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Feb 2026 DOI 10.14302/issn.2372-6601.jhor-25-5944
Y. Berezin MikhailCorresponding author
Background Oxaliplatin, a widely used chemotherapeutic agent, is associated with hematologic toxicities such as anemia, leukopenia, and thrombocytopenia. Despite their clinical relevance, the molecular mechanisms underlying lineage-specific bone marrow suppression remain poorly understood. Methods We administered oxaliplatin to mice over eight weeks and performed RNA-sequencing (RNA integrity >8) on bone marrow alongside peripheral blood analysis and cytokine profiling. Transcriptomic data were analyzed to identify differentially expressed genes (DEGs) and enriched pathways. For that, we applied a thematic Gene Ontology (thematicGO) enrichment method that groups GO terms into biologically meaningful categories, such as hematopoietic lineage disruption, cell cycle arrest, and cytokine signaling. Results Oxaliplatin induced broad transcriptional suppression of erythropoiesis and lymphopoiesis, with 3,691 DEGs identified (FDR<0.05, |FC|>1.5). Upregulation of Cdkn1a and downregulation of E2f2 suggest G1/S cell cycle arrest, correlating with repression of key erythroid maturation genes (e.g., Spta1, Slc4a1, Alas2) and hemoglobin subunits (Hba-a1/2, Hbb-bs/t). Despite a ~3000-fold increase in renal Epo expression, bone marrow Epor was reduced, indicating erythropoietin resistance. B and T cell markers were also significantly downregulated, signifying a collapse in adaptive immunity. Notably, neutrophil populations were largely spared. Cytokine analysis in plasma revealed a pro-inflammatory shift with elevated TNF-α and reduced TGF-β, potentially exacerbating hematopoietic dysfunction. Conclusions Oxaliplatin induces a lineage-dependent suppression of hematopoiesis, driven by coordinated cell cycle arrest, metabolic stress, and disrupted cytokine signaling. RNA-seq analysis enabled integration of transcriptomic findings into coherent biological themes. These findings provide mechanistic insights into oxaliplatin’s hematologic toxicity linking bone marrow failure (potentially reversible) via interconnected inflammatory and metabolic pathways and may inform therapeutic strategies to minimize or restore myelosuppression in cancer patients.
Feb 2018
Zeng JinchengCorresponding author
Dongguan Key Laboratory of Medical Bioactive Molecular Developmental and Translational Research, Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, Guangdong Medical University, Dongguan 523808, China
Gastric cancer is one of the most common types of cancer in the world, usually diagnosed at an advanced stage. Despite the advances in specific anticancer agents' development, the survival rates remain modest, even in early stages. HER2 overexpression was identified on 15% - 20% of gastric cancer patients. Trastuzumab-based chemotherapy provides obvious efficacy improving outcomes of HER2 positive gastric cancer patients. We performed a meta-analysis to estimate the efficacy of the addition of trastuzumab over chemotherapy. We identified randomized controlled trials (RCTs) which compare the addition of trastuzumab therapy to chemotherapy alone reporting progression-free survival (PFS), time to progression (TTP), overall survival (OS), and/or response rates as our eligible trials. Night trials including 1101 patients were eligible for analysis. Trastuzumab therapeutic partners were cisplatin (9 RCTs), 5-fluorouracil (8 RCTs), capecitabine (6 RCTs), irinotecan (1 RCTs), docetaxel (1 RCTs), oxaliplatin (1 RCTs), and leucovorin (1 RCTs). The addition of trastuzumab agents improved OS (HR = 0.80; 95% CI = 0.72 - 0.89), PFS (HR = 0.70; 95% CI = 0.59 - 0.83), TTP (HR = 0.69; 95% CI = 0.57 - 0.83), and overall response rate (RR = 1.22; 95% CI = 0.94 - 1.59), DCR (RR = 1.19; 95% CI = 1.10 - 1.28). Our meta-analysis affirmed the efficacy of adding trastuzumab agent to chemotherapy in HER2 positive gastric cancer.
May 2015 DOI 10.14302/issn.2470-0436.jos-14-527
Sanjay SrinivasanCorresponding author
Ophthalmology and Visual Sciences, Khoo Teck Puat Hospital, Singapore
A 66 year old Chinese male with a medical history of hypertension, diabetes mellitus and hepatitis B carrier was diagnosed with hepatocellular carcinoma in 2009. He underwent treatment with selective internal radiation spheres and sorafenib, and multiple cycles of chemotherapeutic agents such as bevacizumab, erlotinib, OXAFI ( intravenous oxaliplatin and doxorubicin given on days 1, 8 and 15 in a 28-day cycle, a daily continuous infusion of fluorouracil and subcutaneous interferon alfa-2b 5 million units administered thrice weekly), thalidomide, capecitabine, and rapamycin over the course of four years. Along the course of treatment, he developed pulmonary embolism and was initially started on anti-coagulation. Two months later, he developed hemoptysis and the anti-coagulants were stopped. During his routine ophthalmology visit for diabetic eye evaluation, he complained of blurring of vision of his left eye for the past four to five weeks. He was found to have central retinal vein occlusion (CRVO) of the left eye, associated with macular edema. Visual acuity was 6/15 for the right eye and 6/60 for the left eye. Eyelids, conjunctiva, cornea, anterior chamber, pupils, lens and ocular motility were normal. Humphrey visual field testing showed a superior arcuate and basal defect. This is the first reported case of CRVO in hepatocellular carcinoma. The etiology of CRVO is multifactorial, withhepatic malignancy, previous major surgery, multiple cycles of chemotherapy and cessation of anticoagulant therapyas possible aetiological factors. His background medical problems of diabetes and hypertension are further contributors.