[Antitumor Effect of Dihydroartemisinin on Diffuse Large B-Cell Lymphoma].
To investigate the potential antitumor effect and its mechanism of dihydroartemisinin (DHA) on diffuse large B-cell lymphoma (DLBCL).
Lymphoma · LIVING RESEARCH LIBRARY
Ongoing Research for Lymphoma Using Advanced Alternative Medicine
Explore positive published findings by substance, cancer biology, treatment interaction and quality-of-life outcome.
Every entry includes the original study title, year, concise finding and a direct PubMed link.
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Research organized by substance and finding
Browse 21 source-linked studies with the full title, publication year, research focus and a concise finding. Select any linked substance to move directly to its corresponding Sunridge page.
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Artesunate activates the ATF4-CHOP-CHAC1 pathway and affects ferroptosis in Burkitt's Lymphoma.
showed that artesunate induced ferroptosis in DAUDI and CA-46 cells, as evidenced by the protective effect of liproxstatin-1, ferrostatin-1, and desferoxamine, resulting in an endoplasmic reticulum stress response, activation of the ATF4-CHOP-CHAC1 pathway enhanced ferroptosis in DAUDI and CA-46 cells.
Artesunate shows potent anti-tumor activity in B-cell lymphoma.
Artesunate markedly inhibited highly aggressive tumor growth in a xenograft model.
Dihydroartemisinin Induced Apoptosis and Synergized With Chemotherapy in Pleural Effusion Lymphoma Cells.
N-acetylcysteine treatment inhibited DHA-induced ROS elevation and suppressed expression of cleaved caspases leading to significantly reduced PEL apoptosis.
Engineered Artesunate-Naphthalimide Hybrid Dual Drug for Synergistic Multimodal Therapy against Experimental Murine Lymphoma.
Napthalimide-artesunate conjugates inhibit the growth of lymphoma and induce apoptosis, including ready incorporation and reduction in cell viability.
Mechanisms of Dihydroartemisinin and Dihydroartemisinin/Holotransferrin Cytotoxicity in T-Cell Lymphoma Cells.
We found that Jurkat cells (a T-cell lyphoma cell line) were sensitive to DHA treatment with a IC50 of dihydroartemisinin.
Anticancer activities of curcumin on human Burkitt's lymphoma.
Curcumin inhibited proliferation of CA46 cells in a time- and dose-dependent manner, 2.
Co-delivery of Doxorubicin and Curcumin with Polypeptide Nanocarrier for Synergistic Lymphoma Therapy.
Further, combination of DOX with other anticancer drugs, such as curcumin, can enhance the synergistic effects, possibly through epigenetic mechanisms.
Curcumin induces apoptosis via downregulation of SKP2 and induction of GADD45A/CDKN1A expression through generation of ROS in cutaneous T-cell lymphoma cells.
The study found that curcumin induced apoptosis in CTCL cells by activating mitochondrial signaling pathways and caspases leading to growth inhibition.
Antitumor Effect of Epigallocatechin Gallate and Vincristine in Mice with L5178Y Lymphoma.
Therefore, the combination of EGCG with vincristine has a better antineoplastic effect by inhibiting tumor development and increasing survival on both substances independently.
Glutathione overproduction mediates lymphoma initiating cells survival and has a sex-dependent effect on lymphomagenesis.
A subset of lymphoma cells, characterized by an increased abundance of the antioxidant glutathione, escape ROS-induced lethality, a response not seen in non-tumor cells.
Glutathione-S-transferases and Chemotherapy Resistance of Hodgkin's Lymphoma Cell Lines.
Glutathione-S-transferases (GSTs) are associated with multidrug resistance of tumor cells and are involved in drug detoxification and control of apoptosis.
Antitumor potential of ivermectin against T-cell lymphoma-bearing hosts.
These findings collectively support the therapeutic potential of ivermectin as a repurposed anticancer agent, acting through multiple mechanisms including cell cycle arrest, ROS generation, mitochondrial dysfunction, and apoptosis.
Amelioration of Dalton's lymphoma-induced angiogenesis by melatonin.
Dalton's lymphoma ascites induced significant increase in endothelial cell proliferation, migration, and sprouting of the tertiary branching in chorioallantoic membrane and mesentery of Dalton's lymphoma-bearing mice, whereas melatonin treatment led to their inhibition in a dose-dependent manner.
Antitumor Effects of Palladium-α-Lipoic Acid Complex Formulation as an Adjunct in Radiotherapy
Poly-MVA enhanced the antitumor effect of radiation in the reported lymphoma model and also reduced radiation-associated blood-cell and normal-cell DNA effects.
Gut microbiome modulates the outcome in primary central nervous system lymphoma patients undergoing chemotherapy: An ancillary study from the BLOCAGE trial.
Primary central nervous system lymphoma (PCNSL) treatment relies on a high-dose methotrexate-based chemotherapy (HD-MTX-based CT) regimen; however, whether there is a specific microbiota composition association with treatment response and clinical outcomes remains incompletely understood.
Microbiome-Based Modeling of CAR-T Therapy Response in Lymphoma: Insights From Shotgun Metagenomics Sequencing.
We also trained 25 microbiome-based machine-learning (ML) models for response prediction.
Biphasic Rapamycin Effects in Lymphoma and Carcinoma Treatment.
Typical pharmacologic rapamycin (1-8 mg/kg) significantly reduced tumor burden via direct suppression of tumor cell proliferation and improved survival in EL4 challenge independent of antitumor immunity.
Epigenetic Regulation of Apoptosis in Cutaneous T-Cell Lymphoma: Implications for Therapy with Methotrexate, Jak Inhibitors, and Resveratrol.
The study reports epigenetic Regulation of Apoptosis in Cutaneous T-Cell Lymphoma: Implications for Therapy with Methotrexate, Jak Inhibitors, and Resveratrol.
High-dose ascorbic acid synergizes with anti-PD1 in a lymphoma mouse model.
High-dose AA treatment synergized with anti-PD1 therapy in a syngeneic lymphoma mouse model, resulting in marked inhibition of tumor growth compared with either agent alone.
Vitamin D controls apoptosis and proliferation of cutaneous T-cell lymphoma cells.
The study reports vitamin D controls apoptosis and proliferation of cutaneous T-cell lymphoma cells.
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