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P Mehta

Publications and source records attributed to P Mehta.

At least 91 records · Page 5Linked to original sources
PubMed1996

Oxidized LDL decreases L-arginine uptake and nitric oxide synthase protein expression in human platelets: relevance of the effect of oxidized LDL on platelet function.

BACKGROUND: Oxidized LDL (ox-LDL) promotes vasoconstriction and platelet activation. The present study was undertaken to determine the involvement of the L-arginine-nitric oxide (NO) pathway in ox-LDL-mediated platelet activation. METHODS AND RESULTS: Washed human platelets were incubated with native LDL or ox-LDL for 1 hour at 37 degrees C followed by measurement of platelet function and indexes of the L-arginine-NO pathway. Ox-LDL but not native LDL caused a concentration-dependent increase in thrombin-induced platelet aggregation and 14C-serotonin release. These effects of ox-LDL were inhibited by pretreatment of platelets with L-arginine, the precursor of NO. Ox-LDL also caused a concentration-dependent reduction in the uptake of 3H-L-arginine by platelets. In addition, NO synthase activity, measured as conversion of 3H-L-arginine to 3H-L-citrulline, decreased on incubation of platelet cytosol with ox-LDL. Nitrite production was also reduced by treatment of platelets with ox-LDL. These effects of ox-LDL on NO synthase activity and nitrite production were reversed by pretreatment of platelets with L-arginine. Concurrent with the decrease in NO production, cytosolic cGMP was inhibited in ox-LDL-treated platelets. The inhibitory effects of ox-LDL were dependent in part on the increase of cholesterol in the platelets. Western blot analysis demonstrated approximately 50% reduction in the expression of NO synthase protein in platelets treated with ox-LDL. CONCLUSIONS: These observations indicate that the L-arginine-NO pathway is involved in the effects of ox-LDL on platelet function and that ox-LDL stimulates platelet function primarily by diminishing NO synthase expression as well as decreasing the uptake of L-arginine.

Arginine↗
PubMed1996

Nuclear accumulation of p53 protein following kainic acid-induced seizures.

The p53 tumor suppressor gene has been implicated in apoptotic cell death. The present study was conducted to investigate whether expression of p53 protein is increased in association with kainic acid-induced neuronal apoptosis. Adult male Sprague-Dawley rats were treated systemically with the glutamate analog kainic acid, and sacrificed either 4 or 30 h after the onset of seizure activity. Immunohistochemistry was performed on paraffin-embedded sections using an anti-p53 polyclonal antibody. At both time points, increased p53 immuno-reactivity was observed predominantly in the nucleus of apoptotic neurons. These findings lend additional support to the hypothesis that p53 is a marker of neuronal apoptosis in the CNS, and suggest that nuclear accumulation of p53 protein may be an important mediator of neuronal death.

Animals↗
PubMed1996

The design of agents to control DNA methylation adducts. Enhanced major groove methylation of DNA by an N-methyl-N-nitrosourea functionalized phenyl neutral red intercalator.

An N-methyl-N-nitrosourea (MNU) moiety [CH3N(N=O)C(=O)NH-] linked to the C4'-position of the 5-substituted phenyl ring of phenyl neutral red (PNR), 2-methyl-3-amino-5-[p-[[2-[(N-nitroso-N-methylcarbamoyl)amino]ethy l] carbamoyl]phenyl]-7-(dimethylamino)phenazenium chloride (MNU-PNR), has been synthesized as an approach to design a molecule that will deliver alkylating agents with some preference to guanine (Gua) in the major groove of DNA. The PNR nucleus was chosen because previous studies suggested the following: (1) PNR binds with a slight preference for G/C rich sequences; and (2) PNR intercalates into DNA from the major groove with the 5-phenyl ring pointing out into the major groove (Müller, W., Bünemann, H., and Dattagupta, N. (1975) Eur. J. Biochem. 54, 279-291). It is demonstrated that MNU-PNR yields 2.6 and 6.0 times more N7-methylguanine (7-MeGua) than MNU at low salt (10 mM Tris buffer) and high salt (10 mM Tris buffer + 200 mM NaCl), respectively. It is also shown that the ratio of 7-MeGua (a major groove adduct) to N3-methyladenine (a minor groove adduct) is approximately 5 times higher for MNU-PNR than for MNU. The yield of the 7-MeGua adduct is decreased by the coaddition of a nonmethylating analogue of MNU-PNR or NaCl, but increased in the presence of the minor groove intercalator, ethidium bromide. Using a 32P-end-labeled restriction fragment, the enhanced methylation by MNU-PNR at 7-Gua is confirmed, and it is demonstrated that the sequence-dependent formation of 7-MeGua from MNU-PNR is the same as that seen with MNU. UV, circular dichrosism, and viscosity studies are consistent with MNU-PNR binding to DNA via an intercalation-based process.

Adenine↗
PubMed1996

Studies of vascular tolerance to nitroglycerin: effects of N-acetylcysteine, NG-monomethyl L-arginine, and endothelin-1.

Development of vascular tolerance to nitroglycerin (NTG) has been attributed to sulfhydryl (SH) depletion, guanylate cyclase desensitization, or both. Controversy regarding the precise contribution of these mechanisms may be due to variations in experimental design. To examine further the biochemical basis of NTG tolerance, norepinephrine (NE)-precontracted rat aortic rings were exposed to NTG (10(-5)M), which resulted in 84 +/- 6% relaxation. Other rings were first superfused with NTG (10(-6)M) and then contracted with NE. These rings showed a marked tolerance to the vasorelaxant effects of NTG (maximal relaxation 20 +/- 5%, n = 15, p < 0.001 vs. control rings). Similar tolerance to NTG was observed when the vascular rings were first superfused with acetylcholine (ACh 10(-6)M), indicating cross-tolerance between ACh and NTG. Treatment of NTG-tolerant rings with N-acetylcysteine (NAC) (10(-5)M) did not restore vascular smooth muscle (VSM) relaxation in response to NTG (maximal relaxation 23 +/- 5%, n = 8), suggesting that SH depletion may not be the basis of NTG tolerance in these experiments. Parallel sets of NTG-tolerant aortic rings were contracted with endothelin-1 (ET-1, n = 5) or the endothelium-derived relaxing factor (EDRF) synthase inhibitor NG-monomethyl L-arginine (L-NMMA, 10(-4)M, n = 8). In both ET-1- and L-NMMA-contracted rings, vascular relaxation in response to NTG was preserved (80 +/- 6 and 88 +/- 8% relaxation, respectively). Measurement of cyclic GMP in aortic rings showed marked accumulation on initial exposure of tissues to NTG (310 +/- 10 fmol/mg), whereas the NTG-tolerant rings showed much less cyclic GMP accumulation (48 +/- 29 fmol/mg). Rings contracted with L-NMMA or ET-1, but not NE, accumulated cyclic GMP when exposed to NTG (280 +/- 20 fmol/mg). These data indicate that NTG tolerance develops on exposure of vascular rings superfused with NTG or ACh and is probably not related to tissue SH depletion. Contraction of NTG-tolerant rings with ET-1 or L-NMMA restores NTG-mediated relaxation.

Acetylcysteine↗
PubMed1996

Neurological Symptoms, Not Signs, Are Common in Early HIV Infection.

UNLABELLED: Objective. To examine the cross-sectional prevalence of neurological symptoms and signs in a large cohort of human immunodeficiency virus (HIV)-seropositive men, and determine the relationship of the symptoms to disease stage, immunologic markers, and independent variables from neuropsychological (NP) testing and psychiatric interview. METHODS: One hundred-nine controls and 386 HIV-infected volunteers enrolled in the HIV Neurobehavioral Research Center (HNRC) longitudinal study. The majority, without acquired immune deficiency syndrome (AIDS), were screened for alcohol/substance abuse; previous diagnosis of HIV-associated dementia; and HIV-unrelated developmental, neurological, medical, and neurobehavioral conditions which potentially impair cognition; and underwent a structured neurological interview and examination, standardized NP testing, and psychiatric interview as part of a more extensive battery. A large subset (N = 377) underwent lumbar puncture for cerebrospinal fluid (CFS) examination. We examined the relationship of sixteen select but independent variables, using stepwise multiple regressions, from demographic/staging, immunological, NP, and psychiatric domains to neurological symptoms in an effort to identify possible predictors of subclinical nervous systems involvement. Results. All categories of neurological symptoms were significantly more prevalent among medically asymptomatic (CDC stage A) subjects than controls, with a further rise in prevalence in those with more advanced stages of infection. The most marked rise was seen in cognitive and sensorimotor complaints. In contrast, significant findings on neurological examination were evident in only the sicker (stage C) subjects. Stage of illness, serum &beta;2-microglobulin, psychiatric indices of depressed mood or anxiety, and NP "motor" performance were the most significant independent variables associated with the presence of neurological symptoms. CSF pleocytosis was seen early (CDC stage A), and may reflect the presence of HIV in the central nervous system (CNS) at the least stages of infection. We also confirmed the value of CSF &beta;2m and neopterin as important markers of advancing disease stage. Whether they predict subclinical CNS involvement is to be determined by longitudinal observations. Conclusion. Neurological complains are common in medically asymptomatic HIV subjects whereas signs are not. The symptoms correlate with commonly determined independent measures of depression, anxiety, NP tests of fine motor speed and strength, as well as indices of disease worsening (CDC stage, serum &beta;2m).

AIDS Dementia Complex↗
PubMed1996

Platelet inhibitory effect of nitroglycerin in platelet-rich plasma: relevance of glutathione-s-transferases in plasma.

BACKGROUND: Nitroglycerin (NTG) is believed to exert its platelet inhibitory effect via its biotransformation to nitric oxide (NO). We examined the relevance of glutathione-s-transferases (GST) in plasma in the conversion of NTG to NO and the platelet inhibitory effect of NTG. METHODS AND RESULTS: Nitroglycerin (1-100 micrograms/mL) was incubated with human platelet-rich plasma (PRP) for 10-60 minutes. Nitroglycerin caused a concentration-dependent inhibition of platelet aggregation in PRP with IC50 approximately 50 micrograms/mL. NTG also enhanced nitrite levels in PRP and stimulated cyclic GMP accumulation in platelets. In contrast, when NTG was incubated with washed platelets (WP) in concentrations as high as 100 micrograms/mL, there was no inhibition of platelet aggregation, formation of nitrite, or accumulation of cGMP. However, treatment of WP suspension with authentic NO exhibited diminished platelet aggregation, suggesting that NTG delivers NO in plasma that subsequently inhibits platelet aggregation. In keeping with this concept, the aggregation inhibitory effect of NTG in PRP was blocked by oxyhemoglobin. The platelet aggregation inhibition by NTG was potentiated by propylthiouracil (600 micrograms/mL), a GST inducer, and antagonized by ketoprofen (100 micrograms/mL), a GST inhibitor. Direct measurement indeed showed significant GST activity in plasma (24 +/- 3 mU/mL). CONCLUSIONS: We suggest that NTG inhibits platelet aggregation in PRP by its biotransformation to NO in plasma. The presence of GST, and perhaps other cofactors, in plasma is relevant in the platelet inhibitory effects of NTG in PRP.

Adult↗
PubMed1995

Reduction of nitric oxide synthase activity in human neutrophils by oxidized low-density lipoproteins. Reversal of the effect of oxidized low-density lipoproteins by high-density lipoproteins and L-arginine.

Oxidized low-density lipoproteins (ox-LDL) inhibit vascular relaxation by decreasing the synthesis or rapid degradation of endothelium-derived relaxing factor (EDRF), now identified to be nitric oxide (NO). We examined the regulation of NO synthase activity in human neutrophils, which also generate NO, by lipoproteins. Isolated human neutrophils were incubated with native-LDL, ox-LDL (10-50 micrograms protein/mL), high-density lipoproteins (HDL, 100 micrograms protein/mL) or HDL+ox-LDL, and NO synthase activity was measured as conversion of [3H]L-arginine to [3H]L-citrulline. Ox-LDL, but not native-LDL or HDL, significantly decreased NO synthase activity in human neutrophils. This effect of ox-LDL was incubation time and concentration dependent. The incubation of cells with HDL or L-arginine diminished the effects of ox-LDL on NO synthase activity. Thus, ox-LDL decreases the activity of NO synthase enzyme, and this effect of ox-LDL can be modified by HDL and L-arginine.

Arginine↗
PubMed1995

Protein 1a: a major wheat germ agglutinin binding protein on the surface of human granulocytes associated with the cytoskeleton.

Lectin-receptors on leukocyte and endothelial surfaces are becoming more important in the light of increasing evidence which implicates lectin-carbohydrate interactions in diverse physiological phenomena. This study reports the identification of a major 118 kDa granulocyte surface protein, (Protein 1 a) which binds the lectin wheat germ agglutinin (WGA), and is distinctly different from reported WGA binding granulocyte membrane proteins. Protein 1 a has been isolated from the Triton-soluble and Triton-insoluble lysates of normal individuals and patients with Chronic Myeloid Leukemia (CML) using a combination of differential solubilization, lectin affinity, ion exchange chromatography and HPLC. The protein from the detergent lysates of both normal and CML granulocytes has similar pI values, lectin affinities, and hydrophobicity. However, its solubility in Triton is different in the two cell types. In 71% of CML cases examined, Protein 1 a exhibits decreased Triton solubility suggesting its increased association with the cytoskeleton (CSK). Stimulation of normal granulocytes with WGA leads to the translocation of the soluble form of Protein 1 a to the Triton-insoluble fraction. This cytoskeletal recruitment of Protein 1 a is sustained only under conditions of excess WGA and occupied receptor. The CSK disruptive agent dihydrocytochalasin B (H2CB) releases the insoluble form of the receptor into the Triton-soluble fraction. Investigation of a CSK-involving process such as ligand internalization revealed that CML granulocytes exhibit slower kinetics of internalization of fluorescent WGA molecules.(ABSTRACT TRUNCATED AT 250 WORDS)

Antigens, CD↗
PubMed1995

Identification of constitutive and inducible forms of nitric oxide synthase in human platelets.

A number of cell types possess an L-arginine-nitric oxide (NO) pathway. We studied the presence of constitutive and inducible forms of NO synthase in human platelets. N omega-nitro-L-arginine, an inhibitor of NO synthase, potentiated thrombin-induced aggregation of washed human platelets, whereas L-arginine inhibited it. The direct evidence for the presence of constitutive form of NO synthase came from the observation of conversion of tritium-labeled L-arginine to tritium-labeled L-citrulline by washed platelets suspended in Ca(++)-rich but not in Ca(++)-free buffer. Incubation of washed platelets in Ca(++)-free buffer with cytokines (tumor necrosis factor-alpha and interferon-gamma) or cytokines plus lipopolysaccharide caused a marked increase in the conversion of [3H]L-arginine to [3H]L-citrulline, suggesting the presence of inducible form of NO synthase. Gel electrophoresis identified an approximately 130 kd protein band with NO synthase in the platelet cytosol, which on isolation converted [3H]L-arginine to [3H]L-citrulline. This 130 kd protein required the presence of Ca++, reduced nicotinamide adenine dinucleotide phosphate tetrahydro-L-biopterin, and flavin adenine dinucleotide for expression of NO synthase activity. Platelet sonicates demonstrated presence of nitrite, and its concentrations were lowered by preincubation of platelets with NG-nitro-L-arginine methyl ester and enhanced in cytokine-treated platelets. Reverse-transcription polymerase chain reaction demonstrated messenger RNA expression of the constitutive endothelial (but not brain) and inducible isoforms of NO synthase in platelets. These observations indicate that human platelet cytosol possesses both constitutive and inducible forms of NO synthase.

Amino Acid Oxidoreductases↗
PubMed1994

Percutaneous balloon valvuloplasty compared with open surgical commissurotomy for mitral stenosis.

BACKGROUND: Percutaneous balloon mitral valvuloplasty has been proposed as an alternative to open surgical commissurotomy for the treatment of rheumatic mitral-valve stenosis. METHODS: We enrolled 60 patients with severe mitral stenosis and favorable valvular anatomy in a prospective, randomized trial comparing the two procedures. All patients underwent cardiac catheterization before the procedure and one week, six months, and three years thereafter. Hemodynamic data were analyzed by investigators who were blinded to the patients' treatment assignments. RESULTS: Mitral-valve areas improved initially in both groups, from a mean (+/- SD) of 0.9 +/- 0.3 cm2 to 2.1 +/- 0.6 cm2 in the balloon-valvuloplasty group (30 patients; P < 0.01) and from 0.9 +/- 0.3 cm2 to 2.0 +/- 0.6 cm2 in the surgical group (30 patients; P < 0.001). Although improvement was maintained in both groups, mitral-valve areas were greater in the patients in the balloon-valvuloplasty group at three years (2.4 +/- 0.6 cm2, vs. 1.8 +/- 0.4 cm2 in the surgery group, P < 0.001). Restenosis occurred in three patients in the balloon-valvuloplasty group and four in the surgery group. One patient in the balloon-valvuloplasty group died of an apparent stroke after 2.5 years; four patients in the balloon-valvuloplasty group had residual atrial septal defects, and three patients (two in the balloon-valvuloplasty group and one in the surgery group) were judged to have severe mitral regurgitation. Seventy-two percent of the patients who underwent balloon valvuloplasty and 57 percent of the surgically treated patients were in New York Heart Association functional class I (i.e., they had no cardiovascular symptoms) at three years. No patient was lost to follow-up. CONCLUSIONS: In the treatment of mitral stenosis, balloon valvuloplasty and open surgical commissurotomy have comparable initial results and low rates of restenosis, and both produce good functional capacity for at least three years. The potential complications associated with balloon valvuloplasty should be noted. The better hemodynamic results at three years, lower cost, and elimination of the need for thoracotomy suggest that balloon valvuloplasty should be considered for all patients with favorable mitral-valve anatomy.

Adolescent↗
PubMed1994

Congenital coagulopathies and pregnancy: report of four pregnancies in a factor X-deficient woman.

Pregnancy in women with congenital coagulation factor deficiencies has been associated with adverse fetal outcomes. Recurrent spontaneous abortions, placental abruptions, and premature births are reported, the exact reasons for which are not clear, and management of such patients continues to be a challenge. We reviewed the outcome of four pregnancies in a patient with factor X deficiency, and looked at the effect of factor replacement therapy on pregnancy. Her first two pregnancies resulted in the birth of extremely premature babies at 21 and 25 weeks of gestation, both of which died in the neonatal period. The patient was treated with fresh frozen plasma for acute bleeding episodes during these pregnancies. In addition during her second conception she was given factor IX complex [Konyne] prophylactically, but only in the latter half of her pregnancy. During her next two pregnancies she was treated early on during pregnancy, with prophylactic replacement of factor X. She delivered healthy babies at 34 and 32 weeks of gestation, and they are both doing well. We therefore suggest possible mechanisms by which aggressive prophylactic factor support in a female with severe congenital coagulopathy, may improve on fetal outcome.

Adult↗
PubMed1994

Biologic significance of quantitative estrogen receptor immunohistochemical assay by image analysis in breast cancer.

The authors assayed 209 stage I and II mammary carcinomas for the estrogen receptor (ER) with an immunocytochemical assay (ICA) and quantitated the nuclear stain with the SAMBA 4000 Cell Image Analysis System (Imaging Products International, Inc., Chantilly, VA). The cases had been followed for 54-214 months (average, 64 months). The results were correlated with the patients' overall and disease-free survival times. Three of the parameters obtained from the quantitative analysis were evaluated: labeling index, mean optical density, and quick score. Statistical analysis was performed with the Kaplan-Meier product limit estimator for quantitated values and Cox regression for risk of mortality and disease progression. Mean optical density of the nuclei at a cut-off value of 10 produced the strongest association between quantitative ERICA and overall and disease-free survival times in discriminating high- and low-risk groups (P = .016 and P = .018, respectively). When the mean optical density results were categorized into ranges of values of potential biologic significance according to overall survival times, patients with mean optical density greater than 15 were found to be at lowest risk; patients with values between 5 and 15 had a statistically significant intermediate risk; and the group with values less than 5 had the worst outcome (P = .018). The probability of disease-free survival also was statistically significant (P = .038) among the three groups with cut-off points of less than 10, 10-35, and greater than 35. These results showed that quantified optical density has better discriminating power for risk prediction than that obtained by the biochemical assay for ER at a cut-off value of 10 or 20 fmol/mg. Estrogen receptor ICA has been adequately shown to be as or more accurate than ligand-binding assays. Our results corroborate those studies and support the utility of ICA assays for ER by showing that quantitation performed by image analysis is an objective and reproducible method yielding clinical prognostic information of higher reliability than that given by the dextran-coated charcoal ER assay.

Adult↗
PubMed1994

Polymerase chain reaction detection of viruliferous Bemisia tabaci (Homoptera: Aleyrodidae) with two tomato-infecting geminiviruses.

The sweetpotato whitefly, Bemisia tabaci (Gennadius), is an important pest worldwide. A new biotype of sweetpotato whitefly, biotype B, causes damage by direct feeding and by the transmission of plant viruses, such as geminiviruses. In the Mediterranean area, tomato yellow leaf curl geminivirus (TYLCV) is the most serious disease of tomatoes. Another whitefly-transmitted geminivirus, tomato mottle geminivirus (ToMoV), is presently a serious problem in tomato production in west-central and southwestern Florida. Because of the increasing incidence of whitefly-transmitted geminiviruses, it is necessary to develop rapid and simple diagnostic methods for the detection of viruliferous whiteflies. The polymerase chain reaction is a sensitive and specific technique for the detection and identification of plant pathogens. Polymerase chain reaction methods were used successfully to amplify 1.1-kb DNA fragments from individual viruliferous B. tabaci carrying either TYLCV or ToMoV, and no amplified DNA fragments were obtained when nonviruliferous B. tabaci adults were processed similarly. Southern hybridization analysis proved that fragments amplified from viruliferous B. tabaci adults were viral DNA. This polymerase chain reaction-based detection method is sensitive enough to detect TYLCV and ToMoV in individual viruliferous B. tabaci in mixed samples of up to 25 (1 viruliferous: 24 nonviruliferous) and 10 (1 viruliferous: 9 nonviruliferous) individuals, respectively. The potential uses of this polymerase chain reaction-based detection method in epidermiological studies of geminiviruses are discussed.

Animals↗
PubMed1994

Increased secretion of tumor necrosis factor-alpha and interferon-gamma by mononuclear leukocytes in patients with ischemic heart disease. Relevance in superoxide anion generation.

BACKGROUND: There is growing evidence for a pathogenic role for cytokines in atherogenesis. The presence of certain cytokines has been documented in human atherosclerotic vessels. This study was designed to investigate cytokine production by mononuclear leukocytes from patients with ischemic heart disease. METHODS AND RESULTS: We measured kinetics of secretion of tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) by mononuclear leukocytes from 8 control subjects, 10 patients with stable angina pectoris, and 10 patients with unstable angina pectoris. Mononuclear leukocytes were isolated and incubated with or without the plant lectin mitogen concanavalin A for 48 hours. TNF-alpha and IFN-gamma secretion were measured by ELISA. The effect of TNF-alpha and IFN-gamma on superoxide radical generation by neutrophils was also examined. Secretion of both TNF-alpha and IFN-gamma by mononuclear leukocytes increased progressively over 48 hours, and it was consistently higher (P < .02) in patients compared with control subjects. A similar increase in cytokine secretion was observed in patients with stable or unstable angina pectoris. In addition, there was no relation between the severity of coronary artery disease by angiography and cytokine secretion. Basal neutrophil superoxide radical generation was increased in patients with ischemic heart disease, and incubation with cytokines failed to further stimulate superoxide generation in these patients. CONCLUSIONS: Similar increases in cytokine secretion by mononuclear leukocytes in stable or unstable angina pectoris indicate that the increased cytokine release is not a nonspecific inflammatory response in acute myocardial ischemia. Increased cytokine secretion in ischemic heart disease may play a role in superoxide radical generation, endothelial injury, deposition and activation of cellular elements on the vessel wall, and possibly in the progression of atherosclerosis.

Angina Pectoris↗
PubMed1994

[Expression of p53 in gastric carcinoma. Prognostic value].

P53 gene mutation has been described with variable frequency in gastric cancer and its biological significance remains unclear. We studied 101 gastric carcinomas to evaluate the association between this genetic alteration and the evolution of gastric cancer. Of these, 67 patients were men and 34 were women. The median age at diagnosis was 68 years. The tumors were obtained from gastrectomies. The p53 gene mutation was determined with the monoclonal antibody DO7 (Novocastra). The neoplasms were classified as tumors with high or low level p53 expression according to the intensity and distribution of the nuclear staining. Forty eight tumors showed high level of p53 immunoreactivity. The association of p53 expression with age, sex, tumor size, histologic type, histologic grade, depth of invasion, localization, lymph node metastases, type of surgery and 5 year survival rate was investigated. The results did not demonstrate any significant association between p53 expression and the factors mentioned above.

Adenocarcinoma↗