NYU Langone Health研究人员通过分析来自56名患者共62个肿瘤的443,451个单个胰腺导管腺癌细胞，揭示了这种癌症如何通过持续重写DNA来增强侵袭性、转移能力和治疗耐药性1。研究发现，MYC基因在侵袭性癌细胞中活跃程度显著增强1。通过阻断MYC活性，研究人员成功使侵袭性基底型癌细胞转变为低侵袭性经典型状态，使其更容易被免疫细胞识别1。此外，研究还发现TIGIT基因与肿瘤免疫逃逸相关，而PD1基因的活性则出现降低1。
这项于2026年10月13日发表在《Nature Genetics》期刊上的研究为胰腺癌治疗提供了潜在靶点1。单个肿瘤内包含2-11个不同克隆体，反映出肿瘤的内部多样性1。考虑到胰腺导管腺癌患者诊断后5年内死亡率约为85%，这一发现的临床意义尤为重要1。该研究由Sky Foundation和美国国立卫生研究院提供资金支持1。
Researchers at NYU Langone Health's Perlmutter Cancer Center have identified a mechanism by which pancreatic cancer cells continuously reprogram their genetic material to become more aggressive, metastatic, and resistant to treatment.1 By analyzing nearly 443,451 individual pancreatic ductal adenocarcinoma cells from 62 tumors across 56 patients, the team discovered that the MYC gene becomes hyperactive in invasive cancer cells, enabling this transformation.1 The findings, published in Nature Genetics on October 13, 2026, reveal that blocking MYC activity can convert aggressive basal-like cancer cells into a less invasive classical state that is more recognizable to immune cells.1
The research highlights the remarkable genetic diversity within individual tumors, with each containing between 2 and 11 distinct clonal populations.1 Beyond MYC, scientists identified other genes linked to treatment evasion: the TIGIT gene associated with tumor immune escape and the PD1 gene, which shows reduced activity in resistant cells.1 These findings provide potential therapeutic targets for a disease with a particularly grim prognosis—approximately 85 percent of pancreatic ductal adenocarcinoma patients die within five years of diagnosis.1 The study was supported by the Sky Foundation and the U.S. National Institutes of Health.1
评论
还没有评论，欢迎留下第一条。