RNF43 p.G659fs 通过 PI3K/AKT/mTOR 信号通路和 HLA-E 上调导致 MSI-high 结直肠癌中 NK 细胞功能障碍
RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:Targeting oral tumor microenvironment for effective therapy.
Targeting oral tumor microenvironment for effective therapy.
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口腔癌是常见的头颈部恶性肿瘤之一。针对口腔恶性肿瘤,可采用不同的抗癌治疗方式,如化疗、免疫治疗、放射治疗以及靶向分子治疗。传统上,人们认为仅通过化疗和放疗等抗癌方式靶向恶性细胞即可抑制肿瘤生长。在过去十年中,大量实验证实了肿瘤微环境(TME)中其他细胞和分泌分子在肿瘤进展中的关键作用。细胞外基质和免疫抑制细胞,如肿瘤相关巨噬细胞、髓源性抑制细胞(MDSCs)、癌相关成纤维细胞(CAFs)和调节性T细胞(Tregs),在口腔癌等肿瘤的进展和治疗耐药中发挥关键作用。另一方面,浸润的CD4+和CD8+T淋巴细胞以及自然杀伤(NK)细胞是抑制恶性细胞增殖的关键抗肿瘤细胞。调节细胞外基质和免疫抑制细胞,以及刺激抗癌免疫,已被建议用于更有效地治疗口腔恶性肿瘤。
此外,给予某些佐剂或联合治疗方式可能更有效地抑制口腔恶性肿瘤。在这篇综述中,我们讨论了口腔癌细胞与TME之间的各种相互作用。
此外,我们还综述了口腔TME内可能导致治疗耐药的基本机制。克服口腔癌对各种抗癌方式耐药的潜在靶点和方法也将被综述。针对细胞和潜在治疗靶点的临床研究结果也将被综述。
Oral cancers are among the common head and neck malignancies. Different anticancer therapy modalities such as chemotherapy, immunotherapy, radiation therapy, and also targeted molecular therapy may be prescribed for targeting oral malignancies. Traditionally, it has been assumed that targeting malignant cells alone by anticancer modalities such as chemotherapy and radiotherapy suppresses tumor growth. In the last decade, a large number of experiments have confirmed the pivotal role of other cells and secreted molecules in the tumor microenvironment (TME) on tumor progression.
Extracellular matrix and immunosuppressive cells such as tumor-associated macrophages, myeloid-derived suppressor cells (MDSCs), cancer-associated fibroblasts (CAFs), and regulatory T cells (Tregs) play key roles in the progression of tumors like oral cancers and resistance to therapy.
On the other hand, infiltrated CD4 + and CD8 + T lymphocytes, and natural killer (NK) cells are key anti-tumor cells that suppress the proliferation of malignant cells. Modulation of extracellular matrix and immunosuppressive cells, and also stimulation of anticancer immunity have been suggested to treat oral malignancies more effectively.
Furthermore, the administration of some adjuvants or combination therapy modalities may suppress oral malignancies more effectively. In this review, we discuss various interactions between oral cancer cells and TME.
Furthermore, we also review the basic mechanisms within oral TME that may cause resistance to therapy. Potential targets and approaches for overcoming the resistance of oral cancers to various anticancer modalities will also be reviewed. The findings for targeting cells and potential therapeutic targets in clinical studies will also be reviewed.
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