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2.
Lancet Haematol ; 11(8): e563, 2024 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-39089804

Assuntos
Humanos
5.
BMJ ; 385: q1072, 2024 05 13.
Artigo em Inglês | MEDLINE | ID: mdl-38740428
6.
BMJ ; 385: q795, 2024 04 03.
Artigo em Inglês | MEDLINE | ID: mdl-38569720
7.
BMJ ; 385: q913, 2024 04 19.
Artigo em Inglês | MEDLINE | ID: mdl-38641352
9.
Trends Mol Med ; 30(5): 499-515, 2024 May.
Artigo em Inglês | MEDLINE | ID: mdl-38582623

RESUMO

The clinical use of cell-free DNA (cfDNA) methylation in managing lung cancer depends on its ability to differentiate between malignant and healthy cells, assign methylation changes to specific tissue sources, and elucidate opportunities for targeted therapy. From a technical standpoint, cfDNA methylation analysis is primed as a potential clinical tool for lung cancer screening, early diagnosis, prognostication, and treatment, pending the outcome of elaborate validation studies. Here, we discuss the current state of the art in cfDNA methylation analysis, examine the unique features and limitations of these new methods in a clinical context, propose two models for applying cfDNA methylation data for lung cancer screening, and discuss future research directions.


Assuntos
Biomarcadores Tumorais , Ácidos Nucleicos Livres , Metilação de DNA , Neoplasias Pulmonares , Humanos , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/diagnóstico , Neoplasias Pulmonares/terapia , Ácidos Nucleicos Livres/genética , Biomarcadores Tumorais/genética , Prognóstico , Detecção Precoce de Câncer/métodos , Gerenciamento Clínico
11.
BMJ ; 384: q582, 2024 03 07.
Artigo em Inglês | MEDLINE | ID: mdl-38453189
13.
BMJ ; 384: q608, 2024 03 11.
Artigo em Inglês | MEDLINE | ID: mdl-38467400
14.
BMJ ; 384: q549, 2024 03 04.
Artigo em Inglês | MEDLINE | ID: mdl-38438219
18.
Int Rev Cell Mol Biol ; 383: 41-66, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38359970

RESUMO

Prostate cancer is the second most prevalent cancer in men globally. De novo neuroendocrine prostate cancer (NEPC) is uncommon at initial diagnosis, however, (treatment-induced) t-NEPC emerges in up to 25% of prostate adenocarcinoma (PRAD) cases treated with androgen deprivation, carrying a drastically poor prognosis. The transition from PRAD to t-NEPC is underpinned by several key genetic mutations; TP53, RB1, and MYCN are the main genes implicated, bearing similarities to other neuroendocrine tumours. A broad range of epigenetic alterations, such as aberrations in DNA methylation, histone post-translational modifications, and non-coding RNAs, may drive lineage plasticity from PRAD to t-NEPC. The clinical diagnosis of NEPC is hampered by a lack of accessible biomarkers; recent advances in liquid biopsy techniques assessing circulating tumour cells and ctDNA in NEPC suggest that the advent of non-invasive means of monitoring progression to NEPC is on the horizon. Such techniques are vital for NEPC management; diagnosis of t-NEPC is crucial for implementing effective treatment, and precision medicine will be integral to providing the best outcomes for patients.


Assuntos
Tumores Neuroendócrinos , Neoplasias da Próstata , Masculino , Humanos , Neoplasias da Próstata/genética , Neoplasias da Próstata/patologia , Neoplasias da Próstata/terapia , Antagonistas de Androgênios , Tumores Neuroendócrinos/genética , Tumores Neuroendócrinos/patologia , Epigênese Genética
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