PhD Scientific Days 2017

Budapest, 11-12 April 2017

Oral Presentations: Oncology

Diethylnitrosamine induces lung adenocarcinoma in FVB/N mouse

Előadó neve

Dr. Mervai, Zsolt

Előadó munkahelye

1st Department of Pathology and Experimental Cancer Research

Előadó telefonszáma

+3630 562 14 25

Előadó e-mail címe

mervaizsolt@gmail.com

Az előadás címe

Diethylnitrosamine induces lung adenocarcinoma in FVB/N mouse

Szerző(k) neve és munkahelye

Dr. Zsolt Mervai, Krisztina Egedi, Dr. Ilona Kovalszky, Dr. Kornélia Baghy
1st Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest

Szekció

Oral Presentations: Oncology

Data of the presenter

Doctoral School: Pathology
Program: Oncology
Supervisor: Dr. Baghy Kornélia
E-mail: mervaizsolt@gmail.com
Presentation: Oral presentation preferred (language: Hungarian)

Text of the abstract

Abstract
Background
Diethylnitrosamine is a well known carcinogen that induces cancers of various organs in mice and rats. Using FVB/N mouse strain, here we show that diethylnitrosamine induces primarily lung carcinomas with modest tumor development in the liver.

Aims
Our results may offer a new model to study chemical carcinogenesis in the lung.

Method
Animals were exposed to a single high dose of diethylnitrosamine, and more than 70% of the mice developed lung cancer. To obtain a new transplantable tumor line, pieces of primary tumors were inoculated and maintained subcutaneously in the same mouse strain. We used immunohistochemistry to characterize the tumor for main lung adenocarcinoma markers. We searched for mutations in KRAS exon 2 and EGFR exon 19, 21 with Sanger sequencing. We also compared the normal lung tissue with the diethylnitrosamine induced primary adenocarcinoma, and with the subcutaneously maintained adenocarcinoma using Western blot technique for main cell cycle markers and to identify the main pathways.

Results
Histologically, primary and subcutaneous tumors express cytokeratin-7 and thyroid transcription factor-1, markers characteristic to lung adenocarcinoma. In addition, no mutations were found in the hot spot regions of KRAS and EGFR genes. We found high mTOR activation, but the level of p-Akt Ser 473 and p-Akt 308 decreased in the tumorous samples.

Conclusions
We established a new lung adenocarcinoma model using FVB/N mouse strain and diethylnitrosamine. We believe that this new model system would be highly useful in lung cancer research.

Kind

Szabad

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

1271

Authors (legacy)

Dr. Zsolt Mervai, Krisztina Egedi, Dr. Ilona Kovalszky, Dr. Kornélia Baghy
1st Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest