欢迎来到OAJRC平台！

核心 CSCIED

期刊栏目

投稿

审稿

期刊目次

加入编委

期刊订阅

添加您的邮件地址以接收即将发行期刊数据：

当前位置：国际临床研究杂志 > 2026年 10卷 (9)期

Open Access Article

International Journal of Clinical Research. 2026; 10: (9) ; 23-35 ; DOI: 10.12208/j.ijcr.20260430.

Molecular mechanisms and frontier advances in the diagnosis and treatment of intrahepatic cholangiocarcinoma
肝内胆管癌的分子机制与诊疗前沿进展

作者： 杨真诚, 陈雪健, 胡子豪, 徐力善, 郑宏群 *

哈尔滨医科大学附属第四医院肿瘤外科肝胆外科黑龙江哈尔滨

*通讯作者：郑宏群,单位：哈尔滨医科大学附属第四医院肿瘤外科肝胆外科黑龙江哈尔滨；

发布时间: 2026-09-10 总浏览量: 15 下载量: 加载中...

PDF 全文下载引用本文

摘要

近年来，肝内胆管癌（iCCA）发病率在全球范围内逐年上升，推动因素也从以前的肝吸虫感染及病毒性肝炎转为代谢综合征和非酒精性脂肪性肝病等。而且这种癌症很少通过肝硬化而发展成为恶性肿瘤，这改变了我们对它生物学行为以及发生发展过程的认识。以往的观点是，长期慢性炎症会导致一系列遗传学或表观遗传学变化进而引起恶性肿瘤发生；然而iCCA具有高度异质性，可区分为小胆管型及大导管型两类。小胆管型主要见于FGFR2融合或IDH1/2突变，而大导管型则以KRAS、TP53突变及CDKN2A/B缺失为主。这些不同分子表型为精准治疗指明方向。另外，在组织学上iCCA一个显著特点是富含大量活化癌相关成纤维细胞形成的致密间质，造成一种“免疫排除”型微环境，使得药物难以穿透且缺乏有效的效应性T细胞浸润。尽管手术切除目前仍是最有效的治疗方法，但术后五年复发率仍较高（约50%-70%）。而胆道癌辅助化疗Ⅲ期试验（BILCAP）和日本临床肿瘤研究组1202试验（JCOG1202/ASCOT）两项研究均证实了卡培他滨或者S-1作为术后辅助化疗的有效性，BILCAP研究显示卡培他滨辅助化疗使符合方案集患者中位OS延长至53个月（对照组36个月，HR=0.75）；JCOG1202研究证实S-1可使3年生存率提高至77.1%（对照组67.6%，HR=0.69）。对于可以手术切除患者，樊嘉院士等人开展了一项ZSAB-neoGOLP III期临床试验结果显示，新辅助GOLP治疗能够显著改善高风险患者的无病生存期，较直接手术显著延长中位无事件生存期（18.0 vs. 8.7个月，HR=0.43）并使R0切除率达到95%以上。而在晚期一线治疗中，TOPAZ-1以及KEYNOTE-966两项大型III期临床试验均已明确表明抗PD-L1抗体联合化疗是有效方案。此外，在某些特定分子亚型例如FGFR2融合或IDH1突变情况下，Pemigatinib、Futibatinib等靶向药物以及Ivosidenib等新型抑制剂都显示出巨大潜力。对于不能切除或局限于肝脏病灶者，经动脉化疗栓塞术（TACE）、钇‑90选择性内放射治疗（Y90-SIRT）以及肝动脉灌注化疗（HAIC）等局部区域治疗方法都可以起到一定作用并且可以与全身治疗结合使用。最后，液体活检尤其是ctDNA由于其简便快捷、灵敏度高以及可连续进行监测等优势而在疾病早期发现、复发预警以及耐药机制研究等方面远远优于传统组织活检方法。

关键词： 肝内胆管癌；精准靶向治疗；肿瘤微环境；免疫治疗；液体活检

Abstract

The rate of intrahepatic cholangiocarcinoma (iCCA) has increased over the last several decades in most parts of the world and the underlying cause has shifted as well as liver fluke infections and viral hepatitis to metabolic syndrome and non-alcoholic fatty liver disease. These people may acquire cancer at once without going through cirrhosis, altering the way we perceive the course of the illness. The pathogenesis of iCCA is characterized by an evolutionarily based model of chronic inflammation-genetic and epigenetic changes-malignancy. Cell origin is responsible for a fundamental difference between the two types of cell origin; both have different molecular mutation spectra, stromal reactions, and biological behaviors: the small-duct type has its etiology largely determined by FGFR2 fusions and IDH1/2 mutations, whereas the large-duct type is defined by mutations in the KRAS and TP53 genes and the loss of CDKN2A/B. This molecular plan is the foundation of precision treatment. The hallmark of iCCA in histopathology is the presence of a very dense stroma formed by large numbers of cancer-related fibroblasts that generate an immune-excluded microenvironment that does not allow drugs to penetrate or CD8+ T cells to infiltrate. In connection to treatment, R0 resection is the only potentially curative choice, however, the 5-year postoperative recurrence is 50%-70%. Biliary Cancer Adjuvant Chemotherapy Phase III (BILCAP) and Japan Clinical Oncology Group 1202/Adjuvant S‑1 for Biliary Tract Cancer (JCOG1202/ASCOT) trials have demonstrated capecitabine and S-1 as standards of adjuvant chemotherapy. The BILCAP trial demonstrated that capecitabine adjuvant chemotherapy extended median overall survival in the per protocol population (53.0 vs. 36.0 months; HR=0.75), and the JCOG1202/ASCOT trial confirmed that S-1 improved 3-year survival (77.1% vs. 67.6%; HR=0.69).The most recent perioperative advance has been made by the ZSAB-neoGOLP Phase III trial conducted by Fan Jia and Zhou Jian: the Phase III ZSAB-neoGOLP trial showed that neoadjuvant GOLP significantly improved event-free survival in high-risk patients compared with upfront surgery (median 18.0 vs. 8.7 months; HR=0.43)and the rate of R0 resection was 95%. Durvalumab or pembrolizumab with gemcitabine-cisplatin has become the standard of care in the first-line setting of advanced disease with the TOPAZ-1 and KEYNOTE-966 Phase III studies solidifying this combination. In later lines, survival outcomes of patients with particular molecular subtypes have been significantly improved by agents targeting FGFR2 fusions (pemigatinib, futibatinib), and the IDH1 inhibitor ivosidenib. When it is unresectable but limited to the liver, locoregional treatments [transarterial chemoembolization (TACE), yttrium‑90 selective internal radiation therapy (Y90-SIRT), and hepatic artery infusion chemotherapy (HAIC)] are effective in controlling the disease, and their synergistic benefit with systemic therapy is now better recognized. Throughout the whole course of the disease, liquid biopsy, particularly ctDNA, is showing a potential that cannot be replaced by tissue biopsy, as it overcomes the problems with sampling, gives an early warning of recurrence, and allows monitoring of resistance mutations in real time.

Key words： Intrahepatic cholangiocarcinoma; Precision targeted therapy; Tumor microenvironment; Immuno-therapy; Liquid biopsy

参考文献 References

[1] Benson, A. B., D’Angelica, M. I., Abrams, T., et al. Biliary Tract Cancers, Version 2.2025, NCCN Clinical Practice Guidelines In Oncology. J. Natl. Compr. Canc. Netw. 23, 403–418 (2025).

[2] Valle, J. W., Kelley, R. K., Nervi, B., Oh, D.-Y. & Zhu, A. X. Biliary tract cancer. The Lancet 397, 428–444 (2021).

[3] Shin, H., Oh, J., Masuyer, E., et al. Epidemiology of cholangiocarcinoma: An update focusing on risk factors. Cancer Sci. 101, 579–585 (2010).

[4] Feng, Y., Fang, L. & Cao, G. Epidemiological characteristics and precise prophylaxis and control of HBV-associated primary liver cancer. Hepatoma Res.

https://doi.org/10.20517/2394-5079.2024.132 (2025)

[5] Sithithaworn, P., Yongvanit, P., Duenngai, K., Kiatsopit, N. & Pairojkul, C. Roles of liver fluke infection as risk factor for cholangiocarcinoma. J. Hepato-Biliary-Pancreat. Sci. 21, 301–308 (2014).

[6] Zen, Y. Intrahepatic cholangiocarcinoma: typical features, uncommon variants, and controversial related entities. Hum. Pathol. 132, 197–207 (2023).

[7] Okuda, K. Peripheral cholangiocarcinoma and intrahepatic calculi. J. Gastroenterol. Hepatol. 14, 1141–1143 (1999).

[8] Wang, S., Hu, B., Li, Y., Cai, Z. & Zhou, Y. Risk factors for intrahepatic cholangiocarcinoma: a systematic review and meta-analysis. Preprint at

https://doi.org/10.21203/rs.2.11210/v1 (2019).

[9] Dasgupta, P., Henshaw, C., Youlden, D. R., et al. Global Trends in Incidence Rates of Primary Adult Liver Cancers: A Systematic Review and Meta-Analysis. Front. Oncol. 10, 171 (2020).

[10] Roy, N. P., Gonzalez, Z., Kanth, R. & Roy, P. K. 12 Non-Alcoholic Fatty Liver Disease and Risk for Intrahepatic and Extrahepatic Cholangiocarcinoma: Meta-Analysis of Case Control Studies. Am. J. Gastroenterol. 114, S7–S7 (2019).

[11] Waldner, M. J. & Neurath, M. F. Master regulator of intestinal disease: IL-6 in chronic inflammation and cancer development. Semin. Immunol. 26, 75–79 (2014).

[12] Kafle, A., Suttiprapa, S., Muhammad, M., et al. Epigenetic Biomarkers and the Wnt/β-Catenin Pathway in Opisthorchis viverrini-associated Cholangiocarcinoma: A Scoping Review on Therapeutic Opportunities. PLoS Negl. Trop. Dis. 18, e0012477 (2024).

[13] Huang, C., Wu, Y., Wu, A., et al. Clonorchis sinensis and cholangiocarcinoma: molecular mechanisms and biomarker advances. Parasite 33, 16 (2026).

[14] Wu, M.-J., Kondo, H., Kammula, A. V., et al. Mutant IDH1 inhibition induces dsDNA sensing to activate tumor immunity. Science 385, eadl6173 (2024).

[15] Kendall, T., Verheij, J., Gaudio, E., et al. Anatomical, histomorphological and molecular classification of cholangiocarcinoma. Liver Int. 39, 7–18 (2019).

[16] Goyal, L., Meric-Bernstam, F., Hollebecque, A., et al. Futibatinib for FGFR2 -Rearranged Intrahepatic Cholangiocarcinoma. N. Engl. J. Med. 388, 228–239 (2023).

[17] Zhu, A. X., Borger, D. R., Kim, Y., et al. Genomic Profiling of Intrahepatic Cholangiocarcinoma: Refining Prognosis and Identifying Therapeutic Targets. Ann. Surg. Oncol. 21, 3827–3834 (2014).

[18] Mahipal, A., Tella, S. H., Kommalapati, A., Anaya, D. & Kim, R. FGFR2 genomic aberrations: Achilles heel in the management of advanced cholangiocarcinoma. Cancer Treat. Rev. 78, 1–7 (2019).

[19] Jiao, Y., Pawlik, T. M., Anders, R. A., et al. Exome sequencing identifies frequent inactivating mutations in BAP1, ARID1A and PBRM1 in intrahepatic cholangiocarcinomas. Nat. Genet. 45, 1470–1473 (2013).

[20] Voss, J. S., Holtegaard, L. M., Kerr, S. E., et al. Molecular profiling of cholangiocarcinoma shows potential for targeted therapy treatment decisions. Hum. Pathol. 44, 1216–1222 (2013).

[21] Meric-Bernstam, F., Makker, V., Oaknin, A., et al. Efficacy and Safety of Trastuzumab Deruxtecan in Patients With HER2-Expressing Solid Tumors: Primary Results From the DESTINY-PanTumor02 Phase II Trial. J. Clin. Oncol. 42, 47–58 (2024).

[22] 中国临床肿瘤学会(CSCO)胆道肿瘤专家委员会. 胆道恶性肿瘤精准检测与分子诊断专家共识. 临床肿瘤学杂志 29, 797 (2024).

[23] Argenziano, M. E., Montori, M., Scorzoni, C., et al. The role of tumor microenvironment in cholangiocarcinoma. Hepatoma Res. 9, 9 (2023).

[24] Affὸ, S., Sererols-Viñas, L., Garcia-Vicién, G., et al. Cancer-Associated Fibroblasts in Intrahepatic Cholangiocarcinoma. Am. J. Pathol. 195, 378–396 (2025).

[25] Affo, S., Nair, A., Brundu, F., et al. Promotion of cholangiocarcinoma growth by diverse cancer-associated fibroblast subpopulations. Cancer Cell 39, 866-882.e11 (2021).

[26] Cogliati, B., Yashaswini, C. N., Wang, S., Sia, D. & Friedman, S. L. Friend or foe? The elusive role of hepatic stellate cells in liver cancer. Nat. Rev. Gastroenterol. Hepatol. 20, 647–661 (2023).

[27] Wu, F., Yang, J., Liu, J., et al. Signaling pathways in cancer-associated fibroblasts and targeted therapy for cancer. Signal Transduct. Target. Ther. 6, 218 (2021).

[28] Heij, L., Bednarsch, J., Tan, X., et al. Expression of Checkpoint Molecules in the Tumor Microenvironment of Intrahepatic Cholangiocarcinoma: Implications for Immune Checkpoint Blockade Therapy. Cells 12, 851 (2023).

[29] Zabransky, D. J., Kartalia, E., Lee, J. W., et al. Tumor-derived CCL2 drives tumor growth and immunosuppression in IDH1-mutant cholangiocarcinoma. Hepatology 82, 599–611 (2025).

[30] Ullman, N. A., Ruffolo, L. I., Jackson, K. M., et al. Association of CXCR2+ granulocytic myeloid derived suppressor cells with the development of cholangiocarcinoma: A possible target for intervention. J. Clin. Oncol. 38, 565–565 (2020).

[31] Wu, M.-J., Shi, L., Dubrot, J., et al. Mutant IDH Inhibits IFNγ–TET2 Signaling to Promote Immunoevasion and Tumor Maintenance in Cholangiocarcinoma. Cancer Discov. 12, 812–835 (2022).

[32] Nishida, N. & Kudo, M. Genetic/Epigenetic Alteration and Tumor Immune Microenvironment in Intrahepatic Cholangiocarcinoma: Transforming the Immune Microenvironment with Molecular-Targeted Agents. Liver Cancer 13, 136–149 (2024).

[33] 科技部传染病防治重大专项课题“病毒性肝炎相关肝癌外科综合治疗的个体化和新策略研究”专家组. 肝内胆管癌外科治疗中国专家共识（2020版）. 中华消化外科杂志 20, 1 (2021).

[34] Primrose, J. N., Fox, R. P., Palmer, D. H., et al. Capecitabine compared with observation in resected biliary tract cancer (BILCAP): a randomised, controlled, multicentre, phase 3 study. Lancet Oncol. 20, 663–673 (2019).

[35] Kobayashi, S., Ikeda, M., Nakachi, K., et al. A Multicenter Survey on Eligibility for a Randomized Phase III Trial of Adjuvant Chemotherapy for Resected Biliary Tract Cancer (JCOG1202, ASCOT). Ann. Surg. Oncol. 30, 7331–7337 (2023).

[36] Edeline, J., Benabdelghani, M., Bertaut, A., et al. Gemcitabine and Oxaliplatin Chemotherapy or Surveillance in Resected Biliary Tract Cancer (PRODIGE 12-ACCORD 18-UNICANCER GI): A Randomized Phase III Study. J. Clin. Oncol. 37, 658–667 (2019).

[37] Shi, G.-M., Huang, X.-Y., Liang, F., et al. Neoadjuvant GOLP in Resectable High-Risk Intrahepatic Cholangiocarcinoma. N. Engl. J. Med. 394, 983–995 (2026).

[38] Maithel, S. K., Javle, M. M., Mahipal, A., et al. NEO-GAP: A phase II single-arm prospective feasibility study of neoadjuvant gemcitabine/cisplatin/nab-paclitaxel for resectable high-risk intrahepatic cholangiocarcinoma. J. Clin. Oncol. 40, 4097–4097 (2022).

[39] Branch of Biliary SurgeryChinese Society of SurgeryChinese Medical Association. 胆道恶性肿瘤转化治疗专家共识（2025）. 中华外科杂志 63, 453 (2025).

[40] Anteby, R., Vierra, B. M. & Shah, S. A. Liver transplant for intrahepatic cholangiocarcinoma: current evidence and clinical practice recommendations. J. Gastrointest. Surg. 29, 102211 (2025).

[41] Ierardi, A. M., Angileri, S. A., Patella, F., et al. The role of interventional radiology in the treatment of intrahepatic cholangiocarcinoma. Med. Oncol. 34, 11 (2017).

[42] Gairing, S. J., Thol, F., Müller, L., et al. The Addition of Transarterial Chemoembolization to Palliative Chemotherapy Extends Survival in Intrahepatic Cholangiocarcinoma. J. Clin. Med. 10, 2732 (2021).

[43] Braccischi, L., Garducci, P. F., Taninokuchi Tomassoni, M., et al. Long-Term Outcomes and Prognostic Factors After Yttrium-90 Resin-Based Radioembolization for Unresectable Intrahepatic Cholangiocarcinoma: A Single-Center Experience. Cardiovasc. Intervent. Radiol. 49, 514–526 (2025).

[44] Xu, Q., Wang, C., You, R., et al. Hepatic arterial infusion chemotherapy (HAIC) plus Lenvatinib and PD-1 inhibitors versus systemic chemotherapy for unresectable intrahepatic cholangiocarcinoma. Discov. Oncol. 16, 775 (2025).

[45] Liu, P., Ye, H., Song, L., et al. Outcomes of stereotactic body radiotherapy for unresectable cholangiocarcinoma: a meta-analysis and systematic review. PeerJ 13, e19909 (2025).

[46] Bale, R. & Pawlik, T. M. Treatment of intrahepatic cholangiocarcinoma: evidence for the role of percutaneous ablation. Hepatoma Res. https://doi.org/10.20517/2394-5079.2023.71 (2023).

[47] Li, S., Yu, G., Wang, M., et al. Efficacy and safety of local–regional therapy combined with chemotherapy, immune checkpoint inhibitors and lenvatinib as first-line treatment in advanced intrahepatic cholangiocarcinoma: a multicenter retrospective cohort study. Cancer Immunol. Immunother. 74, 229 (2025).

[48] Valle, J., Wasan, H., Palmer, D. H., et al. Cisplatin plus Gemcitabine versus Gemcitabine for Biliary Tract Cancer. N. Engl. J. Med. 362, 1273–1281 (2010).

[49] Vogel, A., Sahai, V., Hollebecque, A., et al. An open-label study of pemigatinib in cholangiocarcinoma: final results from FIGHT-202. ESMO Open 9, 103488 (2024).

[50] Goyal, L., Meric-Bernstam, F., Hollebecque, A., et al. Abstract CT010: Primary results of phase 2 FOENIX-CCA2: The irreversible FGFR1-4 inhibitor futibatinib in intrahepatic cholangiocarcinoma (iCCA) with FGFR2 fusions/rearrangements. Cancer Res. 81, CT010–CT010 (2021).

[51] Javle, M. M., Roychowdhury, S., Kelley, R. K., et al. Final results from a phase II study of infigratinib (BGJ398), an FGFR-selective tyrosine kinase inhibitor, in patients with previously treated advanced cholangiocarcinoma harboring an FGFR2 gene fusion or rearrangement. J. Clin. Oncol. 39, 265–265 (2021).

[52] Zhu, A. X., Macarulla, T., Javle, M. M., et al. Final Overall Survival Efficacy Results of Ivosidenib for Patients With Advanced Cholangiocarcinoma With IDH1 Mutation: The Phase 3 Randomized Clinical ClarIDHy Trial. JAMA Oncol. 7, 1669 (2021).

[53] Saha, S. K., Parachoniak, C. A., Ghanta, K. S., et al. Mutant IDH inhibits HNF-4α to block hepatocyte differentiation and promote biliary cancer. Nature 513, 110–114 (2014).

[54] Bridgewater, J. A., Gardini, A. C., Wilmink, H., et al. 262MO Preliminary efficacy outcomes of ivosidenib in patients with IDH1-mutated cholangiocarcinoma (mIDH1 CCA): Initial results from the phase IIIb ProvIDHe study. Ann. Oncol. 36, S103 (2025).

[55] Harding, J. J., Fan, J., Oh, D.-Y., et al. Zanidatamab for HER2-amplified, unresectable, locally advanced or metastatic biliary tract cancer (HERIZON-BTC-01): a multicentre, single-arm, phase 2b study. Lancet Oncol. 24, 772–782 (2023).

[56] Trigo, J., Subbiah, V., Besse, B., et al. Lurbinectedin as second-line treatment for patients with small-cell lung cancer: a single-arm, open-label, phase 2 basket trial. Lancet Oncol. 21, 645–654 (2020).

[57] Kelley, R. K., Ueno, M., Yoo, C., et al. Pembrolizumab in combination with gemcitabine and cisplatin compared with gemcitabine and cisplatin alone for patients with advanced biliary tract cancer (KEYNOTE-966): a randomised, double-blind, placebo-controlled, phase 3 trial. The Lancet 401, 1853–1865 (2023).

[58] Chen, J., Amoozgar, Z., Liu, X., et al. Reprogramming the Intrahepatic Cholangiocarcinoma Immune Microenvironment by Chemotherapy and CTLA-4 Blockade Enhances Anti–PD-1 Therapy. Cancer Immunol. Res. 12, 400–412 (2024).

[59] Alizadeh, D. & Larmonier, N. Chemotherapeutic Targeting of Cancer-Induced Immunosuppressive Cells. Cancer Res. 74, 2663–2668 (2014).

[60] Oh, D.-Y., Ruth He, A., Qin, S., et al. Durvalumab plus Gemcitabine and Cisplatin in Advanced Biliary Tract Cancer. NEJM Evid. 1, (2022).

[61] 中国临床肿瘤学会(CSCO)胆道肿瘤专家委员会. 《胆道恶性肿瘤免疫检查点抑制剂治疗中国专家共识(2025版)》. 临床肿瘤学杂志 30, 598 (2025).

[62] Zhang, P., Niu, Z., Guo, H., et al. The multi-kinase inhibitor tinengotinib as monotherapy or combined with atezolizumab in advanced solid tumors: a phase Ib/II trial. Nat. Commun. https://doi.org/10.1038/s41467-026-72541-2 (2026).

[63] Florou, V., Rosenberg, A. E., Wieder, E., et al. Correction to: Angiosarcoma patients treated with immune checkpoint inhibitors: a case series of seven patients from a single institution. J. Immunother. Cancer 7, 285 (2019).

[64] Klein, O., Kee, D., Nagrial, A., et al. Evaluation of Combination Nivolumab and Ipilimumab Immunotherapy in Patients With Advanced Biliary Tract Cancers: Subgroup Analysis of a Phase 2 Nonrandomized Clinical Trial. JAMA Oncol. 6, 1405 (2020).

[65] Nagrial, A., Carlino, M. S., Gunjur, A., et al. Nivolumab and ipilimumab combination treatment in patients with advanced intrahepatic cholangiocarcinoma and gallbladder cancer: Results from the phase II MoST-CIRCUIT trial. Clin. Cancer Res. https://doi.org/10.1158/1078-0432.CCR-25-4009 (2026)

[66] Fotiadis, N., De Paepe, K. N., Bonne, L., et al. Comparison of a coaxial versus non-coaxial liver biopsy technique in an oncological setting: diagnostic yield, complications and seeding risk. Eur. Radiol. 30, 6702–6708 (2020).

[67] de Scordilli, M., Bortolot, M., Torresan, S., et al. Precision oncology in biliary tract cancer: the emerging role of liquid biopsy. ESMO Open 10, 105079 (2025).

[68] Guo, D., Huang, A., Wang, Y., et al. Early detection and prognosis evaluation for hepatocellular carcinoma by circulating tumour DNA methylation: A multicentre cohort study. Clin. Transl. Med. 14, e1652 (2024).

[69] Wang, Y., Li, Y., Liang, Z., et al. Circulating tumor DNA in cholangiocarcinoma: current clinical applications and future perspectives. Front. Cell Dev. Biol. 13, 1616064 (2025).

[70] Kim, K.-H., Yi, H.-S., Lee, H., Bae, G.-E. & Yeo, M.-K. Targeting the Sequences of Circulating Tumor DNA of Cholangiocarcinomas and Its Applications and Limitations in Clinical Practice. Int. J. Mol. Sci. 24, 7512 (2023).

[71] Mundhava, M., Jangid, P., Jangir, K., et al. Integrating Circulating Tumor DNA (ctDNA) Into Postoperative Surveillance After the Resection of Intrahepatic Cholangiocarcinoma: A Proposed Hybrid Imaging-Molecular Framework. Cureus

https://doi.org/10.7759/cureus.103966 (2026)

[72] Yu, J., He, A. R., Ouf, M., et al. Detecting Early Recurrence With Circulating Tumor DNA in Stage I-III Biliary Tract Cancer After Curative Resection. JCO Precis. Oncol. e2400443 (2025).

[73] Gutmans, J. & Mechahougui, H. Biliary tract cancers: advances in diagnostic and management. Explor. Target. Anti-Tumor Ther. 6, 1002328 (2025).

[74] Liu, C., Wang, X., Liu, E., et al. Deciphering cholangiocarcinoma heterogeneity and specific progenitor cell niche of extrahepatic cholangiocarcinoma at single-cell resolution. J. Hematol. Oncol. 18, 66 (2025).

[75] Hogenson, T. L., Xie, H., Phillips, W. J., et al. Culture media composition influences patient-derived organoid ability to predict therapeutic responses in gastrointestinal cancers. JCI Insight 7, e158060 (2022).

引用本文

杨真诚, 陈雪健, 胡子豪, 徐力善, 郑宏群, 肝内胆管癌的分子机制与诊疗前沿进展[J]. 国际临床研究杂志, 2026; 10: (9) : 23-35.

入驻平台

回到顶部

搜索文章: