PDF(Pubmed)
Abstract：
BACKGROUND: Classical Hodgkin Lymphomas (HL) are a unique malignant growth with an excellent initial prognosis. However, 10-30% of patients will still relapse after remission. One primary cellular function that has been the focus of tumor progression is autophagy. This process can preserve cellular homeostasis under stressful conditions. Several studies have shown that autophagy may play a role in developing HL. Therefore, this review aimed to explore chemotherapy\'s effect on autophagy in HL, and the effects of autophagy on HL.
METHODS: A scoping review in line with the published PRISMA extension for scoping reviews (PRISMA-ScR) was conducted. A literature search was conducted on the MEDLINE database and the Cochrane Central Register of Controlled Trials (CENTRAL). All results were retrieved and screened, and the resulting articles were synthesized narratively.
RESULTS: The results showed that some cancer chemotherapy also induces autophagic flux. Although the data on HL is limited, since the mechanisms of action of these drugs are similar, we can infer a similar relationship. However, this increased autophagy activity may reflect a mechanism for increasing tumor growth or a cellular compensation to inhibit its growth. Although evidence supports both views, we argued that autophagy allowed cancer cells to resist cell death, mainly due to DNA damage caused by cytotoxic drugs.
CONCLUSIONS: Autophagy reflects the cell\'s adaptation to survive and explains why chemotherapy generally induces autophagy functions. However, further research on autophagy inhibition is needed as it presents a viable treatment strategy, especially against drug-resistant populations that may arise from HL chemotherapy regimens.
METHODS: A scoping review in line with the published PRISMA extension for scoping reviews (PRISMA-ScR) was conducted. A literature search was conducted on the MEDLINE database and the Cochrane Central Register of Controlled Trials (CENTRAL). All results were retrieved and screened, and the resulting articles were synthesized narratively.
RESULTS: The results showed that some cancer chemotherapy also induces autophagic flux. Although the data on HL is limited, since the mechanisms of action of these drugs are similar, we can infer a similar relationship. However, this increased autophagy activity may reflect a mechanism for increasing tumor growth or a cellular compensation to inhibit its growth. Although evidence supports both views, we argued that autophagy allowed cancer cells to resist cell death, mainly due to DNA damage caused by cytotoxic drugs.
CONCLUSIONS: Autophagy reflects the cell\'s adaptation to survive and explains why chemotherapy generally induces autophagy functions. However, further research on autophagy inhibition is needed as it presents a viable treatment strategy, especially against drug-resistant populations that may arise from HL chemotherapy regimens.
摘要：
背景：经典霍奇金淋巴瘤（HL）是一种独特的恶性生长，具有良好的初始预后。然而,10-30%的患者在缓解后仍会复发。已经成为肿瘤进展焦点的一种主要细胞功能是自噬。该过程可以在压力条件下保持细胞稳态。多项研究表明，自噬可能在HL的发展中起作用。因此,本综述旨在探讨化疗对HL细胞自噬的影响,以及自噬对HL的影响。
方法：进行了与已发布的PRISMA扩展范围审查（PRISMA-ScR）相一致的范围审查。在MEDLINE数据库和Cochrane中央对照试验注册中心（CENTRAL）上进行了文献检索。对所有结果进行检索和筛选,并对所得文章进行了叙述合成。
结果：结果显示，某些癌症化疗也会诱导自噬通量。虽然HL上的数据有限，由于这些药物的作用机制相似，我们可以推断出类似的关系。然而,这种自噬活性的增加可能反映了增加肿瘤生长的机制或细胞补偿以抑制其生长。尽管有证据支持这两种观点，我们认为自噬允许癌细胞抵抗细胞死亡，主要是由于细胞毒性药物引起的DNA损伤。
结论：自噬反映了细胞对生存的适应，并解释了为什么化疗通常会诱导自噬功能。然而,自噬抑制需要进一步研究，因为它提出了可行的治疗策略，特别是针对HL化疗方案可能产生的耐药人群。
方法：进行了与已发布的PRISMA扩展范围审查（PRISMA-ScR）相一致的范围审查。在MEDLINE数据库和Cochrane中央对照试验注册中心（CENTRAL）上进行了文献检索。对所有结果进行检索和筛选,并对所得文章进行了叙述合成。
结果：结果显示，某些癌症化疗也会诱导自噬通量。虽然HL上的数据有限，由于这些药物的作用机制相似，我们可以推断出类似的关系。然而,这种自噬活性的增加可能反映了增加肿瘤生长的机制或细胞补偿以抑制其生长。尽管有证据支持这两种观点，我们认为自噬允许癌细胞抵抗细胞死亡，主要是由于细胞毒性药物引起的DNA损伤。
结论：自噬反映了细胞对生存的适应，并解释了为什么化疗通常会诱导自噬功能。然而,自噬抑制需要进一步研究，因为它提出了可行的治疗策略，特别是针对HL化疗方案可能产生的耐药人群。
