ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016
Stimulation of the hypoxia pathway modulates chemotherapy resistance in Hodgkin's lymphoma cells.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- MEPED as salvage therapy for relapsed/refractory Hodgkin's lymphoma incorporating edited non-oncogene addiction: mTOR as a bottleneck.Frontiers in pharmacology · 2025Review
- Hodgkin lymphoma: hypodense lesions in mediastinal masses.Scientific reports · 2024Article
- Multidrug Resistance of Gastric Cancer: The Mechanisms and Chinese Medicine Reversal Agents.Cancer management and research · 2020Review
- Sustain, Adapt, and Overcome-Hypoxia Associated Changes in the Progression of Lymphatic Neoplasia.Frontiers in oncology · 2019Review
- Tumor necrosis factor receptor 2 may promote the proliferation and drug resistance of Kapras299 and L428 lymphoma cells via the AKT and WNT/β-catenin signaling pathways.Oncology letters · 2018Article
- Identification of target gene of venous thromboembolism in patients with lymphoma via microarray analysis.Oncology letters · 2017Article
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Authors and funding
4 authors at 2 institutions in 1 country.
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Abstract
Hodgkin's lymphoma (HL) is a malignant disease of the lymphatic system. The therapy has been improved during the last decades but there are still patients who cannot be cured, and the therapy is associated with several adverse late effects. Therefore, we asked which genes might be involved in the chemotherapy resistance of HL cells. We observed that HL cells became more resistant against cisplatin after treatment with cobalt chloride. Therefore, we analyzed which genes were differentially expressed between cells incubated in medium with or without cobalt chloride. We found several genes which were up- or downregulated in the presence of cobalt chloride and might be involved in the modulation of chemotherapy resistance. Cobalt chloride is a hypoxia-mimetic agent. Therefore, we tested chemo-resistance and gene expression of HL cells under hypoxic conditions and confirmed the results from the cobalt chloride experiments. Taken together, activation of the hypoxia pathway led to altered gene expression and drug resistance of HL cells. Differentially expressed genes might be interesting targets for the development of future treatment strategies against drug-resistant HL.
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