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前列腺癌中的谱系可塑性:超越内在改变的视角。

Lineage plasticity in prostate cancer: Looking beyond intrinsic alterations.

机构信息

Department for BioMedical Research, University of Bern, Bern, 3008, Switzerland.

Department for BioMedical Research, University of Bern, Bern, 3008, Switzerland; Bern Center for Precision Medicine, Inselspital, University Hospital of Bern, Bern, 3008, Switzerland.

出版信息

Cancer Lett. 2022 Nov 1;548:215901. doi: 10.1016/j.canlet.2022.215901. Epub 2022 Sep 6.

Abstract

Emergence of small cell prostate cancer is linked to the plasticity of tumour cells and avoidance of environmental pressures. This process is thought to be reversable, however to-date evidence of this has been demonstrated in small-cell prostate cancer. To study the plasticity of prostate tumours, we look to clinical cohorts of patients covering the spectra of malignancy subtypes and utilise in vitro and in vivo models of disease progression. Current models have assisted in the understanding of the extremities of this plasticity, elucidating internal mechanisms and adaptations to stressors through transition to altered cell states. By interrogating the tumour microenvironment and earlier time points, we are beginning to form a deeper understanding of the full spectra of tumour plasticity. It could be proffered that this deeper understanding will lead to better patient outcome, with earlier interventions more likely to reverse plasticity and prevent trans-differentiation to the aggressive, small cell phenotype.

摘要

小细胞前列腺癌的发生与肿瘤细胞的可塑性和逃避环境压力有关。尽管人们认为这个过程是可逆的,但迄今为止,这种可逆性仅在小细胞前列腺癌中得到了证实。为了研究前列腺肿瘤的可塑性,我们研究了涵盖恶性肿瘤亚型谱的患者临床队列,并利用疾病进展的体外和体内模型。目前的模型有助于了解这种可塑性的极端情况,通过向改变的细胞状态转变来阐明内部机制和对胁迫的适应。通过研究肿瘤微环境和更早的时间点,我们开始更深入地了解肿瘤可塑性的全貌。可以说,这种更深入的了解将导致更好的患者结果,早期干预更有可能逆转可塑性并防止向侵袭性小细胞表型的转化。

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