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1.
J Med Screen ; 28(2): 210-212, 2021 06.
Artigo em Inglês | MEDLINE | ID: mdl-33663240

RESUMO

The COVID-19 pandemic has led to delays in cancer diagnosis, in part due to postponement of cancer screening. We used Google Trends data to assess public attention to cancer screening during the first peak of the COVID-19 pandemic. Search volume for terms related to established cancer screening tests ("colonoscopy," "mammogram," "lung cancer screening," and "pap smear") showed a marked decrease of up to 76% compared to the pre-pandemic period, a significantly greater drop than for search volume for terms denoting common chronic diseases. Maintaining awareness of cancer screening during future public health crises may decrease delays in cancer diagnosis.


Assuntos
COVID-19 , Detecção Precoce de Câncer , Comportamento de Busca de Informação , Armazenamento e Recuperação da Informação/tendências , Ferramenta de Busca/tendências , Neoplasias da Mama/diagnóstico por imagem , Colonoscopia/tendências , Feminino , Humanos , Neoplasias Pulmonares/diagnóstico , Masculino , Mamografia/tendências , Ferramenta de Busca/estatística & dados numéricos , Esfregaço Vaginal/tendências
2.
Cell Rep ; 34(11): 108864, 2021 03 16.
Artigo em Inglês | MEDLINE | ID: mdl-33730582

RESUMO

N-Nitrosodimethylamine (NDMA) is a DNA-methylating agent that has been discovered to contaminate water, food, and drugs. The alkyladenine DNA glycosylase (AAG) removes methylated bases to initiate the base excision repair (BER) pathway. To understand how gene-environment interactions impact disease susceptibility, we study Aag-knockout (Aag-/-) and Aag-overexpressing mice that harbor increased levels of either replication-blocking lesions (3-methyladenine [3MeA]) or strand breaks (BER intermediates), respectively. Remarkably, the disease outcome switches from cancer to lethality simply by changing AAG levels. To understand the underlying basis for this observation, we integrate a suite of molecular, cellular, and physiological analyses. We find that unrepaired 3MeA is somewhat toxic, but highly mutagenic (promoting cancer), whereas excess strand breaks are poorly mutagenic and highly toxic (suppressing cancer and promoting lethality). We demonstrate that the levels of a single DNA repair protein tip the balance between blocks and breaks and thus dictate the disease consequences of DNA damage.


Assuntos
Replicação do DNA/genética , Mutagênese/genética , Neoplasias/genética , Neoplasias/patologia , Animais , Biomarcadores Tumorais/metabolismo , Morte Celular , Instabilidade Cromossômica/genética , Dano ao DNA/genética , DNA Glicosilases/deficiência , DNA Glicosilases/metabolismo , Reparo do DNA/genética , Dietilnitrosamina , Suscetibilidade a Doenças , Histonas/metabolismo , Recombinação Homóloga/genética , Fígado/patologia , Neoplasias Hepáticas/patologia , Camundongos Endogâmicos C57BL , Camundongos Transgênicos , Micronúcleos com Defeito Cromossômico , Nitrosaminas , Fenótipo , Fosfoproteínas/metabolismo , Fosforilação
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