Immunohistochemical observations on tumor suppressor gene p53 status in mouse fibrosarcoma following in-vivo photodynamic therapy: the role of xanthine oxidase activity

1997 ◽  
Author(s):  
Piotr P. Ziolkowski ◽  
Krzysztof Symonowicz ◽  
Artur Milnerowicz ◽  
Beata J. Osiecka
Keyword(s):  
Photodynamic Therapy ◽  
Tumor Suppressor ◽  
Xanthine Oxidase ◽  
Tumor Suppressor Gene ◽  
Oxidase Activity ◽  
Suppressor Gene ◽  
P53 Status ◽  
Tumor Suppressor Gene P53

Molecular Pathogenesis of Adenocarcinomas in Barrett’s Esophagus: Role of the Tumor Suppressor Gene p53

1997 ◽  
Vol 20 (1) ◽  
pp. 36-40
Author(s):  
P.M. Schneider ◽  
A.G. Casson ◽  
A.H. Hölscher ◽  
S. Schweighart ◽  
S. Mizumoto ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Barrett’S Esophagus ◽  
Barrett's Esophagus ◽  
Suppressor Gene ◽  
Molecular Pathogenesis ◽  
Tumor Suppressor Gene P53

Mutational analysis of a dominant oncogene (c-Ki-ras-2) and a tumor suppressor gene (p53) in hamster lung tumorigenesis

1992 ◽  
Vol 6 (3) ◽  
pp. 199-202 ◽  
Author(s):  
Victor I. C. Oreffo ◽  
Hsiu-Wei Lin ◽  
Paul H. Gumerlock ◽  
Susan A. Kraegel ◽  
Hanspeter Witschi
Keyword(s):  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Mutational Analysis ◽  
Suppressor Gene ◽  
Lung Tumorigenesis ◽  
Tumor Suppressor Gene P53

scholarly journals Genetic determinants of EGFR-Driven Lung Cancer Growth and Therapeutic Response In Vivo

2020 ◽  
Author(s):  
Giorgia Foggetti ◽  
Chuan Li ◽  
Hongchen Cai ◽  
Jessica A. Hellyer ◽  
Wen-Yang Lin ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Tumor Growth ◽  
Lung Adenocarcinoma ◽  
Tumor Suppressor Gene ◽  
Suppressor Gene ◽  
Genetic Alterations ◽  
Putative Tumor Suppressor ◽  
Lung Adenocarcinomas ◽  
Gene Alterations

AbstractCancer genome sequencing has uncovered substantial complexity in the mutational landscape of tumors. Given this complexity, experimental approaches are necessary to establish the impact of combinations of genetic alterations on tumor biology and to uncover genotype-dependent effects on drug sensitivity. In lung adenocarcinoma, EGFR mutations co-occur with many putative tumor suppressor gene alterations, however the extent to which these alterations contribute to tumor growth and their response to therapy in vivo has not been explored experimentally. By integrating a novel mouse model of oncogenic EGFR-driven Trp53-deficient lung adenocarcinoma with multiplexed CRISPR–Cas9-mediated genome editing and tumor barcode sequencing, we quantified the effects of inactivation of ten putative tumor suppressor genes. Inactivation of Apc, Rb1, or Rbm10 most strongly promoted tumor growth. Unexpectedly, inactivation of Lkb1 or Setd2 – which are the strongest drivers of tumor growth in an oncogenic Kras-driven model – reduced EGFR-driven tumor growth. These results are consistent with the relative frequency of these tumor suppressor gene alterations in human EGFR- and KRAS-driven lung adenocarcinomas. Furthermore, Keap1 inactivation reduces the sensitivity of EGFR-driven Trp53-deficient tumors to the EGFR inhibitor osimertinib. Importantly, in human EGFR/TP53 mutant lung adenocarcinomas, mutations in the KEAP1 pathway correlated with decreased time on tyrosine kinase inhibitor treatment. Our study highlights how genetic alterations can have dramatically different biological consequences depending on the oncogenic context and that the fitness landscape can shift upon drug treatment.

scholarly journals Correlation of primary tumor size and axillary nodal status with tumor suppressor gene p53 in breast carcinoma

2002 ◽  
Vol 59 (1) ◽  
pp. 29-32 ◽  
Author(s):  
Brano Topic ◽  
Nebojsa Stankovic ◽  
Dragutin Savjak ◽  
Slavko Grbic
Keyword(s):  
Prognostic Factors ◽  
Breast Carcinoma ◽  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Tumor Size ◽  
Primary Tumor ◽  
Suppressor Gene ◽  
Nodal Status ◽  
Primary Tumor Size ◽  
Tumor Suppressor Gene P53

Correlation of standard path morphological prognostic parameters, primary tumor size and axillary nodal status with new prognostic factor in breast carcinoma: tumor suppressor gene p53 was analyzed. The studied sample included 65 women who underwent surgery for breast carcinoma at the Surgical Clinic of Clinical Center Banja Luka, from January 1st 1997 till January 1st 1999. Statistical data analysis was performed and correlation of prognostic factors was determined. The majority of authors in this field agree that the primary tumor size and axillary nodal status are the two most important prognostic factors. These factors are the best predictors of prognosis and survival of women who had the tumor and were operated on. Tumor markers were immunohistochemically determined in the last ten years and, according to the majority of authors, are still considered the additional or relative prognostic factors in breast carcinoma. Their prognostic value and significance increase almost daily. Most frequently determined tumor markers are bcl-2, pS2, Ki-67 and p53. There was a positive, directly proportional relationship between primary tumor size and tumor suppressor gene p53, but there was no positive correlation between the axillary nodal status and tumor suppressor gene p53. Significance of determination of new tumor markers as the prognostic factors was emphasized. These markers represent a powerful tool in the early detection and prevention of breast carcinoma.

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