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Topic: P53 gene

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P53

Tumor supressor gene

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	P53 - Wikipedia, the free encyclopedia
		p53 also known as Tumor protein 53 (TP53) is a protein (EC 2.7.1.37) that regulates the cell cycle and hence functions as a tumor suppressor.
		In normal cells p53 is usually inactive, bound to the protein MDM2, which prevents its action and promotes its degradation.
		Although it was initially presumed to be an oncogene, its character as a tumor suppressor gene was revealed in 1989.
	en.wikipedia.org /wiki/P53_gene (1206 words)

	CHEST: An atypical carcinoid tumor of the lung with mutations in the p53 gene and the retinoblastoma gene (Site not responding. Last check: 2007-10-25)
		An atypical carcinoid tumor of the lung with mutations in the p53 gene and the retinoblastoma gene
		We have investigated the abnormalities in the p53 gene and the Rb gene in lung cancer specimens obtained by biopsy, operation, or autopsy One of the autopsy cases was diagnosed as atypical carcinoid and one metastatic lesion on the pericardium was rendered to molecular analysis.
		Although D'Amico et al[4] reported that the p53 gene mutation in SCLC was not associated with tumor response to therapy or to patient survival, the incidence of the p53 gene mutations in established lung cancer cell lines is higher than in nonimmortalized lung neoplasms.
	www.findarticles.com /p/articles/mi_m0984/is_n5_v104/ai_14636683 (1140 words)

	Alcohol Impairs Tumor-Suppressing Gene in Smokers
		They found that mutations in the gene known as p53 in the cancer cells of patients with the most common type of lung cancer were strongly associated with both cigarette smoking and alcohol use.
		The p53 tumor suppressor gene is the most frequently mutated gene in human cancer, and plays a significant role in the early events leading to the development of lung cancer, says Dr. Ahrendt.
		The p53 gene normally suppresses cell growth, permitting repair of damaged DNA prior to cell division.
	healthlink.mcw.edu /article/964718193.html (575 words)

	P53 Gene
		P53 protein is activated when DNA damage occurs, and serves to block DNA replication and hence allow time for repair of DNA.
		For this reason p53 gene is a prime target for the development of novel anti cancer therapies such as "gene therapy".
		This consists of injecting the "normal p53 gene" (it is called p53 wild type) into the ill human body.
	www.york.ac.uk /inst/ltc/efl/courses/Found_n/2001/p53gene.htm (287 words)

	Gene P53ID88
		Although the number of genes activated by p53 is rather large, the outcome of p53 activation is either cell cycle arrest in G1 (by p21), in G2 (by 14-3-3 g) or apoptosis (by BAX, PUMA or NOXA).
		P53 is mutated in 30% of breast cancers; preferentially observed in advanced and aggressive forms; probably a late event; hotspots at codons 175, 248, and 273.
		P53 is mutated in 50% of oesophagus cancers (70% in squamous cell carcinoma and 45% of adenocarcinoma); probably an early event; hotspots at codons 175, 248 and 273.
	www.infobiogen.fr /services/chromcancer/Genes/P53ID88.html (1444 words)

	First Adenoviral-p53 Gene Therapy Trial Shows Success In Lung Cancer
		The study was a dose escalation trial; each of the 21 patients received the p53 treatment once a month (given via an adenovirus delivery system (vector) directly into a single primary or metastatic tumor); nine also received cisplatin intravenously over two hours, given three days prior to being injected with p53 gene.
		No adverse side effects attributable to the p53 gene were observed in any of the patients enrolled in the study.
		p53 is a tumor suppressor gene that encodes a protein which responds to damage involving a cell's DNA.
	www.docguide.com /dg.nsf/PrintPrint/41ECFDB788B15E118525649F004DFEA5 (769 words)

	The p53 tumor suppressor protein (Site not responding. Last check: 2007-10-25)
		The p53 gene like the Rb gene, is a tumor suppressor gene, i.e., its activity stops the formation of tumors.
		If a person inherits only one functional copy of the p53 gene from their parents, they are predisposed to cancer and usually develop several independent tumors in a variety of tissues in early adulthood.
		Mutant p53 can no longer bind DNA in an effective way, and as a consequence the p21 protein is not made available to act as the 'stop signal' for cell division.
	www.ncbi.nlm.nih.gov /books/bv.fcgi?call=bv.View..ShowSection&rid=gnd.section.107 (262 words)

	Upregulation of the Elongation Factor-1alpha Gene by p53 in Association With Death of an Erythroleukemic Cell Line -- ... (Site not responding. Last check: 2007-10-25)
		It was also reported that upregulation of the bax gene and downregulation of the bcl-2 gene by p53 are associated with apoptosis of a murine leukemic cell line M1 and that Fas, a transducer of a signal for apoptosis, is upregulated by p53 in non-small-cell lung adenocarcinoma and erythroleukemia.
		In the case of pGVP-E3E4, the luciferase activity of the cells with wild-type p53 was twofold to 2.5-fold of that of cells without wild-type p53 (Fig 2B).
		gene by p53 may be enough to induce apoptosis without significant changes in the expression of the apoptosis-associated genes in 1-2-3 cells.
	www.bloodjournal.org /cgi/content/full/90/4/1373 (3326 words)

	Resistance to Therapy: p53 and Chemosensitivity in Gastric Cancer by James M Ford, MD
		P53 in normal cells, normal mammalian systems, is a central player in response to DNA damage of a variety of sorts.
		This is a larger schema of the regulation of P53 both upstream and downstream, and I think it is one of the major points I want to make today, which is that simply looking at P53 status in isolation is not surprisingly confusing in terms of trying to make predictions, given this very complicated regulation.
		And these are genes that appear to be involved in this mitotic spindle check point regulated by P53 and these are starting to be identified, and they include the MAD genes and the BUB genes, which are homologous of yeast genes involved in that process.
	www.webtie.org /sots/Meetings/Gastrointestinal/March62001/lectures/FORD/transcripts/transcripts.htm (3242 words)

	p53, "Molecule of the Year" (Site not responding. Last check: 2007-10-25)
		The p53 gene was originally discovered in 1979 by Arnold Levine of Princeton University (now a member of HHMI's Scientific Review Board in Genetics), David Lane of the University of Dundee, Scotland (now an HHMI International Research Scholar), and William Old of the Memorial Sloan-Kettering Cancer Center in New York City.
		In its normal form, p53 acts to stop cell division whenever it senses that a cell's DNA is damaged, thus giving the cell a chance to repair the DNA before its errors are duplicated and passed on to daughter cells.
		The p53 found in normal cells acts as a transcription factor, a protein that binds to a particular DNA sequence and regulates its expression, Vogelstein reported, but the mutant forms of p53 seen in colorectal cancers have lost this function.
	www.hhmi.org /annual95/b140.html (1098 words)

	Energy Citations Database (ECD) - Energy and Energy-Related Bibliographic Citations
		Purpose/Objective: To investigate the use of the wild-type p53 gene as a radiosensitizer of human malignant cells and tumors.
		Results: Cells expressing the p53 gene product were more sensitive to radiation than control cells expressing the luciferase gene in in vitro clonogenic survival assays.
		We also demonstrate that intra-tumoral injection of an adenoviral vector containing the wild type p53 gene increases the radiation responsiveness of established tumors, consistent with the radiosensitizing activity of the wild type p53 gene demonstrated in vitro.
	www.osti.gov /energycitations/product.biblio.jsp?osti_id=20420889 (408 words)

	Baylor Health Care System: Cancer treatment involving the p53 gene
		One gene found to play a critical role in preventing the cancerous transformation of a cell is a tumor suppressor gene known as p53.
		Inactivation of the p53 protein—one of the most common alterations observed in human cancer cells—may be enhanced by some viral infections, such as the human papillomavirus, thus allowing malignant transformations to take place.
		Mutations of this gene are associated with transformation to a malignant phenotype.
	www.baylorhealth.edu /proceedings/12_2/12_2_nemunaitis.html (3676 words)

	Reisman Lab p53 Home Page (Site not responding. Last check: 2007-10-25)
		The wild type p53 gene is a tumor suppressor gene which encodes a protein that regulates a cell cycle checkpoint and the induction of programmed cell death (apoptosis) in response to DNA damage, cell stress or the aberrant expression of some oncogenes.
		In a number of cases elevated transcription of the p53 gene contributes the overall high levels of the mutant protein in tumor cells.
		The ability of many mutant and oncogenic tumor-derived p53 alleles to modulate gene expression may be of prime importance in their transforming and oncogenic activities since missense mutations are very rarely observed in either the amino terminal transactivation domain of the protein or in the nuclear localization signals.
	www.biol.sc.edu /~reisman (519 words)

	The p53 Tumor Suppressor Gene and Apoptosis
		Pathol Res Pract 1999;195(3):129-35 p53 gene alterations in prostate cancer after radiation failure and their association with clinical outcome: a molecular and immunohistochemical analysis.
		Cancer 1999 Mar 15;85(6):1293-9 p53 protein overexpression is associated with increased cell proliferation in patients with locally recurrent prostate carcinoma after radiation therapy.
		Clin Cancer Res 1998 Apr;4(4):835-46 Adenovirus-mediated p53 gene therapy and paclitaxel have synergistic efficacy in models of human head and neck, ovarian, prostate, and breast cancer.
	www.psa-rising.com /medsci/p53.htm (1240 words)

	p53 gene (Site not responding. Last check: 2007-10-25)
		Using the new approach, the UC Davis team demonstrated that p53 abnormalities are much more common in localized prostate cancer than previously thought and that in about one-third of the cases the abnormalities are multiple rather than single.
		Mutations of p53, for example, have been shown to be critical in the development of colon cancer.
		The new approach seems to detect p53 mutations in early as well as late stage prostate cancer, but additional research is needed to determine whether p53 mutations are a good marker for prostate cancer progression or response to therapy.
	www.ucdmc.ucdavis.edu /news/medicalnews/p53.html (606 words)

	Exon 5 of the p53 gene is a target for deletions in ovarian cancer -- Angelopoulou et al. 44 (1): 72 -- Clinical ...
		Exon 5 of the p53 gene is a target for deletions in ovarian cancer -- Angelopoulou et al.
		gene in the same reaction mixture was used (20).
		p53, a transdominant regulator of transcription whose function is ablated by mutations occurring in human cancer.
	www.clinchem.org /cgi/pmidlookup?view=long&pmid=9550561 (2909 words)

	THE 1993 WALTER-HUBERT-LECTURE - THE ROLE OF THE P53 TUMOR-SUPPRESSOR GENE IN TUMORIGENESIS (Site not responding. Last check: 2007-10-25)
		Overexpression of the p53 protein results either in arrest in the G(1) phase of the cell cycle or in the induction of apoptosis.
		Thus, the role of p53 in suppressing tumorigenesis may be to rescue the cell or organism from the mutagenic effects of DNA damage.
		Loss of p53 function accelerates the process of tumorigenesis and alters the response of cells to agents that damage DNA, indicating that successful strategies for radiation therapy may well need to take into account the tissue of origin and the status of p53 in the tumour.
	www.carelife.com /cancer/med_onc/p53a.html (282 words)

	A novel case with germline p53 gene mutation having concurrent multiple primary colon tumours -- Miyaki et al. 52 (2): ...
		Germ-line transmission of a mutated p53 gene in a cancer-prone family with Li-Fraumeni syndrome.
		Genetic changes of both p53 alleles associated with the conversion from colorectal adenoma to early carcinoma in familial adenomatous polyposis and non-familial adenomatous polyposis patients.
		Prevalence and spectrum of germline mutations of the p53 gene among patients with sarcoma.
	gut.bmjjournals.com /cgi/content/full/52/2/304 (1920 words)

	LHC p53 Resources Page
		The p53 protein is a multi-functional transcription factor involved in the control cell cycle progression, DNA integrity and apoptosis in cells exposed to DNA-damaging agents.
		Since the identification of tumor-specific, missense p53 mutations in 1989, there has been a widespread interest in the possibility that the localization and the characteristics of these mutations may reveal clues about the etiology and the molecular pathogenesis of human cancer (Greenblatt et al., 1994.
		In this respect, the p53 gene differs from other tumor suppressor genes such as Rb, APC and ATM which are frequently inactivated by deletion or nonsense mutations, and from the oncogenes of the ras family, which are activated by mutation at a small number of well-defined codons.
	www3.cancer.gov /intra/LHC/p53ref.htm (417 words)

	An Infrequent Point Mutation of the p53 Gene in Human Nasopharyngeal Carcinoma -- Sun et al. 89 (14): 6516 -- ...
		Point mutations in the p53 gene have been detected in a variety of human cancers; the mutations are clustered in four "hot-spots" located in the coding region of exons 5, 7, and 8, which coincide with the four most highly conserved regions of the gene.
		C mutation at codon 280 (exon 8), position 2, of the p53 gene in a nasopharyngeal carcinoma (NPC) cell line, originating from Guangdong, a province in the People's Republic of China that leads the world in NPC incidence.
		We conclude from this study that mutational or other alterations of the p53 gene are not common in nasopharyngeal carcinogenesis and that a codon-280 mutation of p53 may be involved in <10% of NPC cases.
	www.pnas.org /cgi/lookup?vol=89&fp=6516&view=abstract (542 words)

	eMedicine - Li-Fraumeni Syndrome : Article Excerpt by: Gary R Jones, MD (Site not responding. Last check: 2007-10-25)
		Mutations can be inherited or can arise as de novo mutations early in embryogenesis or in one of the parent's germ cells.
		Somatic (ie, nongermline) TP53 tumor suppressor gene mutations are very common human cancers, suggesting that TP53 alterations play an important role in the development of cancer.
		Alterations are the result of either loss of function of wild type p53, increased or aberrant protein function, or dominant negative effects.
	www.emedicine.com /ped/byname/li-fraumeni-syndrome.htm (535 words)

	Novel p53 gene-based therapy boosts immune system and reduces tumor size
		The therapy, known as Advexin, also showed evidence that the p53 protein it was delivering was actually being replaced in the targeted tumors, and that the treatment produced beneficial and possibly sustained local immune responses in the patients tested.
		About half of patients with locally advanced breast cancer have mutations in their p53 gene, which plays a critical role in suppressing cancer development.
		In the study, 12 eligible patients with locally advanced breast cancer, each of whom had large tumors (an average of eight centimeters, larger than a silver dollar), received several injections of Advexin directly into the tumor, followed by a course of chemotherapy.
	www.eurekalert.org /pub_releases/2004-12/plos-npg120304.php (407 words)

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