Mutant p53 and the Response to Chemotherapy and Radiation

2014 ◽  
pp. 133-159 ◽  
Author(s):  
Leila Tchelebi ◽  
Hani Ashamalla ◽  
Paul R. Graves
Keyword(s):  
Mutant P53 ◽  
Response To Chemotherapy

Mutant p53 Gain of Function and Chemoresistance: The Role of Mutant p53 in Response to Clinical Chemotherapy

Chemotherapy ◽  
2016 ◽  
Vol 62 (1) ◽  
pp. 43-53 ◽  
Author(s):  
Chao He ◽  
Lun Li ◽  
Xuan Guan ◽  
Li Xiong ◽  
Xiongying Miao
Keyword(s):  
B Cell Lymphoma ◽  
Chemotherapeutic Agents ◽  
Lymphocytic Leukemia ◽  
Chemotherapy Response ◽  
Mutant P53 ◽  
Gain Of Function ◽  
Pubmed Database ◽  
Response To Chemotherapy ◽  
The Impact

Purpose: To review mechanisms underlying mutant p53 (mutp53) gain of function (GOF) and mutp53-induced chemoresistance, and to investigate the role of mutp53 in response to clinical chemotherapy. Methods: We searched the PubMed database for clinical studies from the past decade, including data evaluating the impact of mutp53 in clinical chemotherapy response. Results: Interactions between mutp53 and transcriptional factors, proteins or DNA structures, as well as epigenetic regulation, contribute to mutp53 GOF. Major mechanisms of mutp53-induced chemoresistance include enhanced drug efflux and metabolism, promoting survival, inhibiting apoptosis, upregulating DNA repair, suppressing autophagy, elevating microenvironmental resistance and inducing a stem-like phenotype. Clinically, mutp53 predicted resistance to chemotherapy in diffuse large B-cell lymphoma, and esophageal and oropharyngeal cancers, but its impact on chronic lymphocytic leukemia was unclear. In bladder cancer, mutp53 did not predict resistance, whereas in some breast and ovarian cancers, it was associated with sensitivity to certain chemotherapeutic agents. Conclusion: mutp53 has an intricate role in the response to clinical chemotherapy and should not be interpreted in isolation. Furthermore, when predicting tumor response to chemotherapy based on the p53 status, the drugs used should also be taken into consideration. These concepts require further investigation.

Immunogold labeling of Pneumocystis carinii for Electron microscopy

1991 ◽  
Vol 49 ◽  
pp. 270-271
Author(s):  
Michael P. Goheen ◽  
Marilyn S. Bartlett ◽  
James W. Smith
Keyword(s):  
Electron Microscopy ◽  
Pneumocystis Carinii ◽  
Severe Pneumonia ◽  
Culture Fluid ◽  
Immunogold Labeling ◽  
Antigenic Sites ◽  
Transmission Electron ◽  
Response To Chemotherapy ◽  
Acquired Immunodeficiency ◽  
Immunodeficiency Syndrome

Studies of the biology of Pneumocystis carinii (PC) are of increasing importance because this extracellular pathogen is a frequent source of severe pneumonia in patients with acquired immunodeficiency syndrome (AIDS) and is a leading cause of mortality in these patients. Immunoelectron microscopic localization of antigenic sites on the surface of PC would improve the understanding of these sites and their role in pathenogenisis of the disease and response to chemotherapy. The purpose of this study was to develop a methodology for visualizing immunoreactive sites on PC with transmission electron microscopy (TEM) using immunogold labeled probes.Trophozoites of PC were added to spinner flask cultures and allowed to grow for 7 days, then aliquots of tissue culture fluid were centrifuged at 12,000 RPM for 30 sec. Pellets of organisims were fixed in either 1% glutaraldehyde, 0.1% glutaraldehyde-4% paraformaldehyde, or 4% paraformaldehyde for 4h. All fixatives were buffered with 0.1M Na cacodylate and the pH adjusted to 7.1. After fixation the pellets were rinsed in 0.1M Na cacodylate (3X), dehydrated with ethanol, and immersed in a 1:1 mixture of 95% ethanol and LR White resin.

Mutant p53 inhibits helicobacter-induced premalignant lesions through downregulation of Th1 proinflammatory responses

2001 ◽  
Vol 120 (5) ◽  
pp. A87-A87
Author(s):  
J FOX ◽  
B SHEPPARD ◽  
C DANGLER ◽  
M WHARY ◽  
M IHRIG ◽  
...  
Keyword(s):  
Premalignant Lesions ◽  
Mutant P53 ◽  
Proinflammatory Responses

Chemotherapy-induced apoptosis in pancreatic cancer with mutant p53 involves p73 and is mediated via the extrinsic and the intrinsic pathway

2011 ◽  
Vol 49 (08) ◽  
Author(s):  
M Soboletzki ◽  
S Staemmler ◽  
N Joschko ◽  
A Lovas ◽  
W Stremmel ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Mutant P53 ◽  
Intrinsic Pathway ◽  
Induced Apoptosis
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