Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04637 (p53)
 77,613 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oral cancer accounts for 40 to 50% of cancers diagnosed in India. Oral cancer is preceeded in most cases by pre malignant lesions-leukoplakia, submucous fibrosis and lichen planus. Stoppage of causative agents reverts premalignant lesions in some of the cases only. Thus anti oxidant therapy is being used to revert premalignant change to normal. Few studies available, have taken clinical parameters as indicators of response to therapy. Extensive medline search failed to reveal any study at the cellular level. This study attempts to investigate for the first time the role of p53 and bcl2 as markers of prognosis following vitamin A therapy. 24 cases of pre malignant lesions of oral cavity were studied. 1 lakh IU of vitamin A were given orally twice a week for 3 months. Biopsies were done before and after therapy. Haematoxylin and Eosin stain was done to confirm diagnosis. Immunostaining for mutant p53 and bcl2 was done on paraffin sections. 500 cells were counted over an average of 5 HPF and percentage positivity was calculated. Statistical analysis was done by applying the paired t tests. In 19 cases (79.2%) of premalignant lesions mutant p53 expression was zero before therapy, and remained unchanged even after the therapy. 3 cases (12.5%) had high mutant p53 values which reduced following therapy (p = 0.037). Therapy thus proved effective in these cases. However, in 2 cases (8.3%) pre therapy values of zero showed an increase after vitamin A therapy. These were the cases which had dysplasia and were chronic smokers. In 2 cases (8.3%) pre therapy values of bcl2 were zero and remained unchanged even after therapy and these cases did not stop smoking even during the vitamin A therapy. In 12 cases (50.0%) higher pre therapy values were reduced after therapy (p < 0.0001). Vitamin A therapy was effective in these cases. However, in 10 cases (42.0%) expression of bcl2 increased subsequent to therapy. Therapy failed in these cases because of chronic heavy smoking and tobacco chewing. Thus, in the majority of cases vitamin A was effective in preventing mutation of p53 (91.7%) and expression of bcl2 (58.0%). In effect, these two oncoproteins can be used as prognostic markers and follow up for anti oxidant therapy.
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PMID:Role of p53 and bcl2 as markers of vitamin A response in premalignant lesions of the oral cavity. 1747 47

To study the influence of microwave induced thermo-chemotherapy on high-grade urothelial cell carcinomas. Five groups of each three patients were formed of whom initial biopsies and cystectomy samples were collected. Patients were treated 2 days prior to cystectomy with mitomycin-C (group 1), hyperthermia (group 2) or thermo-chemotherapy (group 3). Group 4 patients had been treated with a cycle of six thermo-chemotherapy treatments prior to cystectomy and group 5 patients served as control (no treatment). Tumour samples were stained with Haematoxylin and Eosin, monoclonal antibody Ki-67 and the monoclonal antibody p53. In six out of the nine patients treated with hyperthermia a decrease in proliferation activity in the tumour was found. Seven out of nine patients treated with hyperthermia showed a decrease in p53 activity. A decrease in proliferation activity and p53 activity illustrate the potential role of thermo-chemotherapy as a promising intravesical treatment.
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PMID:The influence of thermo-chemotherapy on bladder tumours: an immunohistochemical analysis. 1757 92

Ganglioglioma with a glioblastomatous component and high-grade atypia of neuronal cells are extremely rare findings. In this paper, we report the case of a 60-year-old man who presented with a tumor of the left temporal lobe. Hematoxylin-Eosin stained slides revealed a complex tumor with features of glioblastoma and marked atypia of neuronal cells. Glial cells were highlightened by antibodies to GFAP and neuronal cells by chromogranin and synaptophysin markers. There was an accumulation of p53-positive cells. There was a high Ki-67 labelling index (19%).
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PMID:Ganglioglioma with glioblastoma component. 1875 48

This study was conducted to investigate the prognostic value and therapeutic response of treatment modalities on p53 protein expression and AgNOR index in squamous cell carcinoma (SCC). Furthermore, based on data, we proposed a new p53 immunohistochemistry (IHC) scoring system. Sixty albino mice were given 7,12-dimethylbenz[a]anthracine (DMBA) and 12-O-tetradecanoly Phorbol-13-acetate (TPA) to produce skin tumors. The retinoids were given after the development of tumors. p53 immunohistochemical and AgNOR staining was performed on the sections taken before and after the retinoid administration. p53 protein was expressed in 31 of the lesions (60.8%). AgNOR index was high in all 51 (100%) of the pretreated lesions. There was a marked decrease in the expression of p53 protein in 16/51 (31.4%) and AgNOR index in 36/51 (70.6%) in post-treated mice. There was no decrease in the expression of both markers in mice harboring malignant neoplasms. p53 IHC scores were 0, I, and II in epidermal hyperplasia, papilloma, and dysplasia, respectively, while they were II, III, IV, and V in SCC in situ, well-differentiated, moderately differentiated, and poorly differentiated SCCs, respectively. Alteration of p53 and AgNOR index occured during the development of SCC. The p53 IHC scores are directly related to the grades of malignancy. Both markers might be used as a supportive tool with routinely performed Hematoxylin and Eosin staining and may help in the diagnosis of SCC. The newly proposed p53 IHC scoring system will help histopathologists in making their differential diagnosis among benign, premalignant, and malignant lesions. It will also help the oncologists to assess the prognosis and effectiveness of their chemotherapy.
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PMID:Prognostic significance of new immunohistochemistry scoring of p53 protein expression in cutaneous squamous cell carcinoma of mice. 1883 75

Single high-dose irradiation has become a safe and encouraging form of radiation therapy but variations in the histological changes after irradiation have not been fully understood in clinical settings. The aim of this study was to investigate the histological changes of tumor cells after single high-dose, direct irradiation with a case of cutaneous squamous cell carcinoma that developed on a burn scar. The patient received irradiation followed by radical resection of the tumor. Tissues before and after irradiation were stained with Hematoxylin and Eosin (H&E), TdT-mediated dUTP-X nick end labeling (TUNEL), and by immunohistochemistry for MIB-1, p53, and p21. Massive necrosis was noted after irradiation but a few viable tumor cells remained. Preradiation histology revealed MIB-1 and p53 as positive, and p21 tumor cells as partially positive. These expressions were reduced after irradiation. The TUNEL stain was consistently negative. It was established that tumor cell death after single high-dose irradiation was caused mainly by necrosis rather than apoptosis in clinical settings.
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PMID:Histological changes after single high-dose irradiation for squamous cell carcinoma arising from a burn scar. 1921 12

We evaluated the medical record of patients with salivary gland neoplasms diagnosed at Timisoara City Hospital from 2002 to 2009. A study has been carried out for seven years on 204 cases of salivary gland tumors and only two cases of salivary gland lymphomas were diagnosed. The two cases were females of 71- and 49-year-old, respectively. The formalin-fixed paraffin-embedded tissue samples were cut in 4 mum thick sections and stained with Hematoxylin and Eosin. The primary monoclonal antibodies for the immunohistochemical analysis were the followings: LCA (2B11, Dako), CD20 (L26, Dako), cytokeratin (MNF116, Dako), p53 (DQ-7, Dako), and PCNA (PC-10, Dako). The histopathology and immunohistochemistry suggested in the first case a low-grade diffuse large B-cell mucosa associated lymphoid tissue lymphoma and in the second case a high-grade extranodal marginal zone B-cell lymphoma.
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PMID:Primary malignant non-Hodgkin's lymphomas of salivary glands. 1994 68

We present a case of basal cell adenocarcinoma (BCAC) in the tongue in a 65-year old male. This is an extremely rare presentation. BCAC generally occurs in the parotid gland and rarely involves the minor salivary glands. Few cases have been reported in literature with a variable presentation. The biopsy was formalin-fixed and paraffin-embedded. The sections were stained with routine Hematoxylin and Eosin. Immunohistochemistry was performed. Hematoxylin and eosin staining showed tumour composed of variable sized and shaped, nests and sheets of basaloid epithelial cells having hyperchromatic to vesicular nuclei. Immunohistochemistry was positive for Pancytokeratin, Epithelial membrane antigen and p53. The clinicopathological features and the cellular immunophenotype addressed the diagnosis towards BCAC of the tongue. The goal of this report is to increase awareness of this rare disease and to review and discuss the differential diagnosis and important considerations in treatment.
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PMID:Basal cell adenocarcinoma in the tongue: an unusual presentation. 2115 83

Kolaviron is a phytochemical isolated from Garcina kola (G. kola); a common oral masticatory agent in Nigeria (West Africa). It is a bioflavonoid used--as an antiviral, anti-inflammatory and antioxidant--in relieving the symptoms of several diseases and infections. In this study we have evaluated the neuroprotective and regenerative effect of kolaviron in neurons of the prefrontal cortex (Pfc) before or after exposure to sodium azide (NaN3) induced oxidative stress. Separate groups of animals were treated as follows; kolaviron (200 mg/Kg) for 21 days; kolaviron (200 mg/Kg for 21 days) followed by NaN3 treatment (20 mg/Kg for 5 days); NaN3 treatment (20 mg/Kg for 5 days) followed by kolaviron (200 mg/Kg for 21 days); 1 ml of corn-oil (21 days-vehicle); NaN3 treatment (20 mg/Kg for 5 days). Exploratory activity associated with Pfc function was assessed in the open field test (OFT) following which the microscopic anatomy of the prefrontal cortex was examined in histology (Haematoxylin and Eosin) and antigen retrieval Immunohistochemistry to show astroglia activation (GFAP), neuronal metabolism (NSE), cytoskeleton (NF) and cell cycle dysregulation (p53). Subsequently, we quantified the level of Glucose-6-phosphate dehydrogenase (G6PDH) and lactate dehydrogenase (LDH) in the brain tissue homogenate as a measure of stress-related glucose metabolism. Kolaviron (Kv) and Kolaviron/NaN3 treatment caused no prominent change in astroglia density and size while NaN3 and NaN3/Kv induced astroglia activation and scar formation (astrogliosis) in the Pfc when compared with the control. Similarly, Kolaviron and Kv/NaN3 did not alter NSE expression (glucose metabolism) while NaN3 and NaN3/Kv treatment increased cortical NSE expression; thus indicating stress related metabolism. Further studies on enzymes of glucose metabolism (G6PDH and LDH) showed that NaN3 increased LDH while kolaviron reduced LDH in the brain tissue homogenate (P < 0.001). In addition kolaviron treatment before (P < 0.001) or after (P < 0.05) NaN3 treatment also reduced LDH expression; thus supporting its role in suppression of oxidative stress. Interestingly, NF deposition increased in the Pfc after kolaviron treatment while Kv/NaN3 showed no significant change in NF when compared with the control. In furtherance, NaN3 and NaN3/Kv caused a decrease in NF deposition (degeneration). Ultimately, the protective effect of KV administered prior to NaN3 treatment was confirmed through p53 expression; which was similar to the control. However, NaN3 and NaN3/Kv caused an increase in p53 expression in the Pfc neurons (cell cycle dysregulation). We conclude that kolaviron is not neurotoxic when used at 200 mg/Kg BW. Furthermore, 200 mg/Kg of kolaviron administered prior to NaN3 treatment (Kv/NaN3) was neuroprotective when compared with Kolaviron administered after NaN3 treatment (NaN3/Kv). Some of the observed effects of kolaviron administered before NaN3 treatment includes reduction of astroglia activation, absence of astroglia scars, antioxidation (reduced NSE and LDH), prevention of neurofilament loss and cell cycle regulation.
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PMID:Kolaviron was protective against sodium azide (NaN3) induced oxidative stress in the prefrontal cortex. 2591 84

Aim. Evaluate tumor proliferation marker (Ki67) and p53 tumor suppressor marker in Wilms tumor and correlate with histology, anaplasia, and staging. Design. Prospective, hospital based study conducted at a tertiary pediatric referral centre in south India. Setting. Wilms tumor is the most common childhood renal malignancy worldwide. Anaplasia on histology is associated with treatment resistance but not with aggressiveness clinical presentation. Chemotherapy for Wilms tumor is based on histology and staging. Most patients respond to current chemotherapy protocol. However, a small fraction relapses or metastasizes. Affordable prognostic markers are needed for histopathological evaluation of this tumor. Subjects. Cases of histologically confirmed Wilms tumor over five years. Cases after chemotherapy were excluded as the immunostaining was inconsistent in necrotic areas. Methods. The clinical and radiological findings of 31 cases of Wilms tumor were documented at a tertiary pediatric referral hospital over five years. In addition to Hematoxylin and Eosin staining, Ki67 proliferation index and p53 expression were correlated with tumor histology and staging. Results. Age incidence was 3-8 years with female preponderance. Significant correlation was noted between Ki67 proliferation index and tumor staging. p53 expression was not useful in stratification of Wilms tumor. Conclusion. Ki67 was cost-effective immunohistochemical marker for prognostication of pediatric Wilms tumor.
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PMID:Immunohistochemical Expression of Ki67 and p53 in Wilms Tumor and Its Relationship with Tumor Histology and Stage at Presentation. 2690 59

Aluminum is a light weight and toxic metal present ubiquitously on earth, which has gained considerable attention due to its neurotoxic effects. It also has been linked ecologically and epidemiologically to several neurological disorders, including Alzheimer's disease (AD), Parkinson's disease (PD), Guamanian-Parkinsonian complex and Amyotrophic lateral sclerosis (ALS). The mechanism of aluminum neurotoxicity is poorly understood, but it is well documented that aluminum generates reactive oxygen species (ROS). Enhanced ROS production leads to disruption of cellular antioxidant defense systems and release of cytochrome c (cyt-c) from mitochondria to cytosol resulting in apoptotic cell death. Quercetin (a natural flavonoid) protects it from oxidative damage and has been shown to decrease mitochondrial damage in various animal models of oxidative stress. We hypothesized that if oxidative damage to mitochondria does play a significant role in aluminum-induced neurodegeneration, and then quercetin should ameliorate neuronal apoptosis. Administration of quercetin (10 mg/kg body wt/day) reduced aluminum (10 mg/kg body wt/day)-induced oxidative stress (decreased ROS production, increased mitochondrial superoxide dismutase (MnSOD) activity). In addition, quercetin also prevents aluminum-induced translocation of cyt-c, and up-regulates Bcl-2, down-regulates Bax, p53, caspase-3 activation and reduces DNA fragmentation. Quercetin also obstructs aluminum-induced neurodegenerative changes in aluminum-treated rats as seen by Hematoxylin and Eosin (H&E) staining. Further electron microscopic studies revealed that quercetin attenuates aluminum-induced mitochondrial swelling, loss of cristae and chromatin condensation. These results indicate that treatment with quercetin may represent a therapeutic strategy to attenuate the neuronal death against aluminum-induced neurodegeneration.
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PMID:Quercetin attenuates neuronal death against aluminum-induced neurodegeneration in the rat hippocampus. 2694 3


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