p53 transformation-related protein: Detection by monoclonal antibody in mouse and human cells

Dippold, Wolfgang; Jay, Gilbert; DeLeo, Albert B.; Khoury, George; Old, Lloyd J.

doi:10.1073/pnas.78.3.1695

Cited by 187 publications

(115 citation statements)

References 15 publications

(3 reference statements)

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“…In the present series none of the normal CNS tissue adjacent to the tumours was labelled with PAb 1801 antibody. Also, the labelling of tumour cells is unlikely to represent the somewhat elevated levels of normal p53 seen in actively proliferating cell populations (Dippold et al, 1981;Levin & Momand, 1990) because some tumours with large growth fractions were not labelled with the PAb 1801 antibody, whilst in p53 + ve tumours the p53 LI did not correlate with the growth fraction size. In addition, no endothelial cells were labelled in any of the tumours, even in areas where endothelial proliferation, and Ki-67 labelling were present.…”

Section: Discussionmentioning

confidence: 99%

Prognostic implications of p53 protein, epidermal growth factor receptor, and Ki-67 labelling in brain tumours

Jaros

Perry²,

Adam³

et al. 1992

Br J Cancer

241

114

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Patients with Ki-67 LI >5% had a reduced survival (P< 0.0001) -none survived beyond 86 weeks following diagnosis, whilst 63% of patients with < 5% positive cells were still alive at 100 weeks. The univariate analysis showed that in astrocytomas expression of p53 mutants, EGFR protein, and Ki-67> 5% are associated with malignant progression and poor prognosis. The multivariate analysis revealed that only tumour grade and Ki-67LI were independent prognostic factors for survival.

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Section: Discussionmentioning

confidence: 99%

Prognostic implications of p53 protein, epidermal growth factor receptor, and Ki-67 labelling in brain tumours

Jaros

Perry²,

Adam³

et al. 1992

Br J Cancer

241

114

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Section: Methodsmentioning

confidence: 99%

“…Two p53 monoclonal antibodies (y2a of mouse origin) were used in these studies: hybridoma 20047, described by Dippold et al (23), and PAb 421, described by Harlow et al (24). Several different monoclonal antibodies (y2a) that do not recognize p53 were used as negative controls for the immunofluorescence and immunoprecipitation studies.…”

Section: Methodsmentioning

confidence: 99%

“…The methylcholanthrene-induced BALB/c Meth A sarcoma cell line and the SV40-transformed BALB/c 3T3 cell line 3T3WT have been described (23).…”

mentioning

confidence: 99%

“…Induction of differentiation was determined by the benzidine reaction for hemoglobin (21); commitment to terminal cell division was determined by growth in semisolid medium (22). The methylcholanthrene-induced BALB/c Meth A sarcoma cell line and the SV40-transformed BALB/c 3T3 cell line 3T3WT have been described (23).Antibodies. Two p53 monoclonal antibodies (y2a of mouse origin) were used in these studies: hybridoma 20047, described by Dippold et al (23), and PAb 421, described by Harlow et al (24).…”

mentioning

confidence: 99%

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Protein p53 and inducer-mediated erythroleukemia cell commitment to terminal cell division.

Shen¹,

Real²,

DeLeo³

et al. 1983

Proc. Natl. Acad. Sci. U.S.A.

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Inducer-mediated murine erythroleukemia cell (MELC) differentiation provides a model for examining factors determining terminal cell differentiation. The nuclear protein, p53, has been implicated as a potential determinant of cell cycle progression and cell differentiation. In this study p53 content and synthesis, during inducer-mediated MELC differentiation, has been examined with monoclonal antibodies to p53. A decrease in p53 synthesis and content was demonstrated during induced differentiation. As determined by cell cycle fractionation, the decrease in p53 is manifest at all stages of the cell cycle. Hemin, which induces globin mRNA accumulation but not terminal cell division, fails to decrease p53 content. A MELC variant resistant to inducer-mediated commitment to terminal cell division also fails to decrease p53 levels in response to inducers. These experiments suggest that p53 is implicated in MELC cell proliferation and that an induced decrease in p53 may be responsible for GI phase prolongation and terminal GI arrest.The murine erythroleukemia cell (MELC), a virus-transformed erythroid cell precursor approximating the erythroid colonyforming unit (designated CFUe) stage in the erythropoietic lineage (1), provides a model for study of regulatory mechanisms responsible for coordinate unlinked gene expression (a-and 13-globin mRNA accumulation) and initiation of terminal cell divisions (termed commitment) during cell differentiation (2, 3). MELC can be induced by hexamethylene bisacetamide (HMBA), dimethylsulfoxide (Me2SO), or other chemical agents to initiate a program of differentiation that appears similar to that of normal erythroid precursors (1, 4). Of particular advantage is the availability of different inducers capable of initiating distinct developmental patterns (5, 6) and variant cell lines resistant to inducer-mediated commitment to terminal cell division but competent to express other features of erythroid differentiation (7).An early manifestation of termination of cell division in MELC appears to be a transient prolongation of the GI phase of the cell cycle, which can be detected after cell transit through one complete S phase in the presence of inducer (8-10). After up to 4-5 terminal cell divisions, induced MELC are arrested in a GI-like phase of the cell cycle. Evidence has accumulated suggesting that synthesis of a labile protein during G1 may control entry of cells into S phase (11). A nuclear protein (p53 protein), initially recognized by its elevated levels in transformed cells (12) and by its capacity to bind to simian virus 40 (SV40) tumor antigen (13,14), has been identified as possibly important in determining normal cell cycle progression from G1 to S (15, 16). It also has been suggested that p53 protein levels may be regulated in relation to the differentiation status of a cell lineage (17,18). Based upon a number of observations, it appears that cellular p53 content is determined by both transcriptional and post-transcriptional mechanisms (17)(18)(19)(20). The present...

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Expression of p53 Protein in Advanced Head and Neck Squamous Cell Carcinoma Before and After Chemotherapy

Dunphy

Dunphy²,

Boyd³

et al. 1997

Archives of Otolaryngology - Head and Neck Surgery

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p53 transformation-related protein: Detection by monoclonal antibody in mouse and human cells

Cited by 187 publications

References 15 publications

Prognostic implications of p53 protein, epidermal growth factor receptor, and Ki-67 labelling in brain tumours

Prognostic implications of p53 protein, epidermal growth factor receptor, and Ki-67 labelling in brain tumours

Protein p53 and inducer-mediated erythroleukemia cell commitment to terminal cell division.

Expression of p53 Protein in Advanced Head and Neck Squamous Cell Carcinoma Before and After Chemotherapy

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