Publications by authors named "M Roudier"

Article Synopsis
  • Targeting cell surface molecules with therapies like radioligands and antibodies has been effective in treating various cancers, but the impact of lineage plasticity on these markers is still poorly understood.
  • A specific example of lineage plasticity is the transformation of prostate adenocarcinoma to neuroendocrine prostate cancer, which poses significant treatment challenges and worsens patient survival rates.
  • Research using advanced single-cell analyses and large tumor sample studies revealed significant phenotypic variability and shared gene-regulatory networks between NEPC and small cell lung cancer, raising concerns about the effectiveness of current therapies while suggesting potential for better patient selection in clinical trials.
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Molecular profiling studies have shed new light on the complex biology of prostate cancer. Genomic studies have highlighted that structural rearrangements are among the most common recurrent alterations. In addition, both germline and somatic mutations in DNA repair genes are enriched in patients with advanced disease.

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Therapeutic approaches targeting proteins on the surface of cancer cells have emerged as an important strategy for precision oncology. To capitalize on the potential impact of drugs targeting surface proteins, detailed knowledge about the expression patterns of the target proteins in tumor tissues is required. In castration-resistant prostate cancer (CRPC), agents targeting prostate-specific membrane antigen (PSMA) have demonstrated clinical activity.

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Targeting cell surface molecules using radioligand and antibody-based therapies has yielded considerable success across cancers. However, it remains unclear how the expression of putative lineage markers, particularly cell surface molecules, varies in the process of lineage plasticity, wherein tumor cells alter their identity and acquire new oncogenic properties. A notable example of lineage plasticity is the transformation of prostate adenocarcinoma (PRAD) to neuroendocrine prostate cancer (NEPC)--a growing resistance mechanism that results in the loss of responsiveness to androgen blockade and portends dismal patient survival.

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Therapeutic approaches targeting proteins on the surface of cancer cells have emerged as an important strategy for precision oncology. To fully capitalize on the potential impact of drugs targeting surface proteins, detailed knowledge about the expression patterns of the target proteins in tumor tissues is required. In castration-resistant prostate cancer (CRPC), agents targeting prostate-specific membrane antigen (PSMA) have demonstrated clinical activity.

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