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Results for “Protein expression”

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PubMed1995

Protein expression of the alpha, gamma, delta and epsilon subspecies of protein kinase C changes as C6 glioma cells become contact inhibited and quiescent in the presence of serum.

Total protein kinase C (PKC) activity and protein expression of the alpha and delta subspecies of PKC increases markedly as C6 glioma cells grow from low cell density to the contact-inhibited quiescent state (also known as G(o)) in the presence of serum. At the same time protein expression of PKC subspecies gamma and epsilon decreases while the beta I, beta II, iota and zeta subspecies did not change. Serum deprivation of growing C6 glioma cells does not induce the same changes in PKC subspecies protein expression. The findings support the growing view that there are significant differences between the G(o) states brought about by contact inhibition or serum deprivation.

Blood↗

PubMed2005

Immunosuppression and gingival overgrowth: gene and protein expression profiles of collagen turnover in FK506-treated human gingival fibroblasts.

AIM: FK506 is an immunosuppressive agent that, unlike cyclosporin A (CsA), does not induce gingival overgrowth (GO). CsA-induced GO is caused by quantitative modifications of the extracellular matrix components, particularly collagen (COL). Up to now, clinical trials have only investigated FK506 in relation with GO, so we aimed at analysing the effect of FK506 on COL turnover using a molecular approach, to evaluate the expression of genes and proteins related to this process. MATERIALS AND METHODS: Human gingival fibroblasts were incubated with FK506 or its vehicle (VH) for 24, 48 and 72 h. COL type I (COL-I), matrix metalloproteinases (MMP)-1 and 2, tissue inhibitor of MMP (TIMP)-1 and transforming growth factor (TGF)-beta1 mRNA were assayed by Reverse transcriptase polymerase chain reaction; COL-I protein levels were determined by dot blot, MMP-1 and MMP-2 activity by zymography. RESULTS: Fibroblast proliferation decreased 48 and 72 h after treatment. COL-I gene and protein expression, TGF-beta1 and TIMP-1 mRNA levels were not significantly affected, whereas MMP-1 gene and protein expression and MMP-2 mRNA levels rose significantly in treated fibroblasts compared with VH. CONCLUSIONS: These findings suggest that increased MMP-1 gene and protein expression may be important for regulating COL-I homeostasis in the gingival connective compartment of FK506-immunosuppressed subjects.

Adult↗

PubMed2005

Role of phosphorylation in p53 acetylation and PAb421 epitope recognition in baculoviral and mammalian expressed proteins.

Post-translational modifications, such as phosphorylation and acetylation of the tumour suppressor protein p53, elicit important effects on the function and the stability of the resultant protein. However, as phosphorylation and acetylation are dynamic events subject to complex controls, elucidating the relationships between phosphorylation and acetylation is difficult. In the present study we sought to address this problem by comparing full-length wild-type p53 with full-length p53 proteins mutated at specific phosphorylation targets. Recombinant murine p53 proteins were expressed in insect cells (using the baculoviral expression vector system) and in a mammalian in vitro transcription/translation reticulocyte lysate system. In p53 proteins derived from baculoviral expression vectors, S37A (but not S37D) was found to abrogate phosphorylation at S15. Lysine 382 (K382) is constitutively acetylated and was shown to form part of the epitope recognized by PAb421. Lysine 373 (K373) was only acetylated following substitutions at S315 (S315A or S315D) or at S378 (S378A). Importantly, in baculoviral expressed proteins, PAb421 reactivity was independent of K373 acetylation status, indicating that acetylation at K382 specifically determines the PAb421 epitope.

Acetylation↗

PubMed2000

A mammalian germ cell-specific RNA-binding protein interacts with ubiquitously expressed proteins involved in splice site selection.

RNA-binding motif (RBM) genes are found on all mammalian Y chromosomes and are implicated in spermatogenesis. Within human germ cells, RBM protein shows a similar nuclear distribution to components of the pre-mRNA splicing machinery. To address the function of RBM, we have used protein-protein interaction assays to test for possible physical interactions between these proteins. We find that RBM protein directly interacts with members of the SR family of splicing factors and, in addition, strongly interacts with itself. We have mapped the protein domains responsible for mediating these interactions and expressed the mouse RBM interaction region as a bacterial fusion protein. This fusion protein can pull-down several functionally active SR protein species from cell extracts. Depletion and add-back experiments indicate that these SR proteins are the only splicing factors bound by RBM which are required for the splicing of a panel of pre-mRNAs. Our results suggest that RBM protein is an evolutionarily conserved mammalian splicing regulator which operates as a germ cell-specific cofactor for more ubiquitously expressed pre-mRNA splicing activators.

Animals↗

PubMed2000

Effect of transforming growth factor-beta1 on cytochrome P450 expression: inhibition of CYP1 mRNA and protein expression in primary rat hepatocytes.

Primary hepatocytes are a widely used cell model to analyse the expression and regulation of hepatic cytochrome P450 (CYP) isoenzymes. Transforming growth factor-beta1 (TGF-beta1) was previously shown to inhibit constitutive and induced CYP1 expression in human cell lines and primary hepatocytes but not in rat cells. In the present study we examined the effect of TGF-beta1 on constitutive and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced expression of CYP1 isoenzymes in primary rat hepatocytes in order to address the species-specificity of CYP1 down-regulation by TGF-beta1. The results show an inhibition of TCDD-induced CYP1-related 7-ethoxyresorufin-O-deethylase (EROD), 7-methoxyresorufin-O-demethylase (MROD) activities and mRNA expression (determined by reverse transcriptase polymerase chain reaction, RT-PCR) by 100 pM TGF-beta1 in cells co-treated for 24 h with 1 nM TCDD. However, while TGF-beta1 also down-regulated constitutive EROD and MROD activities as well as CYP1A2 protein expression, it did not change the constitutive mRNA expression of CYP1 isoenzymes. The down-regulation seemed to be specific for CYP1 isoenzymes since constitutive expression of other CYP isoenzymes was unaffected concerning protein levels, as determined by Western blot for CYP2B1/2 and CYP3A1, as well as mRNA levels, as determined by RT-PCR for CYP2B1/2, CYP2E1 and CYP3A1. Thus, TGF-beta1 not only inhibits CYP1 expression in humans but also in rats, indicating that regulation of CYP1 expression in these two species is similar.

Animals↗

PubMed2005

A series of bidirectional tetracycline-inducible promoters provides coordinated protein expression.

Coordinated control of protein expression is highly desirable for functional genomics. Here we show a widely applicable approach to construction and use of custom bidirectional promoters capable of reproducible coexpression of two proteins. The use of a bidirectional promoter system overcomes many of the limitations of current coexpression systems such as unpredictable upstream and downstream expression ratios mediated by an internal ribosome entry site. We present examples of tetracycline-inducible, bidirectional promoter systems that produce simultaneous and rapid coinduction of two separate reporters to predictable levels and ratios. Steric blocking of transcription initiation by simple tetracycline repressors, rather than the use of transcriptional activator/repressor domain fusions, makes the system described here superior for investigating downstream transcriptional consequences of protein expression.

Cell Line↗

PubMed2000

Adipose differentiation related protein: expression, purification of recombinant protein in Escherichia coli and characterization of its fatty acid binding properties.

Adipose differentiation related protein (ADRP) is a 53 kDa protein encoded by a cDNA originally cloned by differential hybridization from murine adipocytes. ADRP is induced during the early onset of the adipose differentiation program and is expressed at high level in mature adipocytes. We have demonstrated that ADRP stimulated the uptake of fatty acids thereby providing evidence for a functional role of ADRP in lipid metabolism. In the present paper, the murine ADRP has been expressed as a recombinant histidine-tagged protein in Escherichia coli, and purified from expressing cultures in order to examine its biochemical properties. We report here that the purified recombinant ADRP binds fatty acids and exhibits stoichiometric saturable binding of NBD-stearic acid with a K(d)=0.145+/-0.003 microM and a B(max)=0.99+/-0.05. Analysis of fluorescence emission spectra indicates that the polarity of the ADRP binding site is near epsilon approximately 23, close to that observed for fatty acid binding sites in other lipid binding proteins such as the liver fatty acid binding protein. The data presented here provide evidence that isolated ADRP purified in the experimental conditions described here can be used for functional studies.

4-Chloro-7-nitrobenzofurazan↗

PubMed2002

Tumour stage, node stage, p53 gene status, and bcl-2 protein expression as predictors of tumour response to platin-fluorouracil chemotherapy in patients with squamous-cell carcinoma of the head and neck.

The purpose of this study was to establish the relative contribution of tumour stage, node stage, p53 gene status, p53 expression, and bcl-2 protein expression to tumour response to platin-fluorouracil chemotherapy in 141 patients with squamous-cell carcinomas of the head and neck. Tumour response was measured at the primary site after three cycles of chemotherapy. Exons 2-10 and the coding part of exon 11 were sequenced on both strands. Bcl-2 or p53 expression was detected by immunohistochemistry. Predictor variables of objective response (reduction of at least 50% of tumour size) were tested in univariate and multivariate analyses. P53 mutations were found in 52 patients (37%). Tumour cells expressed p53 in 84 cases (59%) and bcl-2 in 25 cases (18%). T1 or T2 stage (adjusted odds ratio, 3.3; 95% confidence interval 1.3-8.7; P=0.01), N0 node stage (adjusted odds ratio, 2.7; 95% confidence interval 1.1-6.4; P=0.03), p53 wild-type gene (adjusted odds ratio, 4.0; 95% confidence interval 1.7-9.5; P=0.002), and bcl-2 protein expression (adjusted odds ratio, 20; 95% confidence interval 2.3-170; P=0.006), were positively associated with tumour response. P53 protein expression was not predictive of response. In conclusion, tumour stage, node stage, p53 gene status, and bcl-2 expression are independent predictors of tumour response to platin-fluorouracil in patients with squamous-cell carcinomas of the head and neck.

Adult↗

PubMed2006

Tracheal occlusion in fetal rats alters expression of mesenchymal nuclear transcription factors without affecting surfactant protein expression.

BACKGROUND/PURPOSE: Mesenchymal nuclear transcription factors (MNTF) are involved in lung development and maturation and regulate surfactant protein (SP) expression. Prolonged (>2 weeks) fetal tracheal occlusion (TO) has been shown to accelerate lung growth and inhibit pulmonary surfactant synthesis. The effects of TO on SP expression and MNTF, however, have not been formally assessed. The objectives of this study were to evaluate the effects of short-term (3 days) TO on normal lung growth and protein expression of pulmonary MNTF involved in SP synthesis. METHODS: At E19 (term, 22 days), 2 fetuses per time-dated Sprague-Dawley rats underwent either TO (n = 23) or a sham (n = 22) operation. Lungs were harvested 72 hours post surgery. Pulmonary SP-A; SP-B; SP-C messenger RNA (mRNA) expression; and SP-A and SP-B, Hoxb5, thyroid transcription factor 1, and retinoic X receptor-alpha protein expression were analyzed. RESULTS: Lung weight was significantly increased by TO (TO 0.32 +/- 0.02g vs SHAM 0.14 +/- 0.01 g; P < .001), resulting in 123% increase of the lung-to-body-weight ratio. No difference of SP-A-mRNA (177 +/- 4.3 TO vs 169 +/- 4.4 SHAM; P = .25), SP-B-mRNA (87.7 +/- 0.2 TO vs 87.4 +/- 0.02 SHAM; P = .33), and SP-C-mRNA (186.5 +/- 3.2 TO vs 183.2 +/- 2.7 SHAM; P = .45) expression was found. Surfactant protein A (175.6 +/- 25.3 TO vs 192.5 +/- 19.8 SHAM; P = .59) and SP-B (163.4 +/- 5.2 TO vs 166.8 +/- 9.3 SHAM; P = .75) protein expression were similar in both groups; however, Hoxb5 (70.3 +/- 18.9 TO vs 130.6 +/- 5.1 SHAM; P = .02) and thyroid transcription factor 1 (102.6 +/- 19 TO vs 181.1 +/- 6.3 SHAM; P = .007) expression were significantly decreased. Retinoic X receptor-alpha expression tended to be increased by TO (171.9 +/- 6.0 TO vs 155.4 +/- 6.7 SHAM; P = .06). CONCLUSIONS: Short-term TO late in gestation induces rapid lung growth. Surfactant protein-mRNA and protein expression are not significantly altered. Thyroid transcription factor 1 and Hoxb5 are down-regulated by TO, suggesting that duration and timing of occlusion are important in balancing the effects of TO on lung growth vs lung maturation.

Animals↗

PubMed1997

[Relationship of primary pulmonary carcinoma with P16 protein expression].

This study sought to address the relationship of primary pulmonary carcinoma (PPC) with P16 protein expression. The expression of P16 protein in 65 cases of PPC was examined with immunohistochemical staining. The rate of loss of P16 protein expression in PPC was 36.92% +/- 18.45%. The rate of loss of P16 protein expression in adenocarcinoma (AC) was 28.47 +/- 16.33%, that in squamous cell carcinoma (SCC) was 35.95% +/- 17.36%, and that in adenosquamous cell carcinoma (ASCC) 57.88% +/- 10.18%. There significant differences were in the rate of loss of P16 protein expression between those aged < 60 with SCC and those aged > 60 with SCC, between low differentiated PPC and intermediate differentiated PPC, between AC and ASCC, and between SCC and ASCC (P < 0.05). There were no significant differences in the rate of loss of P16 protein between males and females with PCC, between left and right PPC, and between PPC and metastatic pulmonary carcinoma of lymph node (P > 0.05). These suggest that P16 protein expression may be one of the important standards in estimating the prognosis of patients with PCC.

Adenocarcinoma↗

PubMed1995

Selective humoral immune response of Balb/C mice to Brucella abortus proteins expressed by vaccinia virus recombinants.

Genes encoding Brucella abortus Cu/Zn superoxide dismutase (SOD) and a 54 kDa Escherichia coli HtrA homologue were cloned into shuttle plasmids pUV-1 and pSC11, and transfected into vaccinia virus to develop recombinants vUBSOD and vSB54. Control vaccinia virus recombinants vUV-1 and vSC11, carrying only the beta-gal reporter gene but no B. abortus DNA were also developed. Recombinants were analyzed in Western blotting using a polyclonal B. abortus immune serum. vUBSOD expressed a protein of apparent molecular weight of 28 kDa, composed of the 20 kDa B. abortus Cu/Zn-SOD and a protein approximately 8 kDa encoded by a portion of the vaccinia virus TK gene. vSB54 expressed a 54 kDa protein corresponding to the 54 kDa HtrA homologue. Recombinants vUSV-1 and vSC11 did not express B. abortus proteins. Groups of mice were inoculated intraperitoneally with 10(7) TCID50 of 1 of the 4 different recombinant vaccinia viruses and 5 weeks later their sera were analyzed for antibodies against vaccinia virus and B. abortus proteins. Each group of mice responded with antibodies to vaccinia virus. Sera of vSB54-inoculated mice recognized the 54 kDa HtrA homologue. vUBSOD did not induce a humoral immune response. These results represent the first report on the expression of B. abortus proteins by vaccinia virus recombinants and the first demonstrated immune response against a B. abortus protein expressed by such a recombinant.

Animals↗

PubMed2004

Acute exercise alters Galphai2 protein expressions through the ubiquitin-proteasome proteolysis pathway in rat adipocytes.

The effects of acute exercise on the protein expressions of heterotrimeric G protein alpha subunits were examined in rat adipocytes. Galphai2 protein expression was significantly reduced 0 and 3h after exercise but increased 24h after exercise, without alterations in Galphai2 mRNA expressions. The protein expressions of other alpha subunits, Galphas, Galphai1, and Galphai3, were not influenced. Both the 26S proteasome activity and polyubiquitination of Galphai2 protein were significantly increased 0 and 3h after exercise. Whereas, proteasome activity was decreased, and the polyubiquitination of Galphai2 protein was returned to the control level 24h after exercise. The reductions in Galphai2 protein expressions 0 and 3h after exercise were completely prevented by the injection either of a proteasome inhibitor or of a beta-adrenergic receptor blocker prior to exercise. Thus, acute exercise altered the expression of Galphai2 protein via mechanisms which involve the coupling of beta-adrenergic receptors to an agonist with subsequent ubiquitin-proteasome-dependent proteolysis.

Acetylcysteine↗

PubMed2001

Kainate-induced epilepsy alters protein expression of AMPA receptor subunits GluR1, GluR2 and AMPA receptor binding protein in the rat hippocampus.

Kainic acid induces seizures with consecutive degeneration of highly vulnerable hippocampal CA3 neurons in adult rats. An abnormal influx of calcium through newly synthesized alpha-amino-3-hydroxy-5-methyl-4-isoxazole proprionic acid (AMPA) receptors lacking the GluR2 subunit, which normally renders AMPA receptors calcium impermeable, is thought to play a pivotal role for postictal neuronal death (GluR2 hypothesis). Using a specific GluR2 antiserum, postictal hippocampal GluR2 protein expression was investigated and compared to GluR1 between 6 and 96 h after seizure induction. In addition, postictal protein expression of a recently cloned AMPA receptor binding protein (ABP), which anchors AMPA receptors in the plasma membrane was also analyzed, to address the question of whether its protein expression is associated with neuronal death or survival. At 6 h after seizure induction, GluR2 immunoreactivity (IR) in CA3 was more markedly reduced compared to GluR1, but at 24 h GluR2 IR reattained control levels. More importantly, GluR2 IR was also markedly, but transiently decreased between 6 and 48 h in hippocampal CA1 neurons, but no significant cell loss was observed. These findings modify the GluR2 hypothesis in so far as only a subset of, but not all, hippocampal CA1 and CA3 pyramidal neurons may die due to reduced GluR2 levels with consecutive calcium overload through calcium-permeable AMPA receptors. ABP was induced postictally in presumed CA2 and a subpopulation of CA3 neurons and seems not to be involved in mechanisms of delayed neuronal death.

Animals↗

PubMed2001

[ARHI mRNA and protein expression in pancreatic cancers].

OBJECTIVE: To investigate ARHI mRNA and protein expression in pancreatic cancers. METHODS: Fifty-seven paraffin-embedded resected cancer samples and patient-corresponding normal pancreatic tissues were determined by using immunohistochemistry staining and in situ hybridization method. RESULTS: The positive rate of ARHI mRNA and protein expression in normal control pancreatic tissue was 84.2% and 82.5% respectively, and in cancer group was 52.6% both. The positive rate of mRNA and protein expression in cancer group was markedly decreased (P < 0.01). Yet the protein expression correlated with mRNA. Furthermore, positive staining of ARHI protein and mRNA can be observed in duodenal mucus epithelium, fibroblasts, smooth muscle myocytes, and wall of blood vessels. There was no correlation between positive rate and cancer differentiation, or clinical stages. CONCLUSIONS: ARHI protein expression is down-regulated in pancreatic cancer, possibly plays a role as tumor suppress gene, ARHI protein expressed in multiple types of tissues including duodenal mucus epithelium, fibroblasts and so on.

Adult↗

PubMedDate not supplied

Identification and quantification of differentially expressed proteins in E-cadherin deficient SCC9 cells and SCC9 transfectants expressing E-cadherin by dimethyl isotope labeling, LC-MALDI MS and MS/MS.

A strategy based on isotope labeling of peptides and liquid chromatography matrix-assisted laser desorption ionization mass spectrometry (LC-MALDI MS) has been employed to accurately quantify and confidently identify differentially expressed proteins between an E-cadherin-deficient human carcinoma cell line (SCC9) and its transfectants expressing E-cadherin (SCC9-E). Proteins extracted from each cell line were tryptically digested and the resultant peptides were labeled individually with either d(0)- or d(2)-formaldehyde. The labeled peptides were combined and the peptide mixture was separated and fractionated by a strong cation exchange (SCX) column. Peptides from each SCX fraction were further separated by a microbore reversed-phase (RP) LC column. The effluents were then directly spotted onto a MALDI target using a heated droplet LC-MALDI interface. After mixing with a MALDI matrix, individual sample spots were analyzed by MALDI quadrupole time-of-flight MS, using an initial MS scan to quantify the dimethyl labeled peptide pairs. MS/MS analysis was then carried out on the peptide pairs having relative peak intensity changes of greater than 2-fold. The MS/MS spectra were subjected to database searching for protein identification. The search results were further confirmed by comparing the MS/MS spectra of the peptide pairs. Using this strategy, we detected and compared relative peak intensity changes of 5480 peptide pairs. Among them, 320 peptide pairs showed changes of greater than 2-fold. MS/MS analysis of these changing pairs led to the identification of 49 differentially expressed proteins between the parental SCC9 cells and SCC9-E transfectants. These proteins were determined to be involved in different pathways regulating cytoskeletal organization, cell adhesion, epithelial polarity, and cell proliferation. The changes in protein expression were consistent with increased cell-cell and cell-matrix adhesion and decreased proliferation in SCC9-E cells, in line with E-cadherin tumor suppressor activity. Finally, the accuracy of the MS quantification and subcellular localization for 6 differentially expressed proteins were validated by immunoblotting and immunofluorescence assays.

Amino Acid Sequence↗

PubMed2002

Rapid tissue microarray assay of p16 protein expression for different stage nasopharyngeal carcinoma.

OBJECTIVE: To effectively screen p16 protein expression of different clinical stage nasopharyngeal carcinoma (NPC) by constructing and applying high-throughput tissue microarray/tissue chip. METHODS: A series of tissue chips were prepared by using tissue arrayer with samples from different clinical stage NPC tumors and noncancerous nasopharynx tissue. Specimens from 259 cases of nasopharyngeal lesions were detected immunohistochemically on a tissue chip for p16 protein expression and the correlation of p16 protein expression to clinical stage of NPC was analyzed statistically. RESULTS: p16 protein expression was detected in all 18 histologically normal nasopharyngeal epithelia. No p16 protein was detected in 3 of 3 (100%) stage I NPC, 38 of 44 (86.3%) stage II NPC, 59 of 68 (86.8%) stage III NPC, 23 of 28 (82.1%) stage IV NPC, 87 of 98 (88.8%) unclear stage NPC. The efficiency of p16 protein expression in NPC tissues was significantly lower than that in normal nasopharyngeal epithelia (chi(2) = 82.58, P < 0.001), and there was no apparent relationship between p16 protein expression and clinical stages (chi(2) = 0.09, P = 0.769). CONCLUSIONS: The frequent deletion of p16 protein in NPC suggests that p16 gene has an important role in the development and progression of NPC. The consistency of p16 protein deletion in different stages of NPC suggests that the deletion of p16 protein is an early event in the development of NPC, and it is feasible to utilize tissue microarray for a rapid, economic and accurate screening of clinical tissue specimens on a large scale.

Cyclin-Dependent Kinase Inhibitor p16↗

PubMed2001

Technetium-99m-sestamethoxyisobutylisonitrile scan as a predictor of chemotherapy response in malignant lymphomas compared with P-glycoprotein expression, multidrug resistance-related protein expression and other prognosis factors.

The purpose of the present study was to predict the response of malignant lymphomas (MLs) to chemotherapy using technetium-99m methoxyisobutylisonitrile (Tc-MIBI) scan and to compare it with the predictive ability of P-glycoprotein (P-gp) expression, multidrug resistance-related protein (MRP) expression and other prognosis factors. Twenty-five ML patients were enrolled in this study prior to initiation of chemotherapy. Images were obtained 10 min after intravenous injection of Tc-MIBI, interpreted visually and the tumour-to-background (T/B) ratios calculated. Immunohistochemical analyses were performed on sections of the biopsy specimens to determine P-gp and MRP expression. Chemotherapy response was evaluated in the first 1-2 years after completion of chemotherapy. The mean T/B ratio of the 15 patients with a good response (3.3 +/- 0.6) was significantly higher than that of the 10 patients with a poor response (1.2 +/- 0.1). All 15 patients with a good chemotherapy response had positive Tc-MIBI scan results and negative P-gp and MRP expression. All 10 patients with a poor response had negative Tc-MIBI scan results and either positive P-gp or MRP expression. Other prognosis factors showed no significant difference in the incidence of good and poor responses. Tc-MIBI scan results represent P-gp or MRP expression more accurately than other prognosis factors and predict the chemotherapy response in ML patients.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMedDate not supplied

p53 protein expression in gastrointestinal lymphomas.

We investigated the p53 protein expression in gastrointestinal lymphomas (GIL). Paraffin-embedded samples of 52 patients were examined for this purpose. The avidin-biotin Complex method was used for immunostaining. Nine of the 52 samples (17.3%) showed p53 staining. There was no relationship between the p53 protein expression and clinical characteristics, such as stage, disease localization and tumor burden. Complete remission was higher in patients not expressing this protein, and the p53 protein was more frequently expressed in intermediate and high grade histopathology than low grade lymphomas, but there was no statistically significant difference between the two groups (p = 0.008). Interestingly, patients expressing the p53 protein were younger than the ones not expressing it (30.7 +/- 14.1 vs. 43.6 +/- 15.7 years). We conclude that the p53 protein expression in GILs may be a poor prognostic indicator due to a lower response rate to chemotherapy.

Adult↗