PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Cell Proliferation”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 235 records · Page 13Linked to original sources
PubMed1993

Proliferation cell nuclear antigen (clone 19A2) correlates with 5-bromo-2-deoxyuridine labelling in human colonic epithelium.

Measurements of cell proliferation can be used as biomarkers of preneoplastic change. In this study, two immunocytochemical methods that measure different components of the cell cycle were compared to assess cell proliferation on biopsy samples from human colonic mucosa. These methods are based on a monoclonal antibody against 5-bromo-2-deoxyuridine (BrdU), which is confined to S phase cells, and a more broad assessment of proliferation based on an antibody against proliferating cell nuclear antigen (PCNA, clone 19A2). In the PCNA assay, only strongly immunostained nuclei were included. The proliferation index was assessed in colonic mucosa from patients with no colonic disorders. Correlation between individual total proliferation indices determined by either method was significant with rs = 0.6 (p < 0.05). The mean proliferation index in the study group was 7.79% using BrdU and 7.64% using PCNA immunocytochemistry. Distribution of labelled cells within crypts was similar with respect to the two methods with a peak at the 18th and the 24th percentile in the case of BrdU and at the 23rd percentile for PCNA. Variance component analysis showed that at least two biopsy specimens should be evaluated per subject to allow a precise individual characterisation. It is concluded that PCNA (19A2) immunocytochemistry may be used as an operational marker of cell proliferation in normal colonic mucosa. A significant correlation and an agreement in the mean proliferation index between PCNA (19A2) and BrdU can only be achieved by a strictly standardised enumeration of labelled cells limited to strongly stained nuclei in the PCNA evaluation.

Adult↗
PubMed1994

Cytotoxicity of the anticancer agents cisplatin and taxol during cell proliferation and the cell cycle.

The overt effects of the anti-cancer drugs cisplatin (cis-DDP) and taxol appear to be DNA modification and microtubule stabilization respectively, yet the mechanisms by which these drugs elicit tumor cell death are not well understood. In this report cell sensitivities to cis-DDP and taxol were accurately determined as a function of cell proliferation and cell cycle stage. Quiescent fibroblasts restimulated to synchronously enter the cell cycle become maximally sensitive to cis-DDP immediately preceding DNA synthesis, and resistance increases with onset of DNA synthesis. Mid-log proliferating cells were separated into progressive stages of the cell cycle by centrifugal elutriation or by double thymidine (dThd) block. Cells staged by either method are maximally sensitive to cis-DDP in G1, just prior to the onset of DNA synthesis and minimally sensitive in peak DNA synthesis, with entry into S phase resulting in a 2-fold decrease in sensitivity. Cells that remained blocked at the G1/S phase boundary during cis-DDP treatment remain maximally sensitive after release. Sensitivity to taxol increases at 2 points: transiently during transition of normal cells from quiescence to proliferation and steadily as proliferating cells progress from early G1 to late G2. This 3-fold increase in taxol sensitivity through the cell cycle is rapidly reversed upon cell division. Synchronous cells treated with either drug at points of maximum sensitivity initiate apoptotic DNA fragmentation 12-14 hr post-exposure to drug.

Cell Cycle↗
PubMed2006

Medaka simplet (FAM53B) belongs to a family of novel vertebrate genes controlling cell proliferation.

The identification of genes that regulate proliferation is of great importance to developmental biology, regenerative medicine and cancer research. Using an in situ screen on a cortical structure of the medaka fish brain, we identified the simplet gene (smp), which is homologous to the human FAM53B gene. smp was expressed in actively proliferating cells of the CNS throughout embryogenesis. It belongs to a family of vertebrate-specific genes with no characterized biochemical domains. We showed that FAM53B bound 14-3-3 chaperones, as well as SKIIP proteins, adaptor proteins connecting DNA-binding proteins to modulators of transcription. smp inactivation with morpholinos led to delayed epiboly and reduced embryonic size. Absence of Smp activity did not induce apoptosis, but resulted in a reduced cell proliferation rate and enlarged blastomeres. Moreover, smp was shown to control the expression of the pluripotency-associated oct4/pou5f1 gene. We propose that smp is a novel vertebrate-specific gene needed for cell proliferation and that it is probably associated with the maintenance of a pluripotent state.

14-3-3 Proteins↗
PubMed1997

Uterine leiomyosarcoma has deregulated cell proliferation, but not increased microvessel density compared with uterine leiomyoma.

OBJECTIVE: To investigate the differences of biological aggressiveness in terms of proliferating cell nuclear antigen (PCNA) expression, cell proliferation, and microvessel density between uterine leiomyosarcoma and leiomyoma. STUDY DESIGN: All patients with uterine leiomyosarcoma undergoing surgery at National Cheng Kung University Hospital were eligible. Forty-four patients with uterine myoma were also studied as the benign counterpart. The paraffin-embedded slides were stained with hematoxylin and eosin to confirm the presence of tumor and to quantitate mitoses, PC 10 for measurement of PCNA expression, MIB 1 for measurement of cell proliferation, and factor VIII for quantitation of microvessel density. The immunohistochemical findings of the slides were correlated with clinocopathologic findings of the patients, and the data were analyzed by either chi2 or unpaired t test. RESULTS: Six patients with uterine leiomyosarcoma and 44 patients with uterine leiomyoma were studied. Statistically significant higher mean levels of PCNA and MIB 1 were observed in uterine leiomyosarcoma compared with those of uterine myoma (for PCNA expression, P = 0.0001; for MIB 1, 11.61 +/- 11.42% vs 0.45 +/- 0.21%, P < 0.0001). No significant difference of microvessel density was observed between these two groups (65.73 +/- 48.62 vs 41.97 +/- 28.20, P = 0.084). Among the six patients with leiomyosarcoma, two patients with a higher percentage of MIB 1-positive tumor cells died of recurrent disease. In contrast, two patients with lower MIB 1 counts were disease-free for 3 years or more. CONCLUSION: Deregulated cell growth in uterine leiomyosarcoma may account for the biological aggressiveness of this tumor. Furthermore, the percentage of MIB 1-positive tumor cells seems to be associated with the prognosis or extent of uterine leiomyosarcoma.

Adult↗
PubMed1998

[Relationship between tumor cell proliferating activity and biological behavior, prognosis in laryngeal carcinoma].

Using PC 10, an antibody to proliferating cell nuclear antigen (PCNA) and a standard immunohistochemical staining the authors examined 11 cases of simple hyperplasia of epithelium (SHE), 32 cases of atypical hyperplasia of epithelium (AHE) and 42 cases of laryngeal squamous cell carcinoma (LSCC) for expression of PCNA, a protein associated with DNA polymerase dalta and DNA replication, a marker for tumor cell proliferation. The results revealed that PCNA indices in SHE, AHE and LSCC were 9.5%, 27.33% and 68.05%, respectively. The PCNA indices were 63.68%, 69.57%, 71.18% in the well, moderately and poorly differentiated LSCC, respectively, there were significant differences. The PCNA indices were 63.88%, 70.82%, 66.20% and 69.04%, respectively in stages I, II, III, and IV of LSCC; no significance was found. There was a strong negative correlation betwee survival time and the tumor cell proliferative activity (r = 0.6243). PCNA might provide a useful tool for studying cell proliferation in situ under normal and pathological condition.

Adult↗
PubMed1994

In situ analysis of cellular proliferation in canine, feline and equine tumors by immunohistochemistry: a comparison of bromodeoxyuridine, proliferating cell nuclear antigen, and interchromatin-associated antigen immunostaining techniques.

Cell proliferation in canine, feline, and equine tumors was evaluated using immunohistochemical detection of in vitro 5-bromodeoxyuridine (BrdU) incorporation, proliferating cell nuclear antigen (PCNA), and interchromatin-associated antigen (p105). Ten tumors in each species were analyzed. The tumor proliferative fraction (PF) was defined as the percentage of labeled nuclei for 5,000 tumor nuclei counted. Immunoreactivity was observed with all techniques in all species. A good correlation was observed between the proliferative fractions measured with the BrdU (PFBrdU) and PCNA (PFPCNA) techniques (rs = 0.523, P = 0.0026). There was no correlation between the PFs measured with the BrdU (PFBrdU) and p105 (PFP105) techniques. Using the median values obtained from the different approaches as cutoff points to define slowly and rapidly proliferating tumors, there was an 80% agreement (P = 0.009) between PFBrdU and PFPCNA and no agreement between PFBrdU and PFP105. The results of this study indicate that both BrdU and PCNA labeling methods can be used reliably for identifying proliferating cells in animal tumors. In addition, PCNA could be used to replace the BrdU method to assess tumor proliferative fraction because it does not require pretreatment of tissues.

Animals↗
PubMed1990

Immunocytochemical identification of proliferating cell types in mouse mammary gland.

To study cell proliferation in different cell types and segments of the mammary gland, we devised a dual staining procedure, combining nuclear labeling by 5-bromo-2'-deoxy-uridine (BrdU) uptake (revealed by a dark-brown precipitate) and an alternative (red or blue) cytoplasmic labeling by antibodies specific for the differentiation proteins of epithelial, myoepithelial, and secretory cell types. The following markers, revealed by APAAP or beta-galactosidase procedure, were selected: alpha-smooth muscle actin for the myoepithelial cells, keratin (detected by AE1 monoclonal) for the luminal epithelial cells, alpha-lactalbumin and beta-casein for the secretory cells. To follow the full process of organogenesis, the study was conducted in mouse mammary glands from virgin, primed, and lactating animals and from glands cultured in vitro under specific hormone stimulation. Cell proliferation was localized mainly in focal areas (end buds), and mostly corresponded to "null" undifferentiated cells. Estrogen and progestin stimulation induced a relative increase of proliferating differentiated cells of either epithelial or myoepithelial type, localized in ducts and alveolar structures. Prolactin stimulation induced proliferation in secretory cells.

Animals↗
PubMed1997

Testicular effects of 1,3,5-trinitrobenzene (TNB). II. Immunolocalization of germ cells using proliferating cell nuclear antigen (PCNA) as an endogenous marker.

The applicability of PCNA as a tool for the analysis of germ cells in rats treated with 1,3,5-trinitrobenzene (TNB), a potent testicular toxicant, was evaluated. Male Fischer 344 (F344) rats were gavaged with TNB at 71 mg/kg or with corn oil (vehicle). Rats were killed after 10 daily oral doses or were allowed to recover for 10 or 30 d after the 10 doses. Testes from control rats, treated rats, and rats allowed to recover were immunohistochemically stained for PCNA. PCNA labeling in the control rats was confined to the nuclei of spermatogonia, pachytene spermatocytes, and nuclei of elongate spermatocytes. Conventional (hematoxylin and eosin) staining of testes from rats treated with TNB at 71 mg/kg for 10 d revealed loss of germ cells and cessation of spermatogenesis. Immunohistochemical staining of sections from these treated rats revealed only PCNA-positive spermatogonia. Rats allowed a 10-d recovery had both spermatogonial and spermatocytic staining, indicating partial restoration of germ-cell population. In rats allowed to recover for 30 d, the PCNA staining pattern was identical to the control rats. These results indicate that PCNA can be used to assess the proliferative status of spermatogonia (germ cells) in rodent testes exposed to testicular toxicants.

Animals↗
PubMed2001

Anti-CD3 and concanavalin A-induced human T cell proliferation is associated with an increased rate of arachidonate-phospholipid remodeling. Lack of involvement of group IV and group VI phospholipase A2 in remodeling and increased susceptibility of proliferating T cells to CoA-independent transacyclase inhibitor-induced apoptosis.

In this study arachidonate-phospholipid remodeling was investigated in resting and proliferating human T lymphocytes. Lymphocytes induced to proliferate with either the mitogen concanavalin A or with anti-CD3 (OKT3) in combination with interleukin 2 (OKT3/IL-2) showed a greatly accelerated rate of [3H]arachidonate-phospholipid remodeling compared with resting lymphocytes or with lymphocytes stimulated with OKT3 or IL-2 alone. The concanavalin A-stimulated cells showed a 2-fold increase in the specific activity of CoA-independent transacylase compared with unstimulated cells, indicating that this enzyme is inducible. Stimulation with OKT3 resulted in greatly increased quantities of the group VI calcium-independent phospholipase A2 but not of the quantity of group IV cytosolic phospholipase A2. However, group IV phospholipase A2 became phosphorylated in OKT3-stimulated cells, as determined by decreased electrophoretic mobility. Incubation of cells with the group VI phospholipase A2 inhibitor, bromoenol lactone, or the dual group IV/group VI phospholipase A2 inhibitor, methyl arachidonyl fluorophosphonate, did not block arachidonate-phospholipid remodeling resting or proliferating T cells, suggesting that these phospholipases A2 were not involved in arachidonate-phospholipid remodeling. The incubation of nonproliferating human lymphocytes with inhibitors of CoA-independent transacylase had little impact on cell survival. In contrast, OKT3/IL-2-stimulated T lymphocytes were very sensitive to apoptosis induced by CoA-independent transacylase inhibitors. Altogether these results indicate that increased arachidonate-phospholipid remodeling is associated with T cell proliferation and that CoA-independent transacylase may be a novel therapeutic target for proliferative disorders.

Acyltransferases↗
PubMed2004

Thermal enhancement of oxaliplatin-induced inhibition of cell proliferation and cell cycle progression in human carcinoma cell lines.

Hyperthermia is used to treat intraperitoneal colorectal carcinomatosis. In this setting, the molecular effects of oxaliplatin and hyperthermia, in combination and alone, were deciphered in ovarian and colon cancer cells. The combined antiproliferative effects of hyperthermia and oxaliplatin (Eloxatine) on human IGROV-1 ovarian carcinoma, Caco-2 and HT-29 colon carcinoma cell lines were investigated by cell viability test, cell cycle analysis and modulation of expression of cell cycle-related proteins. Oxaliplatin inhibited growth of all cell lines in a dose-dependent manner. The efficacy of the drug was markedly enhanced by concurrent exposure to mild heat shock (1 h, 42 degree C). In IGROV-1 cells, a low concentration (15 microg/ml) of oxaliplatin in combination with hyperthermia induced a transient G2/M arrest. In both colon carcinoma cell lines, a G1/S arrest with a reduction of the G0/G1 population occurred. In IGROV-1 and Caco-2 cells, growth arrest was accompanied by apoptosis as suggested by the appearance of sub-G1 population. Time-course changes of cell cycle regulatory proteins levels revealed accumulation of cyclins A and B as well as of cdc2 and cdk2 upon exposure of IGROV-1 cells to hyperthermia and oxaliplatin. In this cell line, p53 appeared to be implicated in both G2/M arrest and apoptosis. G1/S arrest of HT-29 cells was linked to up-regulation of cyclin E and p27(Kip1) and accumulation of the hypophosphorylated form of pRB, whereas in Caco-2 cells only the hyperphosphorylated form was detected as well as a down-regulation of the proto-oncogene c-myc. Taken together, the results of these in vitro studies suggest that hyperthermia and oxaliplatin might elicit antiproliferative effects by modulating the expression of cell cycle regulatory proteins through different signalling pathways.

Antineoplastic Agents↗
PubMed1992

Monoclonal antibody JC1: new reagent for studying cell proliferation.

AIM: To characterise a newly developed mouse monoclonal antibody JC1 which recognises a nuclear antigen present in proliferating cells in normal tissues and neoplastic lesions, and which is absent in resting cells. METHODS: The methodology was established using a representative range of frozen sections from normal tissues and from certain tumours which were immunostained with antibodies Ki67 and JC1. The molecular weight of the antigen recognised by JC1 was obtained by western blot analysis and this was compared with that of Ki67. IM-9 cell lysates containing Ki67 derived plasmids were also tested with JC1 antibody. RESULTS: Biochemical investigation indicated that the antigen recognised by JC1 gives two molecular weight bands of 212 and 123 kilodaltons, which is distinct from the well characterised anti-proliferation monoclonal antibody Ki67 (395-345 kilodaltons). In addition recombinant Ki67 protein is not recognised by JC1. Immunohistological reactivity was seen in areas known to contain numerous proliferating cells such as lymphoid germinal centres, splenic white matter, cortical thymocytes and undifferentiated spermatogonia. In tumours many cells from adenocarcinomas, oat cell carcinomas, squamous cell carcinomas of lung, and seminomas were labelled by JC1 with a distribution and proportion similar to that seen with Ki67. In normal tissues the only apparent difference was in testis where JC1 stained a considerably greater number of cells than Ki67. In all cases studied the new antibody showed nuclear reactivity only. JC1 did not show any cytoplasmic crossreactivity with squamous cells as is frequently seen with Ki67. CONCLUSION: Antibody JC1, which recognises a nuclear antigen present in proliferating cells, should provide a useful adjunct to Ki67 as a marker of proliferation especially in those cases such as squamous cell carcinomas where a Ki67 index cannot be determined.

Animals↗
PubMed2002

Cyclin D3 activates Caspase 2, connecting cell proliferation with cell death.

Precancerous cells that enter S phase without appropriate growth and viability factors undergo programmed cell death, suggesting that apoptosis may help guarantee organismic integrity [Evan, G. & Littlewood, T. (1998) Science 281, 1317-1322]. However, the connection between proliferation and cell death has remained unclear. Here, we show that the positive cell cycle regulator cyclin D3 [Matsushime H., Roussel M. F., Ashmun, R. A. & Sherr, C. J. (1991) Cell 65, 701-713] interacts with the death enzyme Caspase 2 [Wang, L., Miura, M., Bergeron, L., Zhu, H. & Yuan, J. (1994) Cell 78, 739-750]. Directed expression of cyclin D3 and Caspase 2 in human cells potentiated apoptosis compared with expression of Caspase 2 alone. Cyclin D3 expression increased the amount of cleaved (active) Caspase 2. We describe a PCR mutagenesis/ligation/two-hybrid/green fluorescent protein approach that facilitates the isolation of missense mutant proteins defective in interaction with particular partners absent other phenotypes or knowledge of the system. We used this approach to isolate Caspase 2 mutants that did not bind cyclin D3 (noninteractors). Noninteractors were sensitive to apoptosis-dependent proteolysis, but did not potentiate apoptosis. Noninteractors did not block apoptosis caused by wild-type Caspase 2. Our results are consistent with the idea that an interaction with cyclin D3 may stabilize Caspase 2, and suggest that a physical interaction between cyclin D3 and Caspase 2 connects the genetic networks that govern cell-cycle progression with those that govern cell death.

Apoptosis↗
PubMed1993

5-Bromodeoxyuridine incorporation and PCNA expression as measures of cell proliferation in transitional cell carcinoma of the urinary bladder.

Cell proliferation in 66 transitional cell carcinomas of the human urinary bladder was evaluated using immunohistochemical detection of in vitro 5-bromodeoxyuridine (BrdUrd) incorporation and of proliferating cell nuclear antigen (PCNA). The labeling index (LI) was defined as percent of labeled nuclei for 2000 tumor nuclei counted. The BrdUrd LI ranged from 0.2% to 38.9%, geometric mean = 8.4% (n = 61), and the PCNA LI ranged from 0.4% to 64.1%, geometric mean = 12.7% (n = 60). For the 55 tumors that were stained by both procedures, the BrdUrd LI showed a highly significant regression on the PCNA LI (BrdUrd LI = 0.74 * PCNA LI, R2 = 0.71, p < 0.0001, coefficient of variation of residual = 17.7%, log transformed data). When compared to clinical and histopathologic criteria, both labeling indices were substantially lower in low grade (Grade 1) versus high grade (Grades 2 and 3) tumors and in Ta tumors versus higher stage T1, T2, and T3 tumors. These studies show that BrdUrd incorporation can be used reliably to measure cell proliferation in fresh bladder tissue, that PCNA labeling is a similar measure of cell proliferation, and that both measures are low in tumors of low histopathologic grade and stage.

Aged↗
PubMed1989

Tumor cell proliferation kinetics and tumor growth rate.

The present knowledge on the growth rate and the proliferation kinetics of human tumor is based on the measurement of the tumor doubling times (DT) in several hundred patients and on the determination of the proportion of proliferating cells with radioactive thymidine or by flow cytometry in large numbers of patients. The results show that the DT of human tumor varies widely, from less than one week to over one year with a median value of approximately 2 months. The DTs are significantly correlated with the histological type. They depend upon 1) the duration of the cell cycle whose mean duration is 2 days with small variations from tumor to tumor, 2) the proportion of proliferating cells and consequently the cell birth rate which varies widely among tumors and which is significantly correlated to the DT, 3) the cell loss factors which also vary widely and which are the greatest when proliferation is most intensive. These studies have several clinical implications: a) they have further increased our understanding of the natural history of human tumor, b) they have therapeutic implications since tumor responsiveness and curability by radiation and drugs are strongly influenced by the cell kinetic parameters of the tumor, c) the proportion of proliferating cells is of great prognostic value in several types of human cancers. The investigation of the molecular defects, which are correlated with the perturbation of control of cell proliferation, should lead to significant fundamental and therapeutic advances.

Cell Cycle↗
PubMed2003

Delphinidin inhibits endothelial cell proliferation and cell cycle progression through a transient activation of ERK-1/-2.

Epidemiological studies have shown that a diet rich in fruits and vegetables might reduce the risk of cardiovascular diseases and protect against cancer by mechanisms that have not been elucidated yet. This study was aimed to define the effect of delphinidin, a vasoactive polyphenol belonging to the class of anthocyanin, on bovine aortic endothelial cells (BAECs) proliferation. Delphinidin inhibited serum- and vascular endothelium growth factor-induced BAECs proliferation. This antiproliferative effect of delphinidin, is triggered by ERK-1/-2 activation, independent of nitric oxide pathway and is correlated with suppression of cell progression by blocking the cell cycle in G(0)/G(1) phase. Furthermore, suppression of cell cycle progression is associated with the modulation of the mitogenic signaling transduction cascade. This includes over-expression of caveolin-1 and p21(WAF1/Cip1) and down-expression of Ras and cyclin D1. In conclusion, the antiproliferative effect of delphinidin may be of importance in preventing both plaque development and stability in atherosclerosis and tumor dissemination in cancer.

Animals↗
PubMed1985

The fate of proliferating cells in skeletal muscle after denervation or tenotomy: an autoradiographic study.

During the first 7 days after denervation or tenotomy of skeletal muscle there is increased cell proliferation, as measured autoradiographically by [3H]thymidine incorporation. By 21 days most of the labelled cells have disappeared. The present experiment was designed to measure residual levels of labelling in skeletal muscles at 21 days after denervation or tenotomy, when [3H]thymidine had been available for the first 7 days. This was to determine the fate of cells labelled at 7 days and to detect whether continued cell proliferation had occurred during the intervening period, as evidenced by the dilution of nuclear label. Tibialis anterior muscles of 16 mice were denervated, tenotomized or sham-operated, and the animals injected with a single daily pulse of [3H]thymidine for the first 7 days only. In denervated muscle the 11% of muscle nuclei and 41% of connective tissue nuclei labelled at 7 days had decreased to 2 and 13%, respectively, by 21 days. These values were still significantly higher than in 21 day controls (0.2 and 1.9%, respectively). In muscle nuclei (myonuclei and satellite cell nuclei) there was a significant decrease in the amount of label per nucleus. This was interpreted as evidence of continued cell proliferation. However, this did not produce an increase in numbers of muscle nuclei. It was concluded that: there was turnover of satellite cells and possibly myonuclei, the latter probably through continued division and incorporation of satellite cells; and the extra satellite cells and myonuclei produced were probably extruded from the fibre to the extracellular space.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Modulation of cell proliferation and cell cycle regulators by vitamin E in human prostate carcinoma cell lines.

PURPOSE: Vitamin E has been identified as a candidate agent for the prevention of prostate cancer. We hypothesize that the mechanism for this effect is in part a result of cell cycle inhibition rather than only due to a reduction in reactive oxygen species. We tested whether vitamin E induces cell cycle arrest in prostate carcinoma, mediated by alterations in cell cycle regulatory proteins, including cyclin E, cdk2 and p27. MATERIALS AND METHODS: Cells were incubated with and without vitamin E (alpha-tocopherol succinate, 20 microg./ml.), fixed and stained with propidium iodide for flow cytometry analysis. In parallel experiments total protein was extracted, immunoprecipitated with cyclin E antibody and analyzed by Western blot for the expression of cell cycle markers. RESULTS: Flow cytometry analysis revealed a dramatic reduction in the S phase percent of LNCaP and PC3 cells in response to vitamin E (69% and 95%, respectively). It was accompanied by over expression of p27 (3-fold increase) with vitamin E treatment. CONCLUSIONS: This study demonstrates that at physiological concentrations vitamin E induced profound cell cycle arrest mediated by up-regulation of p27. This observation provides a theoretical basis for the putative chemopreventive effect of vitamin E.

CDC2-CDC28 Kinases↗