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)

Cervical carcinoma is the most frequent disease of the female reproductive organs. The tumour markers may be helpful: in early diagnosis of cervical cancer, the initial assesment of the extent of the disease, monitoring of tumour growth or tumour volume reduction, recurrence of cancer, and have been used for monitoring of the clinical course of chemotherapy and radiotherapy. In this paper we have focused on the role of new tumour markers, especially cytokines (for example G-CSF, VEGF) and molecular markers of carcinogenesis (for example Bcl-2 and p53), in comparison to typical tumour markers useful in diagnostic of cervical cancer such as CA 125, SCC-Ag, TPA, TPS, CYFRA 21-1.
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PMID:[New tumour markers useful in diagnostics and monitoring of cervical cancer]. 1859 8

We evaluated the occurrence of mutations in P53, K-RAS, COX-2, expression of COX-2 and hTERT and relations among clinicopathological signs. P53 mutations were identified in 34.4% of tumours, the majority of them occurring in SCC (squamous cell carcinoma, 55.6%). K-RAS was mutated in 12.2% of NSCLC tumours, the majority of the mutations being found in ADC (adenocarcinoma, 27.0%). Mutational screening detected three different COX-2 mutations and five different P53 mutations, published for the first time. With RT-PCR we observed that the expression of the tested genes, hTERT and COX-2, was highly significant for ADC (p<0.01) and SCC (p<0.05). Statistical analysis of the combined results revealed significant correlation between expression of COX-2 and hTERT (p<0.001), hTERT expression and staging (p<0.05) and survival (p<0.01). A positive correlation between COX-2 expression and K-RAS mutation (p<0.05) was also observed. This study provides insight into associations between the analysed biomarkers and the clinical-pathological data of the patients.
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PMID:K-RAS and P53 mutations in association with COX-2 and hTERT expression and clinico-pathological status of NSCLC patients. 1895 20

Rhein, an anthraquinone compound, can be found in the rhizome of rhubarb, a traditional Chinese medicine herb showing antitumor activity. In this study, it was observed that rhein induced S-phase arrest through the inhibition of p53, cyclin A and E and it induced apoptosis through the endoplasmic reticulum stress by the production of reactive oxygen species (ROS) and Ca2+ release, mitochondrial dysfunction, and caspase-8, -9 and -3 activation in human tongue cancer cell line (SCC-4). The most efficient induction of apoptosis was observed at 30 microM for 24 h. Mechanistic analysis demonstrated that rhein induced changes in the ratio of Bax/Bcl-2 based on the decrease of Bcl-2 levels, the loss of mitochondrial membrane potential, cytochrome c release from the mitochondria and the activation of caspase-9 and -3. The data demonstrated that rhein induces apoptosis in SCC-4 cells via caspase, ROS and mitochondrial death pathways.
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PMID:Rhein induced apoptosis through the endoplasmic reticulum stress, caspase- and mitochondria-dependent pathways in SCC-4 human tongue squamous cancer cells. 1941 20

Head and neck squamous cell carcinoma (H/N SCC) is a devastating disease in humans and cats, and shares similar features between the two species. The large population of pet cats in the United States, along with the high incidence of oral SCC in the cat, makes the cat an attractive candidate as a natural model for the human disease. There are similarities in pathology, progression, outcome, resistance to treatment, possible aetiologies and p53 expression, and we discuss the benefits of the cat as a natural model. We describe the development of a nude mouse xenograft model of feline oral SCC using the SCCF1 cell line transfected with a luciferase expression construct. In vivo tumour growth and metastasis were measured using serial bioluminescent imaging, and tumours grew best in the subcutis. The cat and nude mouse models will be useful to investigate the pathogenesis and the molecular basis of H/N SCC, and for preclinical drug screening.
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PMID:Feline head and neck squamous cell carcinoma: a natural model for the human disease and development of a mouse model. 1975 18

Squamous cell carcinoma of the head and neck (HNSCC) is the sixth most frequent cancer worldwide. SCC is the most common malignant tumor of the oral cavity with over 35,000 cases and 8,000 deaths reported in the United States each year. Previous case studies have reported increased incidence of HNSCC in patients on immunosuppressive therapy for organ transplantation. The results of these studies indicate that effective immune surveillance is important for preventing emergence of HNSCC. HNSCC may also inhibit immune response to tumor cells, which may be responsible for progression. We previously reported induction of metastatic HNSCC in p53 null mutant mice. Despite induction with the potent carcinogen dimethylbenzanthracene, each mouse developed only 1-2 primary tumors with a relatively long induction period of 22 weeks. We hypothesized that immune surveillance might eliminate early tumor cells resulting in the relatively small number of primary tumors and long induction time. To test this hypothesis we performed the induction protocol in nude mice which have defective T lymphocyte function. Decreased T lymphocyte function resulted in reduced tumor latency and increased tumor formation. Immunohistochemical studies showed that expression of cell cycle regulatory proteins is similar in mouse and human HNSCC. However, distinct differences exist between primary and metastatic tumors from nude and wild-type mice. We also determined that lymphocytes react to metastatic tumor cells by upregulating immunoglobin gene expression but are prone to apoptosis via decreased expression of survival factors and upregulation of cell death genes.
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PMID:Impaired T lymphocyte function increases tumorigenicity and decreases tumor latency in a mouse model of head and neck cancer. 1978 77

Aloe-emodin, one of the anthraquinones, has been shown to have anticancer activity in different kinds of human cancer cell lines. Therefore, the purpose of this study was to investigate the anti-cancer effect of aloe-emodin on human tongue squamous carcinoma SCC-4 cells. The results indicated that aloe-emodin induced cell death through S-phase arrest and apoptosis in a dose- and time-dependent manner. Treatment with 30 microM of aloe-emodin led to S-phase arrest through promoted p53, p21 and p27, but inhibited cyclin A, E, thymidylate synthase and Cdc25A levels. Aloe-emodin promoted the release of apoptosis-inducing factor (AIF), endonuclease G (Endo G), pro-caspase-9 and cytochrome c from the mitochondria via a loss of the mitochondrial membrane potential (DeltaPsi(m)) which was associated with a increase in the ratio of B-cell lymphoma 2-associated X protein (Bax)/B cell lymphoma/leukemia-2 (Bcl-2) and activation of caspase-9 and -3. The free radical scavenger N-acetylcysteine (NAC) and caspase inhibitors markedly blocked aloe-emodin-induced apoptosis. Aloe-emodin thus induced apoptosis in the SCC-4 cells through the Fas/death-receptor, mitochondria and caspase cascade. Aloe-emodin could be a novel chemotherapeutic drug candidate for the treatment of human tongue squamous cancer in the future.
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PMID:Aloe-emodin induces cell death through S-phase arrest and caspase-dependent pathways in human tongue squamous cancer SCC-4 cells. 2003 98

Epidemiologic, clinical, morphologic and molecular evidence show that high risk HPV, particularly type 16, is a prerequisite for some carcinomas of the upper aerodigestive tract (UADT), particularly tonsil and base of tongue. Sexual transmission is an important mode of infection while tobacco use and excessive drinking are not considered risk factors. HPV + tumors are distinct clinically and pathologically. They are more common in young patients (<40 years) with a male to female ratio of 4:1. They usually present as a small or occult primary tumor with advanced neck disease. Microscopically they are non-keratinizing squamous cell carcinomas with basaloid features, excessive mitosis and comedo type necrosis. The tumors have a distinct immunohistochemical profile characterized by strong and diffuse p16 reactivity, low or negative p53 staining and high Ki67 labeling scores. HPV + carcinomas are more radio-sensitive and have a better prognosis than the classical keratinizing SCC of the UADT. An anti-HPV vaccine has recently been made available for prevention of cervical cancer. The impact of the vaccine on the prevalence of HPV related carcinomas of the UADT is currently not known but likely beneficial.
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PMID:Human papillomavirus (HPV) related carcinomas of the upper aerodigestive tract. 2061 73

Patients with an oral squamous cell carcinoma (OSCC) often develop multiple malignant lesions. This report examined whether individual tumours developed in a patient show the same genetic alteration, such as p53 mutations. This case study describes three SCCs and three leukoplakias which developed simultaneously in a single 67-year-old Japanese man. A p53 mutation was detected in two of the three SCCs and one of the three leukoplakias. One SCC had a missense mutation at codon 285 (GAG>AAG, Glu>Lys) and the other a nonsense mutation at codon 336, and the leukoplakia had a missense mutation at codon 273 (CGT>CAT, Arg>His). This case showed that individual oral tumours may have different genetic changes even when they develop in a single patient. Therefore, this report provided strong evidence that in cases of multiple tumours it is necessary to design tailor-made therapies for each individual tumour rather than a single standardised therapy for all multiple tumours.
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PMID:A multiple primary carcinoma consisting of leukoplakia and SCC: a case report with p53 mutation analysis. 2111 40

Head-Neck Squamous Cell Carcinoma (HN-SCC) is a clinically challenging disease associated with a high mortality rate. The chemo-radiotherapy treatments that aim to preserve the organ represent the current gold standard therapy for advanced laryngeal disease, reserving surgery only for non-responsive or relapsed cases. Despite these aggressive approaches, local persistent or recurrent disease remains the primary cause of treatment failure but we still do not have known factors and/or markers able to predict the outcome of the disease and in particular the risk of local relapse. Here we address this point on a series of 54 cases of HN-SCC for whom the presence of local relapse was known. Using immunohistochemistry (IHC) analysis to evaluate protein expression and localization in the recurrence free and recurrence positive samples, we studied the expression of key cell cycle regulators including p53, p16, p27, pRB, Cyclin D1, Cyclin D3, and Stathmin. Overall by analyzing seven different cell cycle regulators we can hypothesize that the alteration of G1/S regulation represents a fundamental event in the onset/progression of HN-SCC cancers and that the associate use of Cyclin D1/p16 expression should be considered as a possible biomarker toward the identification of those patients that will probably develop a recurrent disease and thus should benefit of a more aggressive treatment.
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PMID:Alteration of G1/S transition regulators influences recurrences in head and neck squamous carcinomas. 2141 68

The aberrant expression of p53 and RB proteins was investigated by immunohistochemistry in 73 patients with esophageal SCC, who underwent esophageal resection. Fresh tumor tissues from 21 patients were also tested for p53 mutations in exons 4 through 9 by direct sequencing. Positive nuclear staining with p53 antibody in cancer cells was found in 49.3% (36/73) of the tumors. Mutations in the p53 gene were detected in 66.7% (14/21) by direct sequencing. Nuclear staining with RB antibody in cancer cells was diffuse in 11.0% (8/73) and heterogeneous in 57.5% (42/73) of cases. Ten patients with p53-positive but RB-negative tumors had a significantly higher incidence of stage IV disease than the other patients studied. In addition, 8 patients with tumors with diffuse nuclear staining for RB antibody had a significantly lower survival rate than the other patients. These findings demonstrate that aberrant expression of RB and/or p53 protein is frequent in human esophageal SCC, and is probably associated with tumor progression and unfavorable prognosis.
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PMID:Aberrant expression of p53 and retinoblastoma gene products in human esophageal squamous cell carcinoma. 2152 10


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