by proliferating cell nuclear antigen and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling techni

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14

Chan, Jenq-Shyong, Yang Wang, Virgilius Cornea, Prabir Roy-Chaudhury, and Begoña Campos. "Early Adventitial Activation and Proliferation in a Mouse Model of Arteriovenous Stenosis: Opportunities for Intervention." International Journal of Molecular Sciences 22, no. 22 (2021): 12285. http://dx.doi.org/10.3390/ijms222212285.

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Background: Arteriovenous fistula (AVF) stenosis remains an important cause of AVF maturation failure, for which there are currently no effective therapies. We examined the pattern and phenotype of cellular proliferation at different timepoints in a mouse model characterized by a peri-anastomotic AVF stenosis. Methods: Standard immunohistochemical analyses for cellular proliferation and macrophage infiltration were performed at 2, 7 and 14 d on our validated mouse model of AVF stenosis to study the temporal profile, geographical location and cellular phenotype of proliferating and infiltrating

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15

Virgilio, Maria C., and Kathleen L. Collins. "The Impact of Cellular Proliferation on the HIV-1 Reservoir." Viruses 12, no. 2 (2020): 127. http://dx.doi.org/10.3390/v12020127.

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Human immunodeficiency virus (HIV) is a chronic infection that destroys the immune system in infected individuals. Although antiretroviral therapy is effective at preventing infection of new cells, it is not curative. The inability to clear infection is due to the presence of a rare, but long-lasting latent cellular reservoir. These cells harboring silent integrated proviral genomes have the potential to become activated at any moment, making therapy necessary for life. Latently-infected cells can also proliferate and expand the viral reservoir through several methods including homeostatic pro

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16

Yang, Chung-May, Karl R. Olsen, Eleut Hernandez, and Scott W. Cousins. "Measurement of cellular proliferation within the vitreous during experimental proliferative vitreoretinopathy." Graefe's Archive for Clinical and Experimental Ophthalmology 230, no. 1 (1992): 66–71. http://dx.doi.org/10.1007/bf00166765.

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17

Boerner, Brian P., Nicholas M. George, Natalie M. Targy та Nora E. Sarvetnick. "TGF-β Superfamily Member Nodal Stimulates Human β-Cell Proliferation While Maintaining Cellular Viability". Endocrinology 154, № 11 (2013): 4099–112. http://dx.doi.org/10.1210/en.2013-1197.

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In an effort to expand human islets and enhance allogeneic islet transplant for the treatment of type 1 diabetes, identifying signaling pathways that stimulate human β-cell proliferation is paramount. TGF-β superfamily members, in particular activin-A, are likely involved in islet development and may contribute to β-cell proliferation. Nodal, another TGF-β member, is present in both embryonic and adult rodent islets. Nodal, along with its coreceptor, Cripto, are pro-proliferative factors in certain cell types. Although Nodal stimulates apoptosis of rat insulinoma cells (INS-1), Nodal and Cript

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18

Zempleni, Janos, and Donald M. Mock. "Mitogen-induced proliferation increases biotin uptake into human peripheral blood mononuclear cells." American Journal of Physiology-Cell Physiology 276, no. 5 (1999): C1079—C1084. http://dx.doi.org/10.1152/ajpcell.1999.276.5.c1079.

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We sought to determine whether the proliferation of immune cells affects the cellular uptake of the vitamin biotin. Peripheral blood mononuclear cells (PBMC) were isolated from healthy adults. The proliferation of PBMC was induced by either pokeweed lectin, concanavalin A, or phytohemagglutinin. When the medium contained a physiological concentration of [3H]biotin, nonproliferating PBMC accumulated 406 ± 201 amol [3H]biotin ⋅ 106cells−1 ⋅ 30 min−1. For proliferating PBMC, [3H]biotin uptake increased to between 330 and 722% of nonproliferating values. Maximal transport rates of [3H]biotin in pr

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19

Lopez-Rodriguez, Maria, Alma Viso, Silvia Ortega-Gutierrez, and Ines Diaz-Laviadac. "Involvement of Cannabinoids in Cellular Proliferation." Mini-Reviews in Medicinal Chemistry 5, no. 1 (2005): 97–106. http://dx.doi.org/10.2174/1389557053402819.

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20

Radhika, M., Mary Babu, and P. K. Sehgal. "Cellular proliferation on desamidated collagen matrices." Comparative Biochemistry and Physiology Part C: Pharmacology, Toxicology and Endocrinology 124, no. 2 (1999): 131–39. http://dx.doi.org/10.1016/s0742-8413(99)00042-0.

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21

Castro⁎, J. P., and H. Almeida. "Actin carbonylated aggregates impair cellular proliferation." Free Radical Biology and Medicine 53 (September 2012): S207—S208. http://dx.doi.org/10.1016/j.freeradbiomed.2012.08.435.

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22

IIJIMA, MISA. "CELLULAR DIFFERENTIATION AND PROLIFERATION IN MEDULLOBLASTOMA." KITAKANTO Medical Journal 46, no. 6 (1996): 471–82. http://dx.doi.org/10.2974/kmj1951.46.471.

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23

Guiotto, Paolo. "A Statistical Model for Cellular Proliferation." Stochastic Analysis and Applications 21, no. 6 (2003): 1283–303. http://dx.doi.org/10.1081/sap-120026107.

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24

Brasitus, T. A. "Calcium, cellular proliferation, and colon cancer." Gastroenterology 93, no. 3 (1987): 654–55. http://dx.doi.org/10.1016/0016-5085(87)90932-2.

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25

McDowell, Kristy L., Lesa A. Begley, Nirit Mor-Vaknin, David M. Markovitz, and Jill A. Macoska. "Leukocytic promotion of prostate cellular proliferation." Prostate 70, no. 4 (2009): 377–89. http://dx.doi.org/10.1002/pros.21071.

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26

Gao, Y., U. Simanainen, and D. J. Handelsman. "138. REGION- AND TIME-DEPENDENT CHANGES IN STRUCTURE AND CELLULAR TURNOVER IN ANDROGEN DEPRIVED MOUSE EPIDIDYMIS." Reproduction, Fertility and Development 21, no. 9 (2009): 57. http://dx.doi.org/10.1071/srb09abs138.

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Epididymal maturation of spermatozoa including acquisition of motility and fertilizing ability depends on androgens both directly from testis and indirectly via the circulation. Androgen action via androgen receptor (AR) can cause both proliferative and anti-proliferative effects (1,2) so we have analysed changes in mouse epididymis following androgen deprivation either by orchidectomy or in prostate epithelial AR knockout (PEARKO) males with reduced androgen action also in epididymis (3). Structural changes (stereology), proliferation (PCNA) and apoptosis (TUNEL) were compared between mature

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27

Jacobs, Jacqueline J. L., and Maarten van Lohuizen. "Polycomb repression: from cellular memory to cellular proliferation and cancer." Biochimica et Biophysica Acta (BBA) - Reviews on Cancer 1602, no. 2 (2002): 151–61. http://dx.doi.org/10.1016/s0304-419x(02)00052-5.

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28

Saha, Naresh, Ashutosh K. Dubey, and Bikramjit Basu. "Cellular proliferation, cellular viability, and biocompatibility of HA-ZnO composites." Journal of Biomedical Materials Research Part B: Applied Biomaterials 100B, no. 1 (2011): 256–64. http://dx.doi.org/10.1002/jbm.b.31948.

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29

Aw, Tak Yee. "Cellular Redox: A Modulator of Intestinal Epithelial Cell Proliferation." Physiology 18, no. 5 (2003): 201–4. http://dx.doi.org/10.1152/nips.01448.2003.

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Mucosal proliferation, together with differentiation and apoptosis, are a continuous homeostatic process in the intestinal epithelium. The glutathione/glutathione disulfide redox status plays a key role in intestinal growth control wherein a reduced redox potential maintains a proliferative state. An oxidative shift in this potential elicits growth arrest and cell transition to a differentiated or apoptotic phenotype.

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30

Martín-Sanz, Raquel, José María Sayagués, Pilar García-Cano, et al. "TP53 Abnormalities and MMR Preservation in 5 Cases of Proliferating Trichilemmal Tumours." Dermatopathology 8, no. 2 (2021): 147–58. http://dx.doi.org/10.3390/dermatopathology8020021.

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Proliferating trichilemmal tumours (PTT) are defined by a benign squamous cell proliferation inside a trichilemmal cystic (TC) cavity. A possible explanation of this proliferative phenomenon within the cyst may be molecular alterations in genes associated to cell proliferation, which can be induced by ultraviolet radiation. Among other genes, alterations on TP53 and DNA mismatch repair proteins (MMR) may be involved in the cellular proliferation observed in PTT. Based on this assumption, but also taking into account the close relationship between the sebaceous ducts and the external root sheat

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31

Henriques, S., E. Silva, S. Cruz, et al. "Oestrous cycle-dependent expression of Fas and Bcl2 family gene products in normal canine endometrium." Reproduction, Fertility and Development 28, no. 9 (2016): 1307. http://dx.doi.org/10.1071/rd14245.

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During the oestrous cycle canine endometrium undergoes cyclical cellular proliferation, apoptosis and differentiation. To study the regulation of endometrial apoptosis and proliferation events the expression of apoptosis-related genes was analysed by real-time polymerase chain reaction and cellular expression of their proteins was identified through immunohistochemistry. Cellular apoptosis and proliferation events were detected by TdT-mediated dUTP-biotin nick end labeling (TUNEL) and proliferation marker Ki67 immunostaining, respectively. The highest proliferative index was observed in the fo

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32

Wang, Zheng, Evelyn E. Gurule, Timothy P. Brennan, et al. "Expanded cellular clones carrying replication-competent HIV-1 persist, wax, and wane." Proceedings of the National Academy of Sciences 115, no. 11 (2018): E2575—E2584. http://dx.doi.org/10.1073/pnas.1720665115.

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The latent reservoir for HIV-1 in resting CD4+ T cells is a major barrier to cure. Several lines of evidence suggest that the latent reservoir is maintained through cellular proliferation. Analysis of this proliferative process is complicated by the fact that most infected cells carry defective proviruses. Additional complications are that stimuli that drive T cell proliferation can also induce virus production from latently infected cells and productively infected cells have a short in vivo half-life. In this ex vivo study, we show that latently infected cells containing replication-competent

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33

Yao, Guang. "Quiescence-Origin Senescence: A New Paradigm in Cellular Aging." Biomedicines 12, no. 8 (2024): 1837. http://dx.doi.org/10.3390/biomedicines12081837.

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Cellular senescence, traditionally viewed as a consequence of proliferating and growing cells overwhelmed by extensive stresses and damage, has long been recognized as a critical cellular aging mechanism. Recent research, however, has revealed a novel pathway termed “quiescence-origin senescence”, where cells directly transition into senescence from the quiescent state, bypassing cell proliferation and growth. This opinion paper presents a framework conceptualizing a continuum between quiescence and senescence with quiescence deepening as a precursor to senescence entry. We explore the trigger

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34

Hwang, Hyun Sook, Dong Won Kim, and Soung Soo Kim. "Structure–activity relationships of the human prothrombin kringle-2 peptide derivative NSA9: anti-proliferative activity and cellular internalization." Biochemical Journal 395, no. 1 (2006): 165–72. http://dx.doi.org/10.1042/bj20051300.

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The human prothrombin kringle-2 protein inhibits angiogenesis and LLC (Lewis lung carcinoma) growth and metastasis in mice. Additionally, the NSA9 peptide (NSAVQLVEN) derived from human prothrombin kringle-2 has been reported to inhibit the proliferation of BCE (bovine capillary endothelial) cells and CAM (chorioallantoic membrane) angiogenesis. In the present study, we examined the structure–activity relationships of the NSA9 peptide in inhibiting the proliferation of endothelial cells lines e.g. BCE and HUVE (human umbilical vein endothelial). N- or C-terminal truncated derivatives and rever

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35

Roldán Gallardo, Franco F., Daniel E. Martínez Piñerez, Kevin F. Reinarz Torrado, et al. "Extracellular Vesicles Contribute to Oxidized LDL-Induced Stromal Cell Proliferation in Benign Prostatic Hyperplasia." Biology 13, no. 10 (2024): 827. http://dx.doi.org/10.3390/biology13100827.

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Background: Clinical and experimental evidence has linked Benign Prostatic Hyperplasia (BPH) with dyslipidemic and hypercholesterolemic conditions, though the underlying cellular mechanisms remain unclear. This study investigates the impact of dyslipidemia, specifically oxidized LDL (OxLDL), on prostatic stromal cell proliferation and the release of extracellular vesicles (EVs). Methods: Mice were fed a high-fat diet, and human prostatic stromal cells (HPSCs) were treated with OxLDL. Proliferation assays and EV characterization were performed to assess the role of EVs in BPH progression. Resul

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36

Meng, Qingbing, Jie Zhao, Hongbing Liu, et al. "HMGB1 promotes cellular proliferation and invasion, suppresses cellular apoptosis in osteosarcoma." Tumor Biology 35, no. 12 (2014): 12265–74. http://dx.doi.org/10.1007/s13277-014-2535-3.

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37

Roi, Ciprian, Mircea Riviș, Alexandra Roi, et al. "CD34 and Ki-67 Immunoexpression in Periapical Granulomas: Implications for Angiogenesis and Cellular Proliferation." Diagnostics 14, no. 21 (2024): 2446. http://dx.doi.org/10.3390/diagnostics14212446.

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Background/Objectives: The main mechanism of the formation of granulation tissue is the progression of an infection from the tooth to the periapical bone. At this level, the immune system tries to localize and annihilate the microorganism’s injury. Ki-67 is a protein directly associated with the cell proliferation rate, while CD34 is a biomarker involved in angiogenesis, and studies suggest that they both have a positive correlation with the intensity of the local inflammatory infiltrate. This study will determine the immunoexpression of CD34 and Ki-67 in periapical granulomas and assess their

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38

Tolok, O., and Kh Malysheva. "Regulation of proliferative potential: insights into key signaling cascades and te-lomerase functions." Scientific Messenger of LNU of Veterinary Medicine and Biotechnologies 26, no. 102 (2024): 85–90. https://doi.org/10.32718/nvlvet-f10213.

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Cell proliferation is a fundamental biological process that underpins tissue growth, repair, and regeneration, playing a pivotal role in both normal physiology and pathological conditions. The ability of cells to proliferate is intricately controlled by regulatory networks comprising transcription factors, signaling pathways, and telomerase activity. This review delves into the molecular mechanisms that govern cell proliferation, focusing on the critical signaling cascades – PI3K/Akt, MAPK, Wnt/β-catenin, and NF-κB – which orchestrate cell cycle progression and mediate cellular responses to ex

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39

Costantini, Lara, Romina Molinari, Barbara Farinon, Veronica Lelli, Anna Maria Timperio, and Nicolò Merendino. "Docosahexaenoic Acid Reverted the All-trans Retinoic Acid-Induced Cellular Proliferation of T24 Bladder Cancer Cell Line." Journal of Clinical Medicine 9, no. 8 (2020): 2494. http://dx.doi.org/10.3390/jcm9082494.

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The treatment of solid cancers with pharmacological all-trans retinoic acid (ATRA) concentrations, even if it is a gold standard therapy for the acute promyelocytic leukaemia (APL), is not always effective due to some resistance mechanisms. Here the resistance to ATRA treatment of T24 cell line, bladder cancer, was investigated. T24 was not only resistant to cell death when treated at concentrations up to 20 µM of ATRA, but it was also able to stimulate the cellular proliferation. An over-expression of the fatty acid binding protein 5 (FABP5) in conjunction with the cellular retinol-binding pr

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40

Gerthoffer, William T., Dedmer Schaafsma, Pawan Sharma, Saeid Ghavami, and Andrew J. Halayko. "Motility, Survival, and Proliferation." Comprehensive Physiology 2, no. 1 (2012): 255–81. https://doi.org/10.1002/j.2040-4603.2012.tb00408.x.

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AbstractAirway smooth muscle has classically been of interest for its contractile response linked to bronchoconstriction. However, terminally differentiated smooth muscle cells are phenotypically plastic and have multifunctional capacity for proliferation, cellular hypertrophy, migration, and the synthesis of extracellular matrix and inflammatory mediators. These latter properties of airway smooth muscle are important in airway remodeling which is a structural alteration that compounds the impact of contractile responses on limiting airway conductance. In this overview, we describe the importa

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41

Shani, Samuel, Raja Elina Ahmad, Sangeetha Vasudevaraj Naveen, et al. "Platelet Rich Concentrate Promotes Early Cellular Proliferation and Multiple Lineage Differentiation of Human Mesenchymal Stromal CellsIn Vitro." Scientific World Journal 2014 (2014): 1–12. http://dx.doi.org/10.1155/2014/845293.

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Platelet rich concentrate (PRC) is a natural adjuvant that aids in human mesenchymal stromal cell (hMSC) proliferationin vitro; however, its role requires further exploration. This study was conducted to determine the optimal concentration of PRC required for achieving the maximal proliferation, and the need for activating the platelets to achieve this effect, and if PRC could independently induce early differentiation of hMSC. The gene expression of markers for osteocytes (ALP, RUNX2), chondrocytes (SOX9, COL2A1), and adipocytes (PPAR-γ) was determined at each time point in hMSC treated with

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42

Wikle, Thomas A. "Cellular Tower Proliferation in the United States." Geographical Review 92, no. 1 (2002): 45. http://dx.doi.org/10.2307/4140950.

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43

Day, Regina M., and Yuichiro J. Suzuki. "Cell Proliferation, Reactive Oxygen and Cellular Glutathione." Dose-Response 3, no. 3 (2005): dose—response.0. http://dx.doi.org/10.2203/dose-response.003.03.010.

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A variety of cellular activities, including metabolism, growth, and death, are regulated and modulated by the redox status of the environment. A biphasic effect has been demonstrated on cellular proliferation with reactive oxygen species (ROS)—especially hydrogen peroxide and superoxide—in which low levels (usually submicromolar concentrations) induce growth but higher concentrations (usually >10–30 micromolar) induce apoptosis or necrosis. This phenomenon has been demonstrated for primary, immortalized and transformed cell types. However, the mechanism of the proliferative response to low

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44

Guinee, Donald G., Sherrie L. Perkins, William D. Travis, Joseph A. Holden, Sheryl R. Tripp, and Michael N. Koss. "Proliferation and Cellular Phenotype in Lymphomatoid Granulomatosis." American Journal of Surgical Pathology 22, no. 9 (1998): 1093–100. http://dx.doi.org/10.1097/00000478-199809000-00008.

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45

Shigihara, Yasushi, and Ricardo V. Lloyd. "Apoptosis and Cellular Proliferation in Skin Neoplasms." Applied Immunohistochemistry 5, no. 1 (1997): 29–34. http://dx.doi.org/10.1097/00022744-199703000-00005.

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46

Sabapathy, Kanaga, and Erwin F. Wagner. "JNK2: A Negative Regulator of Cellular Proliferation." Cell Cycle 3, no. 12 (2004): 1520–23. http://dx.doi.org/10.4161/cc.3.12.1315.

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47

Alison, MR. "Review : Assessing cellular proliferation: what's worth measuring?" Human & Experimental Toxicology 14, no. 12 (1995): 935–44. http://dx.doi.org/10.1177/096032719501401201.

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48

Wikle, Thomas A. "Cellular Tower Proliferation in the United States." Geographical Review 92, no. 1 (2002): 45–62. http://dx.doi.org/10.1111/j.1931-0846.2002.tb00133.x.

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Gutierrez-Herrera, E., A. E. Ortiz, A. Doukas, and W. Franco. "Fluorescence excitation photography of epidermal cellular proliferation." British Journal of Dermatology 174, no. 5 (2016): 1086–91. http://dx.doi.org/10.1111/bjd.14400.

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Aranda, Fignacio, and Juan B. Laforga. "Cellular Proliferation in Breast Ductal Infiltrating Carcinoma." Pathology - Research and Practice 193, no. 10 (1997): 683–88. http://dx.doi.org/10.1016/s0344-0338(97)80027-1.

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