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611.
Suppression of mouse skin tumor promotion and induction of apoptosis in HL-60 cells by Alpinia oxyphylla Miquel (Zingiberaceae) 总被引:3,自引:0,他引:3
There have been considerable efforts to search for naturally occurring
substances for the intervention of carcinogenesis. Many components from
dietary or medicinal plants have been identified that possess substantial
chemopreventive properties. An example is curcumin (Curcuma longa Linn.,
Zingiberaceae), which has been shown to inhibit tumor promotion in
experimental carcinogenesis. Alpinia oxyphylla Miquel, another plant of the
ginger family used in oriental herbal medicine, contains diarylheptanoids
whose structures are analogous to that of curcumin. In the present study,
we have tested A.oxyphylla for its ability to suppress tumor promotion.
Thus, topical application of the methanolic extract of dried fruits of
A.oxyphylla significantly ameliorated 12-O-tetradecanoylphorbol-13-acetate
(TPA)-induced skin tumor promotion as well as ear edema in female ICR mice.
In another study, treatment of HL-60 cells with the methanolic extract of
A.oxyphylla significantly reduced the viability of the cells and also
inhibited DNA synthesis. Microscopic examination of the treated cells
showed characteristic morphology of apoptosis. Furthermore, cells treated
with the extract of A.oxyphylla exhibited internucleosomal DNA
fragmentation in time- and concentration-dependent manners. TPA- stimulated
generation of superoxide anion in differentiated HL-60 cells was also
blunted by A.oxyphylla. Taken together, these findings suggest that
A.oxyphylla possesses potential chemopreventive and antitumorigenic
activities.
相似文献
612.
Arnab Ghosh Judith Michels Riccardo Mezzadra Divya Venkatesh Lauren Dong Ricardo Gomez Fadi Samaan Yu-Jui Ho Luis Felipe Campesato Levi Mangarin John Fak Nathan Suek Aliya Holland Cailian Liu Mohsen Abu-Akeel Yonina Bykov Hong Zhong Kelly Fitzgerald Sadna Budhu Andrew Chow Roberta Zappasodi Katherine S. Panageas Olivier de Henau Marcus Ruscetti Scott W. Lowe Taha Merghoub Jedd D. Wolchok 《The Journal of clinical investigation》2022,132(18)
In addition to playing a major role in tumor cell biology, p53 generates a microenvironment that promotes antitumor immune surveillance via tumor-associated macrophages. We examined whether increasing p53 signaling in the tumor microenvironment influences antitumor T cell immunity. Our findings indicate that increased p53 signaling induced either pharmacologically with APR-246 (eprenetapopt) or in p53-overexpressing transgenic mice can disinhibit antitumor T cell immunity and augment the efficacy of immune checkpoint blockade. We demonstrated that increased p53 expression in tumor-associated macrophages induces canonical p53-associated functions such as senescence and activation of a p53-dependent senescence-associated secretory phenotype. This was linked with decreased expression of proteins associated with M2 polarization by tumor-associated macrophages. Our preclinical data led to the development of a clinical trial in patients with solid tumors combining APR-246 with pembrolizumab. Biospecimens from select patients participating in this ongoing trial showed that there was a suppression of M2-polarized myeloid cells and increase in T cell proliferation with therapy in those who responded to the therapy. Our findings, based on both genetic and a small molecule–based pharmacological approach, suggest that increasing p53 expression in tumor-associated macrophages reprograms the tumor microenvironment to augment the response to immune checkpoint blockade. 相似文献
613.
Anne S. Reiner Benjamin H. Durham Mariko Yabe Kseniya Petrova-Drus Jasmine H. Francis Raajit K. Rampal Mario E. Lacouture Veronica Rotemberg Omar Abdel-Wahab Katherine S. Panageas Eli L. Diamond 《British journal of haematology》2023,203(3):389-394
Little is known about outcomes following interruption of targeted therapy in adult patients with histiocytic neoplasms. This is an IRB-approved study of patients with histiocytic neoplasms whose BRAF and MEK inhibitors were interrupted after achieving complete or partial response by 18-fluorodeoxyglucose positron emission tomography (FDG-PET). 17/22 (77%) of patients experienced disease relapse following treatment interruption. Achieving a complete response prior to interruption, having a mutation other than BRAFV600E, and receiving MEK inhibition only were each associated with a statistically significant improvement in relapse-free survival. Relapse is common following treatment interruption however some patients may be suitable for limited-duration treatment. 相似文献