Zobrazeno 1 - 5
of 5
pro vyhledávání: '"Michal Kroupa"'
Autor:
Kristyna Tomasova, Michal Kroupa, Anna Siskova, Josef Horak, Ondrej Vycital, Vaclav Liska, Ludmila Vodickova, Pavel Vodicka
Publikováno v:
Cancer Research. 82:2316-2316
Telomere attrition is a well-known hallmark of malignancy in cancer tissue. Our study analyzed the relative telomere length in adenomas, precursor lesions of colorectal adenocarcinoma. We investigated if the accelerated telomere length shortening occ
Autor:
Michal Kroupa, Kristyna Tomasova, Katerina Saskova, Jana Drabova, Josef Horak, Ludmila Vodickova, Jachym Rosendorf, Vaclav Liska, Pavel Vodicka
Publikováno v:
Cancer Research. 82:760-760
The most common form of genomic instability in sporadic colorectal cancer (CRC) is chromosomal instability, a phenotype characterized by a high frequency of DNA copy number gain (CNG) and loss (CNL). Given the fundamental role of chromosomal instabil
Autor:
Vaclav Liska, Michaela Schneiderova, Michal Kroupa, Markéta Urbanová, Rajesh Kumar, Ludmila Vodickova, Ondrej Vycital, Katerina Jiraskova, Pavel Vodicka, Krishna Rachakonda
Publikováno v:
Cancer Research. 78:1470-1470
Colorectal cancer (CRC) represents a major public health problem, being the fourth leading cause of cancer related deaths mainly due to the late diagnosis and a lack of proper prognostic markers. According to the current knowledge, shortening of telo
Autor:
Katerina Jiraskova, Pavel Vodicka, Alessio Naccarati, Alena Opattova, Michal Kroupa, Sona Vodenkova
Publikováno v:
Cancer Research. 77:1424-1424
Colorectal carcinoma (CRC) is the third most common cancer worldwide with the highest incidence in Central Europe. It is the fourth leading cause of cancer related deaths mainly due to the late diagnosis and low efficacy of treatment. CRC diagnosed i
Autor:
Alessio Naccarati, Ludmila Vodickova, Zdena Polivkova, Michal Kroupa, Rajesh Kumar, Ludovit Musak, Kari Hemminki, Maria Dusinska, Veronika Vymetalkova, Pavel Vodicka, Sona Vodenkova
Publikováno v:
Cancer Research. 76:801-801
Human cancers arise from cells unable to maintain genomic and chromosomal stability, mainly as a sequential consequence of altered DNA repair mechanisms (base and nucleotide excision, mismatch and double-strand breaks). Chromosomal aberrations (CAs)