Clinical trial · Observational
Plasma Sphingolipid Metabolites and Radiotherapy Efficacy in Hepatocellular Carcinoma
Correlation Between Plasma Sphingolipid Metabolites and the Efficacy of Radiotherapy in Hepatocellular Carcinoma
- Source
- ClinicalTrials.gov
- Retrieved
- Sep 8, 2026
- Layer
- normalized (units and labels harmonized; values unchanged)
- Run
- ING-CLINICALTRIALS-20260908-000001
Summary
Brief summary (as posted)
Plasma contains a variety of metabolites, among which sphingolipids, including ceramide, sphingosine, and sphingosine-1-phosphate, serve as important intracellular second messengers and are involved in various cellular signaling pathways, such as apoptosis. We hypothesize that plasma sphingolipid levels may be associated with the efficacy of radiotherapy for liver cancer. This study will utilize LC-MS/MS technology for qualitative and quantitative analysis of plasma sphingolipids in liver cancer patients undergoing radiotherapy. Clinical data related to patient prognosis will also be collected to investigate the correlation between plasma sphingolipid levels and the therapeutic efficacy of liver cancer radiotherapy. The aim is to establish the clinical diagnostic significance of plasma sphingolipid levels in predicting the efficacy of liver cancer radiotherapy, providing new insights to enhance the effectiveness of radiotherapy in liver cancer treatment.
Conditions
Conditions (5)
Free-text conditions as registered, with the CancerIndex entity they were reconciled to and the match type.
| Condition (as posted) | Mapped entity | Match | Confidence |
|---|---|---|---|
| Biomarkers | — | UNRESOLVED | — |
| Hepatocellular Carcinoma | Hepatocellular Carcinoma | ONTOLOGY_EXACT | 0.98 |
| Radiotherapy | — | UNRESOLVED | — |
| Sphingolipids | — | UNRESOLVED | — |
| Treatment Outcome | — | UNRESOLVED | — |
Interventions
Interventions (0)
Data not yet available
Design
Arms and outcomes
Arms (2)
- label
- Radiotherapy Responder Group
- description
- Participants who show a positive response to radiotherapy, as defined by mRECIST 1.1 criteria. This includes patients with Complete Response (CR) or Partial Response (PR) after radiotherapy. A decline in Alpha-Fetoprotein (AFP) levels may also be observed in some responders, serving as a potential biomarker for treatment efficacy.
- label
- Radiotherapy Non-Responder Group
- description
- Participants who do not show a significant response to radiotherapy, as defined by mRECIST 1.1 criteria. This includes patients classified as Stable Disease (SD) or Progressive Disease (PD) after radiotherapy. AFP levels may remain stable or increase in these patients, indicating a lack of significant tumor response to treatment.
Primary outcomes (1)
- measure
- Disease Control Rate (DCR)
- timeFrame
- From the start of treatment to 12 weeks post-treatment assessment
- description
- Disease Control Rate (DCR) is defined as the proportion of patients who achieve complete response (CR), partial response (PR), or stable disease (SD) according to the modified Response Evaluation Criteria in Solid Tumors (mRECIST). mRECIST is commonly used to evaluate tumor response, especially in the context of hepatocellular carcinoma and other solid tumors. DCR is an important measure to assess the overall effectiveness of the treatment in controlling disease progression.
Eligibility
Eligibility (as posted)
- Sex
- All
- Minimum age
- 18 Years
- Maximum age
- 80 Years
Show eligibility criteria text
Inclusion Criteria: * Patients voluntarily signed the informed consent form. * Aged between 18 and 80 years. * Clinically diagnosed with primary liver cancer according to the latest treatment guidelines. * Determined by the treating physician to require radiotherapy. * Expected survival time of more than 3 months. Exclusion Criteria: * Patients who discontinued radiotherapy or did not complete the planned treatment. * Presence of malignancies from other origins. * Severe metabolic diseases such as uncontrolled diabetes, significant obesity, or fatty liver disease. * Uncontrolled comorbidities, such as severe cardiovascular or pulmonary diseases, that may affect treatment or study outcomes.
References
Publications (11)
- RESULTDeng X, Yin X, Allan R, Lu DD, Maurer CW, Haimovitz-Friedman A, Fuks Z, Shaham S, Kolesnick R. Ceramide biogenesis is required for radiation-induced apoptosis in the germ line of C. elegans. Science. 2008 Oct 3;322(5898):110-5. doi: 10.1126/science.1158111. PMID 18832646
- RESULTKumar A, Oskouian B, Fyrst H, Zhang M, Paris F, Saba JD. S1P lyase regulates DNA damage responses through a novel sphingolipid feedback mechanism. Cell Death Dis. 2011 Feb 10;2(2):e119. doi: 10.1038/cddis.2011.3. PMID 21368890
- RESULTTaha TA, Osta W, Kozhaya L, Bielawski J, Johnson KR, Gillanders WE, Dbaibo GS, Hannun YA, Obeid LM. Down-regulation of sphingosine kinase-1 by DNA damage: dependence on proteases and p53. J Biol Chem. 2004 May 7;279(19):20546-54. doi: 10.1074/jbc.M401259200. Epub 2004 Feb 26. PMID 14988393
- RESULTAureli M, Bassi R, Prinetti A, Chiricozzi E, Pappalardi B, Chigorno V, Di Muzio N, Loberto N, Sonnino S. Ionizing radiations increase the activity of the cell surface glycohydrolases and the plasma membrane ceramide content. Glycoconj J. 2012 Dec;29(8-9):585-97. doi: 10.1007/s10719-012-9385-2. Epub 2012 May 17. PMID 22592846
- RESULTCheng JC, Bai A, Beckham TH, Marrison ST, Yount CL, Young K, Lu P, Bartlett AM, Wu BX, Keane BJ, Armeson KE, Marshall DT, Keane TE, Smith MT, Jones EE, Drake RR Jr, Bielawska A, Norris JS, Liu X. Radiation-induced acid ceramidase confers prostate cancer resistance and tumor relapse. J Clin Invest. 2013 Oct;123(10):4344-58. doi: 10.1172/JCI64791. Epub 2013 Sep 16. PMID 24091326
- RESULTGarcia-Barros M, Paris F, Cordon-Cardo C, Lyden D, Rafii S, Haimovitz-Friedman A, Fuks Z, Kolesnick R. Tumor response to radiotherapy regulated by endothelial cell apoptosis. Science. 2003 May 16;300(5622):1155-9. doi: 10.1126/science.1082504. PMID 12750523
- RESULTLiao WC, Haimovitz-Friedman A, Persaud RS, McLoughlin M, Ehleiter D, Zhang N, Gatei M, Lavin M, Kolesnick R, Fuks Z. Ataxia telangiectasia-mutated gene product inhibits DNA damage-induced apoptosis via ceramide synthase. J Biol Chem. 1999 Jun 18;274(25):17908-17. doi: 10.1074/jbc.274.25.17908.