Biomedical subjects

Y Tu

Publications and source records attributed to Y Tu.

At least 91 records · Page 5Linked to original sources

PubMed1998

Nck-2, a novel Src homology2/3-containing adaptor protein that interacts with the LIM-only protein PINCH and components of growth factor receptor kinase-signaling pathways.

Many of the protein-protein interactions that are essential for eukaryotic intracellular signal transduction are mediated by protein binding modules including SH2, SH3, and LIM domains. Nck is a SH3- and SH2-containing adaptor protein implicated in coordinating various signaling pathways, including those of growth factor receptors and cell adhesion receptors. We report here the identification, cloning, and characterization of a widely expressed, Nck-related adaptor protein termed Nck-2. Nck-2 comprises primarily three N-terminal SH3 domains and one C-terminal SH2 domain. We show that Nck-2 interacts with PINCH, a LIM-only protein implicated in integrin-linked kinase signaling. The PINCH-Nck-2 interaction is mediated by the fourth LIM domain of PINCH and the third SH3 domain of Nck-2. Furthermore, we show that Nck-2 is capable of recognizing several key components of growth factor receptor kinase-signaling pathways including EGF receptors, PDGF receptor-beta, and IRS-1. The association of Nck-2 with EGF receptors was regulated by EGF stimulation and involved largely the SH2 domain of Nck-2, although the SH3 domains of Nck-2 also contributed to the complex formation. The association of Nck-2 with PDGF receptor-beta was dependent on PDGF activation and was mediated solely by the SH2 domain of Nck-2. Additionally, we have detected a stable association between Nck-2 and IRS-1 that was mediated primarily via the second and third SH3 domain of Nck-2. Thus, Nck-2 associates with PINCH and components of different growth factor receptor-signaling pathways via distinct mechanisms. Finally, we provide evidence indicating that a fraction of the Nck-2 and/or Nck-1 proteins are associated with the cytoskeleton. These results identify a novel Nck-related SH2- and SH3-domain-containing protein and suggest that it may function as an adaptor protein connecting the growth factor receptor-signaling pathways with the integrin-signaling pathways.

3T3 Cells↗

PubMed1998

Increased Mdm2 expression in rat brain after transient middle cerebral artery occlusion.

The negative regulator of p53 transactivation, Mdm2, increased in the ischemic territory after 90 minutes of transient middle cerebral artery occlusion in spontaneously hypertensive rats compared to sham controls. Increased mdm2 mRNA was detected by semiquantitative reverse transcriptase polymerase chain reaction by 6 hours of reperfusion in the ipsilateral hemisphere. In situ hybridization histochemistry was used to localize increases in mdm2 mRNA which occurred in neurons of ischemic cortex and dorsolateral striatum. The number of labeled neurons increased by approximately 20-fold and the cells displayed five-fold increases of mdm2 mRNA in the cortex. Immunohistochemical staining for Mdm2 revealed that its mRNA was efficiently translated in the ischemic cortex, but not striatum, by 8 to 24 hours of reperfusion. Western blotting confirmed 30- to 40-fold increases in the full-length protein of 90 kd at these time points without evidence of alternative splicing. Because Mdm2 is a negative regulator of the apoptosis promoting activity of p53, increased expression of Mdm2 may be a component of a repair response in injured neurons, and supports Mdm2 being an indicator of DNA damage in the brain early after an ischemic insult in a similar way to Gadd45.

Animals↗

PubMed1998

Calcitonin gene-related peptide protects cultured rat gastric mucosal cells.

Capsaicin exerts its gastroprotective effect by stimulating primary afferent neurons, releasing calcitonin gene-related peptide (CGRP), which in turn increases gastric blood flow. In this work, the effects of capsaicin, rat alpha-CGRP, and relative peptides hCGRP(8-37) and beta-hCGRP, and substance P on cultured gastric mucosal cells independent of neural and vascular mechanisms were studied. Damage was produced by indomethacin, ethanol or taurocholate 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and trypan blue exclusion tests were used to assess viability of the cultured cells. Capsaicin administration alone did not injure gastric cells. However, capsaicin pretreatment potentiated the damaging effect of indomethacin and ethanol. In the sodium taurocholate model, capsaicin slightly protected the cells against injury. Alpha-rCGRP was protective against indomethacin, ethanol and taurocholate in a dose-dependent manner. hCGRP(8-37) and beta-hCGRP both dose-dependently prevented injury caused by indomethacin at concentrations about eight times higher than that of alpha-rCGRP, but substance P was ineffective in the three different damage models. A combination of alpha-CGRP and hCGRP(8-37) was also protective against indomethacin damage to a similar extent as use of either agent alone. The defence mechanism of capsaicin against gastric cell injury may in part be mediated by a direct effect of CGRP on gastric mucosal cells, in addition to effects dependent on neural and vascular mechanisms. hCGRP(8-37) has no antagonist effect against CGRP in this model, suggesting that CGRP receptors in this model may be different from those in other tissues.

Animals↗

PubMed1998

[Immunoprotection in guinea pigs using DNA recombinant plasmid rpDJt and expressed protein P68 in L. interrogans serovar lai].

Immunoprotection against the infection by Leptospira interrogans serogroup Icterohemorrhagiae serovar lai strain 017 was demonstrated in guinea pigs vaccinated with DNA recombinant plasmid rpDJt and expressed protein P68 derived from genomic library of Leptospira strain 017. Thirty days after active immunization, each group received intraperitoneally (1/2 dose) and subcutaneously (1/2 dose) inoculum of L. interrogans serovar lai stain 017; cultures were adjusted to 5 x 10(8) cells/ml. All guinea pigs were observed for 10 days after challenge. Survival (%) of P68 group was 100(7/7); P23 group was 75(3/4); group rpDJt was 77(10/13); group lack recombinant (control) pT7-7 was 25 (3/12), and group with whole-cell inactivated vaccine was 93(13/14). Although the protective antigen in the leptospires has yet to be determined, it is evident that expressed protein P68 conferred a high degree of immunoprotection in guinea pigs.

Animals↗

PubMed1998

[Pathophysiology and surgical treatment on Relaxed Pelvic Floor Syndrome].

OBJECTIVE: To study the pathophysiology of the "Relaxed Pelvic Floor Syndrome (RPFS)" and to assess the value of the "Pelvic Cavity Fixation Operation (PCFO)" for the syndrome. METHOD: 11 patients, who were diagnosed as having RPFS, underwent standardized PCFO. All the patients were followed for a mean time of 19 months (5 - 72 months). RESULT: The main syndromes and signs included difficulty in defecation, inability to empty the rectum properly, fullness of perineum, protrusion of perineum at bearing down, back-inclining uterus, relaxation of the rectum on digital examination. The anorectal dynamics showed that the sequence pressure and rest pressure of the anal cannel were lower and the time of contraction of the anal cannel decreased than that of the normal controls. The rectum sensation was damaged slightly. Defeacography showed that there were relaxing changes in several systems in the pelvic cavity. Operatively, it was easy to see the relaxation of the supporting structure of the colon, rectum, uterus and the lower position of the peritoneal cavity. PCFO has achieved good results. Seven patients were free of symptoms completely and 4 improved. CONCLUSION: The relaxing changes of the supporting tissue of many viscus fefer to several systems are the pathophysiologic of the RPFS. "Pelvic Cavity Fixation Operation" is useful in the treatment of the syndrome.

Adult↗

PubMed1998

[Effect of dihydroquinghaosu on the development of Plasmodium yoelii yoelii in Anopheles stephensi].

AIM: To observe the effect of dihydro qinghaosu (DQHS) on the development of Plasmodium yoelii yoelii in Anopheles stephensi and to explore the possibility of whether DQHS has preventive effect against malaria. METHODS: Plasmodium yoelii yoelii-infected mice that had been administered with a single dose of different dosages (60 mg/kg, 120 mg/kg, 180 mg/kg and 240 mg/kg) of DQHS were exposed to mosquitoes to suck blood. The development of malaria parasites in the mosquitoes of the control group and the treated group were observed by light microscopy (LM) and transmission electron microscopy (TEM). RESULTS: DQHS exhibited certain inhibitory effect on the infectivity of gametocyte. The degree of inhibition was related to the developmental stages of gametocyte and the drug dosage. Immature gametocytes were more sensitive to DQHS than the mature gametocytes. With the increases in dosage, the positive rate and the density of oocyst and sporozoite decreased. However, the difference in the density of sporozoite between 180 mg/kg and 240 mg/kg treated groups was insignificant. TEM result showed damage of the membrane system and vacuolation in the cytoplasm of the oocysts (12-13 d) on mosquito midgut of 60 mg/kg 16 h treated group. The oocysts in the mosquitoes continued to develop after treated with 120 mg/kg of DQHS for 16 h on 3-day-instar. There was no significant difference (P > 0.05) in the density of oocyst and sporozoite between the control group and the treated group. CONCLUSION: DQHS can affect the infectivity of gametocyte and decrease the malaria transmission but cannot inhibit the sorogonic stage directly.

Animals↗

PubMed1997

Inhibition of brain Gz GAP and other RGS proteins by palmitoylation of G protein alpha subunits.

Palmitoylation of the alpha subunit of the guanine nucleotide-binding protein Gz inhibited by more than 90 percent its response to the guanosine triphosphatase (GTPase)-accelerating activity of Gz GAP, a Gz-selective member of the regulators of G-protein signaling (RGS) protein family of GTPase-activating proteins (GAPs). Palmitoylation both decreased the affinity of Gz GAP for the GTP-bound form of Galphaz by at least 90 percent and decreased the maximum rate of GTP hydrolysis. Inhibition was reversed by removal of the palmitoyl group by dithiothreitol. Palmitoylation of Galphaz also inhibited its response to the GAP activity of Galpha-interacting protein (GAIP), another RGS protein, and palmitoylation of Galphai1 inhibited its response to RGS4. The extent of inhibition of Gz GAP, GAIP, RGS4, and RGS10 correlated roughly with their intrinsic GAP activities for the Galpha target used in the assay. Reversible palmitoylation is thus a major determinant of Gz deactivation after its stimulation by receptors, and may be a general mechanism for prolonging or potentiating G-protein signaling.

Animals↗

PubMed1997

Parathyroid hormone (1-34)-mediated interleukin-6 induction.

Parathyroid hormone (PTH) functions in part by regulating osteoblast cytokine expression. We recently demonstrated that PTH induced a rapid and transient increase in interleukin-6 (IL-6) mRNA expression in rat bones in vivo. To determine the molecular basis of this effect, we analyzed the human IL-6 promoter fused (-1,179 to +9) with the chloramphenicol acetyltransferase (CAT) reporter gene in stable transfections into human osteoblast-like osteosarcoma SaOS-2 cells. We compared the effects of PTH on IL-6 expression with adenylate cyclase activator forskolin, PKC activator phorbol 12-myristate 13-acetate (PMA), calcium ionophore A23187, interleukin-1 alpha (IL-1 alpha), prostaglandin E-2 (PGE-2), RS-66271 (a parathyroid hormone-related peptide analog), and platelet-derived growth factor-BB (PDGF-BB). Analyses of cell clones showed that IL-6 promoter expression was extremely low in the unstimulated state. Exposure to PTH (0.001-100 nM) for 12 h stimulated CAT expression in a dose-dependent manner (200-500% of control). Treatment with IL-1 alpha was more potent than PTH in inducing transcription of the IL-6 promoter (900-1,000%). Activation of the cAMP-PKA pathway by treatment with forskolin induced a comparable level of induction with PTH. Together, the effects of PTH and forskolin were additive. RS-66271, previously shown to have PTH-like effects, induced a comparable level of IL-6 promoter expression. When examined together, PTH+RS-66271 effects were comparable to PTH effects alone. Exposure to PGE-2, PMA, PDGF-BB, or A23187 for 12 h did not significantly alter IL-6 promoter expression. These results demonstrate PTH, forskolin, the PTHrP analog RS-66271, and IL-1 alpha stimulate IL-6 expression by stimulating gene transcription. The response to forskolin suggests that the messenger system mediated by PKA is sufficient to induce IL-6 expression.

Becaplermin↗

PubMed1997

Sequence-specific and domain-specific DNA repair in xeroderma pigmentosum and Cockayne syndrome cells.

Xeroderma pigmentosum (XP) and Cockayne syndrome (CS) cells have specific DNA repair defects. We had previously analyzed repair rates of cyclobutane pyrimidine dimers at nucleotide resolution along the human JUN gene in normal fibroblasts and found very efficient repair of sequences near the transcription initiation site but slow repair along the promoter. To investigate sequence-specific repair rate patterns in XP and CS cells, we conducted a similar analysis in XPA, XPB, XPC, XPD, and CSB fibroblasts. XPA cells were almost completely repair-deficient at all sequences analyzed. XPC cells repaired only the transcribed DNA strand beginning at position -20 relative to the transcription start site. Both XBP and XPD cells were deficient in repair of nontranscribed DNA and also very inefficiently repaired the transcribed strand including sequences near the transcription start site. CSB cells exhibited rapid repair near the transcription initiation site but were deficient in repair of sequences encountered by RNA polymerase during elongation (beginning at position +20). Since transcription of the JUN gene was UV-induced in all fibroblast strains, including CSB, the defective repair of the transcribed strand in CSB cannot be explained by a lack of transcription; rather, it appears to be a true DNA repair defect.

Base Sequence↗

PubMed1997

A GTPase-activating protein for the G protein Galphaz. Identification, purification, and mechanism of action.

A GTPase-activating protein (GAP) specific for Galphaz was identified in brain, spleen, retina, platelet, C6 glioma cells, and several other tissues and cells. Gz GAP from bovine brain is a membrane protein that is refractory to solubilization with most detergents but was solubilized with warm Triton X-100 and purified up to 50,000-fold. Activity is associated with at least two separate proteins of Mr approximately 22,000 and 28,000, both of which have similar specific activities. In an assay that measures the rate of hydrolysis of GTP pre-bound to detergent-soluble Galphaz, the GAP accelerates hydrolysis over 200-fold, from 0.014 to 3 min -1 at 15 degrees C, or to >/=20 min-1 at 30 degrees C. It does not alter rates of nucleotide association or dissociation. When co-reconstituted into phospholipid vesicles with trimeric Gz and m2 muscarinic receptor, Gz GAP accelerates agonist-stimulated steady-state GTP hydrolysis as predicted by its effect on the hydrolytic reaction. In the single turnover assay, the Km of the GAP for Galphaz-GTP is 2 nM. Its activity is inhibited by Galphaz-guanosine 5'-O-thiotriphosphate (Galphaz-GTPgammaS) or by Galphaz-GDP/AlF4 with Ki approximately 1.5 nM for both species; Galphaz-GDP does not inhibit. G protein betagamma subunits inhibit Gz GAP activity, apparently by forming a GTP-Galphazbetagamma complex that is a poor GAP substrate. Gz GAP displays little GAP activity toward Galphai1 or Galphao, but its activity with Galphaz is competitively inhibited by both Galphai1 and Galphao at nanomolar concentrations when they are bound to GTPgammaS but not to GDP. Neither phospholipase C-beta1 (a Gq GAP) nor several adenylyl cyclase isoforms display Gz GAP activity.

Animals↗

PubMed1997

Rejection of spontaneously accepted rat liver allografts with recipientinterleukin-2 treatment or donor irradiation.

While MHC incompatible DA (RTl(a)) to Lewis (RT1(1), LEW) rat liver allografts are acutely rejected, the reciprocal LEW to DA liver grafts are spontaneously accepted. The mechanism of this acceptance remains unclear. We evaluated the effect of donor treatment with total body irradiation (TBI) or gadolinium chloride (GdCl3), and recipient treatment with exogenous IL-2 after transplantation on the survival of the spontaneously accepted liver grafts. Male LEW and DA rats were used as donors and recipients for orthotopic liver allo- or iso-graft transplants. The LEW liver donor was treated by TBI (10 gray) 7 days before transplantation, or LEW donor Kupffer cell phagocytosis was blocked with GdCl3 (7 mg/kg) on days -2 and -1 pretransplant. In an attempt to reverse LEW liver graft acceptance, 180,000 units human IL-2 (hIL-2) were administered daily IP to the DA liver recipients from days 1 to 7 after liver grafting. While untreated LEW recipients rejected DA liver grafts within 13 days, DA recipients accepted LEW livers indefinitely (>302 days). In contrast, irradiation of the LEW liver donor prevented the spontaneous acceptance by DA recipients, and resulted in acute rejection of the liver grafts in 9-20 days. However, spontaneous graft tolerance was restored by parking the irradiated LEW donor liver in naive LEW rats for 48 hr before retransplantation to DA recipients (>50 days). When LEW donors were treated with GdCl3, which is known to block Kupffer cell phagocytosis and antigen processing, the spontaneous acceptance of the LEW liver grafts by DA recipients was unaffected. However, when exogenous rhIL-2 was given daily, LEW liver allografts were rejected by the DA recipients. The resulting liver failure correlated with a progressive increase in serum bilirubin and the development of a predominantly lymphocytic portal tract infiltration, bile duct epithelial damage, and portal vein endothelitis, which is consistent with acute allograft rejection. LEW and DA recipients of liver isografts developed no toxicity and survived indefinitely (>100 days) when treated with the same dose of IL-2. These results indicate that spontaneous rat liver allograft acceptance is associated with the presence of radiosensitive cells in the donor liver that may interact with recipient T cells to inhibit (Th1) production of IL-2.

Animals↗

PubMed1997

Relationship between progression of gastric mucosal atrophy and Helicobacter pylori infection: retrospective long-term endoscopic follow-up study.

A retrospective long-term endoscopic follow-up study was designed to examine atrophic changes in the gastric mucosa over time in Helicobacter pylori-positive patients. Over a period of 8-17 years (mean, 13.4 years) 22 subjects (5 men, 17 women, mean age, 55 years) without localized gastroduodenal lesions underwent serial endoscopic examinations and serological and microbiological assessments of H. pylori infection. The extent of atrophic mucosa in the gastric body was expressed using the Kimura-Takemoto classification of atrophic pattern. Atrophic patterns were unchanged over time in 7 H. pylori-seronegative and culture-negative subjects with normal stomach, and in 1 seropositive and culture-negative subject with severe atrophy. Seven of 10 H. pylori culture-positive subjects not including three with the O-3 pattern, i.e., open type atrophic pattern, exhibited a cephalad shift of atrophic pattern. The cumulative progression rates of atrophy in the culture-positive subjects excluding O-3 subjects, were 10% after 2 years, 20% after 4 years, 50% after 6 years, and 70% after 8 years. The increases in the extent of the atrophic area were discontinuous, in terms of age, in the H. pylori-positive individuals and occasionally advanced rapidly within periods of several years with no relation to age.

Adult↗

PubMed1997

Mechanism of anti-beta-adrenoceptor antibody mediated myocardial damage in dilated cardiomyopathy.

Antibodies against beta(1)-adrenoceptor can be detected in serum of patients with dilated cardiomyopathy (DCM), which have beta-agonist-like activity, and induce a positive chronotropic effect on cardiac myocytes by its persistence at full strength. Effects of the antibodies against beta-adrenoceptor from sera of patients with DCM on myocardial cytotoxicity and cytoplasmic free Ca(2+)-concentration ([Ca2+]i) were observed in the cultured single layer SD rat ventricular cells by using the cytotoxicity assay and fluorescent Ca(2+)-indicator fura-2/AM. The positive sera of the anti-beta-adrenoceptor antibodies from patients with DCM markedly enhanced myocardial [Ca2+]i. Betaloc, a beta(1)-receptor blocker, might inhibit the increase of the antibody-mediated myocardial [Ca2+]i, and the sera from healthy donors had no effect on myocardial [Ca2+]i. Our results suggest that the anti-beta-adrenoceptor antibody might increase myocardial [Ca2+]i and result in myocardial damage. The antibodies might activate receptor-gating Ca(2+)-channel, thereby causing myocardial [Ca2+]i rise and calcium overload. Early use of betaloc is recommended in the treatment of dilated cardiomyopathy.

Adult↗

PubMed1997

Effect of intra-arachnoid space perfusion on thromboxane A and prostacycline in experimental spinal cord injury.

In order to understand the relation between TXA2-PGI2 and secondary trauma and the effect of intra-arachnoid perfusion of dexamethasone and verapamil on alteration of TXA2-PGI2 following spinal cord injury, TXB2 and 6-keto-PGF alpha concentration and pathological changes in injured site 1, 2, 4, and 6 h after injury were studied using a rabbit spinal cord injury model by Allen's weight drop method.

6-Ketoprostaglandin F1 alpha↗

PubMed1997

A model of subarachnoid cavity drugs perfusion and its clinical application in treatment of spinal cord injury.

An animal model of subarachnoid cavity drugs perfusion and its prelimilary clinical application in treatment of acute spinal cord injury (SCI) were reported. Analysis of the heart rate (HR), ECG blood pressure (CVP, CAP) cerebrospinal fluid (CSF) pressuer and CSF gas and pH values of 10 healthy adult goats during subarachnoid daxamethasone verapamil perfusion showed that this model was safe anti reliable. 26 patients with acute SCI were selected for a clinical obseration. Good results were obtained in 7 cases who received this treatment of subarachnoid cavity perfusion with dexamethasone and verapamil.

Adolescent↗

PubMed1997

Apoptotic vs. nonapoptotic cytotoxicity induced by hydrogen peroxide.

The regulation of cellular cytotoxicity induced by hydrogen peroxide (H2O2) over a wide concentration range was assessed. Three distinct patterns were detected: the highest concentrations (> 10 mM) rapidly induced a necrotic form of death characterized by smeared patterns of DNA digestion and morphological evidence of primary cytoplasm and plasma membrane damage; In contrast, 10 and 5 mM H2O2 induced endonucleosomal DNA digestion concurrently with cytotoxicity and target cell death was associated with morphologic evidence of apoptosis. Apoptosis was inhibited by cycloheximide, emetine, aminobenzamide (ABA), aurintricarboxylic acid, and calcium depletion. The lowest concentrations of H2O2 (0.5 and 0.1 mM)-induced delayed cytotoxicity (at 24 or 48 hr), which was not associated with DNA ladder formation or morphologic evidence of apoptosis, but was inhibited by ABA. Enforced expression of BCL-2 induced resistance to 0.5 and 0.1 mM H2O2 but had no effect on cytotoxicity induced by 5 and 10 mM. Exposure of isolated nuclei to H2O2 in the absence of calcium or magnesium failed to induce endonucleosomal fragmentation. These data indicate that distinct pathways of H2O2-induced cytotoxicity can be distinguished by their different concentration dependences, and that BCL-2 can protect against some forms of H2O2-induced cytotoxicity.

Animals↗

PubMed1997

Evidence against the hypothesis that BCL-2 inhibits apoptosis through an anti-oxidant effect.

We contrasted possible protection against apoptosis afforded by either BCL-2 expression or anti-oxidant inhibitors in the same tumor target challenged by two distinct triggers of apoptosis. Exposure of L929 fibroblasts to tumor necrosis factor (TNF) or etoposide (VP-16) induced apoptotic death with similar kinetics. Enforced expression of BCL-2 significantly protected against apoptosis induced by VP-16 but had no effect against TNF-induced apoptosis. In contrast, the anti-oxidants desferrioxamine, butylated hydroxyanisol and N-acetyl cysteine all inhibited TNF-induced apoptosis in a concentration-dependent fashion. Although exposure to VP-16 resulted in a significant generation of intracellular oxyradicals, the above three anti-oxidant inhibitors had no effect on VP-16-induced apoptotic death. Interestingly, enforced expression of BCL-2 also inhibited the ability of VP-16 to generate oxy-radicals and to depress intracellular glutathione levels. These results indicate that BCL-2 can exert anti-oxidant effects but argue against the hypothesis that these effects are critical to its protection against apoptosis.

Journal Article↗

PubMed1997

Multiple myeloma cells are protected against dexamethasone-induced apoptosis by insulin-like growth factors.

Multiple myeloma cell lines express functional receptors for insulin-like growth factors (IGFs) and several cell types that make up the bone marrow microenvironment produce these cytokines. This suggests that IGFs may play a role in survival and/or expansion of the malignant clone within the marrow in patients with multiple myeloma. We tested the effects of these growth factors on myeloma cells challenged with dexamethasone. Dye exclusion and MTT assays demonstrated that both IGF-I and IGF-II protected the 8226 and dox-40 myeloma cell lines and three primary myeloma cultures from dexamethasone-induced cytotoxicity in a dose-dependent fashion. Morphologic studies of target cells and their nuclei as well as DNA electrophoresis confirmed the IGFs afforded protection against dexamethasone-induced apoptosis. Insulin also protected but was less impressive and required much higher concentrations. IGFs also protected against cycloheximide-induced apoptosis but were ineffective against serum starvation, topoisomerase II inhibitors, or anti-fas antibodies. IGF-induced protection against dexamethasone was not associated with any alteration in quantitative or qualitative expression of BCL-2, BAX or BCL-X proteins. These data indicate that insulin-like growth factors may play a role in maintenance of the malignant clone in patients with myeloma by protecting tumour cells from apoptotic death.

Animals↗