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interferon (DS Sumiferon / Humoferon / Sumiferon)

✓ Approved

Pacific Pharmaceuticals · IFNAR2

什么是 interferon？

interferon 是一种治疗药物，由Pacific Pharmaceuticals研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Intramuscular (IM) Injection、Subcutaneous Injection。

药物档案

商品名DS Sumiferon, Humoferon, Sumiferon
公司Pacific Pharmaceuticals
分子靶点IFNAR2
给药途径Injectable (Others), Intramuscular (IM) Injection, Subcutaneous Injection
状态Approved
来源： ClinicalTrials.gov, Pacific Pharmaceuticals

作用机制

分子靶点

interferon 作用于 1 个分子靶点：

IFNAR2interferon alpha and beta receptor subunit 2 (IFNARB, IFN-alpha-REC)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

interferon 针对 9 个适应症，涉及 2 个治疗领域。

治疗领域疾病/病症分期
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Hairy cell leukaemia✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Respiratory papilloma✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Chronic myeloid leukaemia✓ Approved
Infections and infestationsHepatitis B✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Plasma cell myeloma✓ Approved

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相关研究文献

PubMedThoracic cancer2026-09-11

Extent of Endobronchial Ultrasound Nodal Sampling and Risk of Pathologic N2 Upstaging in Clinical N0-N1 Non-Small Cell Lung Cancer.

Kim Min Jee MJ, Lee Jae Cheol JC, Choi Chang-Min CM, Lee Sei Won SW et al.

Endobronchial ultrasound (EBUS)-guided transbronchial needle aspiration (TBNA) is strongly recommended for mediastinal staging in resectable non-small cell lung cancer (NSCLC). However, the optimal sampling extent remains uncertain. This study aimed to evaluate whether the extent of nodal sampling during staging EBUS is associated with pathologic N2 upstaging in clinical N0-N1 NSCLC. This retrospective cohort included patients with cN0-N1 NSCLC who underwent preoperative EBUS-TBNA between January 2022 and December 2023. Patients were stratified into three groups according to the number of sampled lymph node stations at the N2/N3 levels: Group 1, ≤ 1 mediastinal station at N2 or N3; Group 2, one N2 and one N3 station; Group 3, ≥ 3 stations, including at least one N2 and one N3. The primary outcome was pathologic N2 upstaging, defined as N2 disease confirmed on surgical pathology despite preoperative stage N0-N1. A total of 418 patients were included (mean age, 68.6 years; 64.1% male). Most had adenocarcinoma (75.4%) and cN0 disease (94.7%). Group distribution was 140 (33.5%) in Group 1, 92 (22.0%) in Group 2, and 186 (44.5%) in Group 3. Pathologic N2 upstaging occurred in 21/140 (15.0%) in Group 1, 8/92 (8.7%) in Group 2, and 8/186 (4.3%) in Group 3. The rate decreased with increasing sampling, with Group 3 showing a lower rate than Group 1 (p = 0.005). Comprehensive staging EBUS-TBNA with ≥ 3 N2/N3 stations was associated with a lower rate of occult N2 upstaging in clinical N0-N1 NSCLC, underscoring the importance of comprehensive nodal evaluation for accurate staging.

PMID 42723359
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PubMedTranslational cancer research2026-09-11

Midkine restrains T-cell mediated anti-tumor immunity by suppressing macrophage M1 polarization in lung adenocarcinoma.

Qian Ting T, Sun Zijian Z, Wang Xin X, Sun Yan Y

Lung adenocarcinoma (LUAD) is characterized by a highly immunosuppressive tumor microenvironment (TME), which limits the efficacy of current anti programmed cell death protein 1 (anti-PD-1) immunotherapy. Midkine (MDK), a heparin-binding growth factor, is frequently overexpressed in various malignancies; however, its specific role in regulating anti-tumor immunity in LUAD remains unclear. This study aimed to investigate the immunomodulatory role of MDK in LUAD, and to evaluate the therapeutic potential of MDK neutralization. In this study, we analyzed single-cell sequencing datasets and validated MDK expression across multiple non-small cell lung cancer (NSCLC) cell lines. To explore the immunomodulatory functions of MDK, we established ex vivo co-culture models using human peripheral blood mononuclear cells (PBMCs) and LUAD cells. We assessed the impact of recombinant MDK and an MDK-neutralizing antibody (α-MDK) on T cell proliferation, differentiation, and cytotoxicity, as well as macrophage polarization, using flow cytometry, lactate dehydrogenase (LDH) release assays, and multiplex cytokine measurement. We confirmed that MDK is significantly upregulated in malignant LUAD cells compared to normal lung epithelial cells. Functional analysis revealed that MDK signaling suppresses T cell-mediated anti-tumor immunity by inhibiting the expansion of cytotoxic CD8+ T cells and restricting T helper type 1 cell (TH1) polarization. Furthermore, MDK impaired the polarization of macrophages towards the pro-inflammatory M1 phenotype, and dampened antigen-presenting cell function. Notably, blocking MDK signaling with a neutralizing antibody effectively reversed these immunosuppressive effects, restoring T cell cytotoxicity and enhancing the secretion of pro-inflammatory cytokines such as interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α). Our findings demonstrate that MDK acts as a key regulator in the LUAD TME by simultaneously restraining T cell activation and M1 macrophage polarization. These data suggest that targeting MDK offers a promising therapeutic strategy to overcome immune suppression and improve clinical outcomes in LUAD.

PMID 42724375
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PubMedAmerican journal of cancer research2026-09-11

High-fat diet-responsive DNM1 promotes hepatocellular carcinoma progression and predicts poor prognosis in viral-associated patients.

Chen Po-Ming PM, Huang Huai-Yi HY, Chen Hsin-Hung HH, Chen Rong-Fu RF et al.

Hepatocellular carcinoma (HCC) arises from diverse etiologies, among which metabolic dysfunction-associated liver disease and chronic viral hepatitis are the two major drivers worldwide. However, the molecular mechanisms linking metabolic stress to HCC progression remain incompletely understood. Dynamin-1 (DNM1), primarily known for its role in vesicular trafficking, has emerged as a potential oncogene, yet its prognostic and functional significance in HCC remains largely unexplored. Here, we investigated the role of DNM1 in high-fat diet (HFD)-associated hepatocarcinogenesis. Transcriptomic profiling was conducted to identify differentially expressed genes between normal and high-fat diet murine models, with human orthologs mapped. Clinical relevance was validated using The Cancer Genome Atlas (TCGA-LIHC) dataset. Survival analysis, GSEA (Gene Set Enrichment Analysis), and subgroup stratifications based on viral hepatitis status were performed. In vitro, loss-of-function assays (shRNA knockdown) were executed in HepG2 and SK-Hep1 cell lines to assess cell viability and migration. DNM1 was significantly upregulated in high-fat diet models. In the TCGA-LIHC cohort, high DNM1 expression was an independent risk factor for poor overall survival (HR=1.44, P=0.039) and correlated with advanced tumor stages (Stage III+IV, P=0.010). In vitro knockdown of DNM1 profoundly impaired cell proliferation and migration in HCC cell lines. Strikingly, DNM1 expression was further elevated in patients with concurrent viral hepatitis (P=0.009). GSEA revealed that high DNM1 expression was positively associated with viral infection pathways and negatively correlated with critical immune responses, including interferon-alpha/gamma responses and host immune cytolysis. Survival analysis stratified by four subgroups demonstrated that patients with both viral infection and high DNM1 expression exhibited the worst prognosis (Overall Log-rank P < 0.001). Our findings identify DNM1 as a high-fat diet-responsive regulator that links metabolic stress to hepatocellular carcinoma progression. Elevated DNM1 expression promotes malignant phenotypes in HCC and identifies a subgroup of viral-associated patients with particularly poor prognosis, highlighting DNM1 as a potential prognostic biomarker and therapeutic target.

PMID 42724488
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PubMedTranslational cancer research2026-09-11

Survival outcomes of postoperative radiotherapy and chemotherapy in early-stage cervical cancer: a Surveillance, Epidemiology, and End Results database-based stratified analysis.

Weng Changmei C, Wang Yan Y, Chen Wenbin W, Chen Shengchi S et al.

For early-stage cervical cancer, surgery constitutes the standard therapeutic approach. Whether adjuvant radiotherapy and chemotherapy should be administered to patients with intermediate- or high-risk pathological characteristics continues to generate debate. Controversy persists regarding the ideal postoperative adjuvant treatment approach for this patient population. Using the Surveillance, Epidemiology, and End Results (SEER) database, this study compared survival outcomes among early-stage cervical cancer patients managed with observation, postoperative radiotherapy (PORT), or postoperative concurrent chemoradiotherapy (POCRT). Patients with stage I-II cervical cancer who underwent surgical treatment from 2004 to 2020 were identified through the SEER database. Patients were classified into three cohorts based on their postoperative management: observation, PORT, and POCRT. Overall survival (OS) and cancer-specific survival (CSS) were assessed through Cox proportional hazards regression, competing risk modeling, Kaplan-Meier survival curves, and subgroup analyses. Among 13,687 eligible patients, 9,868 underwent postoperative observation, 1,237 received PORT, and 2,582 received POCRT. In the unmatched overall cohort, patients receiving adjuvant therapy had higher mortality rates and higher-risk baseline profiles. Stratified analysis demonstrated that postoperative observation was associated with better survival than PORT and POCRT in stage I patients (P<0.001), whereas POCRT was associated with better survival compared with observation and PORT in stage II patients (P=0.04). Subgroup analyses suggested associations between postoperative adjuvant therapy and better survival among patients with T2 disease, N1 status, multiple primary malignancies (≥2), or age ≥60 years. For patients with early-stage cervical cancer, the decision regarding PORT and chemotherapy should remain guided by current guideline-based risk stratification. Our findings suggest that tumor (T) stage, node (N) stage, multiple primary malignancies, and age warrant further investigation as potential effect modifiers.

PMID 42724481
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PubMedBrain communications2026-09-11

A meta-analysis of periodic and aperiodic electrophysiological features in Parkinson's disease.

Norouzi Hamzeh H, Ietswaart Magdalena M, Adair Jason J, Learmonth Gemma G

Parkinson's disease is characterized by a range of motor and non-motor changes that can negatively impact quality of life. Many studies have identified potential clinical electrophysiological correlates of Parkinson's disease with an aim of developing new methods of identifying at-risk patients and forming the basis of therapeutic interventions. However, these studies do not present consistent results, and a formal meta-analysis is warranted to identify reliable EEG or magnetoencephalography (M/EEG) characteristics across datasets. In this meta-analysis of open-access M/EEG datasets (n = 6; 4 EEG and 2 MEG), we compared periodic and aperiodic characteristics of resting-state recordings in 368 patients with Parkinson's disease and 570 age-matched healthy controls. Specifically, we compared the power and peak frequency of unadjusted and aperiodic-adjusted alpha- and beta-band oscillations, and the exponent and offset, across the two groups. Parkinson's patients had a consistently elevated aperiodic exponent and offset. Patients also had higher unadjusted beta-band power, but this was no longer present when the aperiodic features were removed, suggesting that previous findings of elevated beta activity in Parkinson's disease could be confounded by aperiodic activity rather than reflecting true oscillatory differences. Patients also had higher adjusted and unadjusted alpha-band power and a slower alpha peak frequency compared with controls, whereas no group difference in beta peak frequency was identified. In conclusion, this large cohort meta-analysis points to a broadly consistent pattern of both periodic and aperiodic changes in Parkinson's patients in M/EEG signals that may be used to develop diagnostics and targeted interventions in the future.

PMID 42724388
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PubMedTranslational cancer research2026-09-11

Predicting the prognosis of small intestinal stromal tumors in the post-imatinib era: a study based on the SEER database.

Sun Ying Y, Ren Xia X, Xu Xiaodan X, Liu Luojie L

The prognosis of small intestinal stromal tumors (SISTs) in the post-imatinib era is influenced by a complex interplay of clinicopathological factors. This study aimed to develop and validate predictive models for overall survival (OS) and cancer-specific survival (CSS) in patients with SISTs using data from the Surveillance, Epidemiology, and End Results (SEER) database. We retrospectively analyzed 3,504 patients diagnosed with SISTs between 2012 and 2023. Patients were randomly divided into a training cohort (n=2,453) and a testing cohort (n=1,051). Cox proportional hazards regression analyses were performed in the training cohort to identify independent prognostic factors for OS and CSS. Significant predictors were used to construct nomograms for predicting 1-, 3-, and 5-year survival probabilities. The models' performance was evaluated using receiver operating characteristic (ROC) curves, calibration plots, and decision curve analysis (DCA) in both the training and testing cohorts. Multivariate Cox regression analysis identified age ≥65 years, male sex, high tumor grade (III/IV), distant metastasis (M1), no surgery, unmarried status, and no chemotherapy as independent risk factors for worse OS (all P<0.01). For CSS, independent risk factors included age ≥65 years, high tumor grade (III/IV), lymph node metastasis (N1), distant metastasis (M1), and no surgery (all P<0.05). These factors were incorporated into the nomograms, which demonstrated satisfactory predictive accuracy. In the testing cohort, the area under the curve (AUC) for the OS nomogram at 1, 3, and 5 years were 0.763, 0.728, and 0.758, and for the CSS nomogram were 0.763, 0.784, and 0.801. Calibration curves showed good agreement between predicted and observed survival, and DCA confirmed the clinical utility of the nomograms. We developed and validated promising nomograms for predicting OS and CSS in patients with SISTs. These models, incorporating readily available clinicopathological factors, may serve as a supplementary tool for individualized risk stratification and clinical decision-making in the post-imatinib era.

PMID 42724818
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