sorafenib

The combination of Tislelizumab and Sorafenib demonstrates promising antitumor activity in the first-line treatment of hepatocellular carcinoma, with a relatively high objective response rate (ORR) and acceptable safety profile. Baseline CTC PD-L1 positivity can serve as a predictive marker for selecting hepatocellular carcinoma patients for PD-1/PD-L1 blockade therapy, and dynamic measurement of CTC changes can be used to monitor treatment efficacy.

Notably, high-risk patients demonstrated higher sensitivity to Sorafenib, Oxaliplatin and MK-2206, underscoring the promise of these lncRNAs as precise therapeutic targets in bladder cancer. By revealing the predictive importance of disulfidptosis-associated lncRNAs in bladder cancer, our research offers new perspectives and pinpoints potential therapeutic targets in clinical environments.

We found that a positive feedback loop between ALDH1L2 and NRF2 promotes HCC progression by activating the IL-6/Jak2/STAT3 signaling axis and tumor-associated macrophage polarization. In addition, we found that ALDH1L2 knockdown enhances the anti-HCC effect of sorafenib.

Our research demonstrated that DGKH is a crucial oncometabolic regulator of cancer stemness and therapy resistance, suggesting that inhibiting DGKH may lead to more effective HCC treatment.

All-trans retinoic acid (ATRA) is well known for its effectiveness in acute promyelocytic leukemia (APL) treatment and has already been shown to have synergistic effects combined with another TKI, sorafenib. Finally, in a xenotransplantation model ATRA plus AC220 was more efficient to reduce the leukemic burden than monotherapy with ATRA or AC220. Taken together, our results are a proof of the concept that ATRA and AC220 have synergistic anti-leukemic effects.

All the target compounds were evaluated against CAIX enzyme compared to dorzolamide and acetazolamide, subsequently the most potent CAIX inhibitors (3a, 3b, 3o, 6d, 6g, and 6i) were selected to evaluate their inhibitory activity against VEGFR-2 using sorafenib as a reference drug. Physicochemical predictions were examined using in silico techniques. In conclusion, these scaffolds present promising leads and furnish promising chemical backbones for the design of potent dual CAIX and VEGFR-2 inhibitors.b.

The results demonstrated that MALAT1-IN1 significantly enhanced sorafenib efficacy for the treatment of HCC both in vitro and in vivo. Collectively, our work brings new insights into the epigenetic mechanisms of sorafenib resistance and offers an alternative therapeutic strategy targeting ferroptosis for sorafenib-resistant HCC patients.

Our study reveals a novel mechanism underlying sorafenib-induced HCC cell death.

Chemotherapeutic agents such as gefitinib and sorafenib were predicted to be effective against high HJURP-expressing tumors. Its high expression correlates with specific genetic alterations and immune profiles, highlighting its potential as a therapeutic target. Future studies should validate these findings in larger cohorts.

Compound 5 was the most active derivative against HepG-2 and HuH-7 cell lines with IC50 = 0.75 ± 0.04 and 3.43 ± 0.16 μM, respectively, in contrast to Sorafenib which shows IC50 values of 5.23 ± 0.31 and 4.58 ± 0.21 μM, respectively...Hybrid 5 stops HepG-2's cell cycle at the S phase 48.02 % higher than untreated. Docking experiments assessed AKT and VEGFR2 binding patterns.

Sorafenib (SB), an anticancer drug was loaded onto MX-ZIF-8 and further modified with a liposomes (LPs) lipid bilayer to create (SB-MX-ZIF-8@LPs) nanocomposites...These findings were consistent with experimental results, highlighting the favorable interaction between MXene and SB. ADMET analysis confirmed that MX-ZIF-8@LPs possessed favorable drug carrier properties, including high intestinal absorption (96.6%), and low toxicity supporting its potential as an effective DDS for cancer therapy.

Additionally, patients in the low-risk group exhibited improved response to TACE and sorafenib treatments compared to the high-risk group. In contrast, the high-risk group exhibited reduced sensitivity to immunotherapy and increased sensitivity to paclitaxel. In the in-house cohort, high-risk patients displayed higher rates of early recurrence, along with an increased frequency of elevated alpha-fetoprotein, microvascular invasion, and aggressive MRI features associated with HCC. This study has successfully developed a risk score based on MTM and VETC-related genes, providing a promising tool for prognosis prediction and personalized treatment strategies in HCC patients.

P3, N=537, Active, not recruiting, Children's Oncology Group | Trial completion date: Jun 2026 --> Dec 2026 | Trial primary completion date: Jun 2026 --> Dec 2026

Consequently, decreased HNF4A-AS1 levels caused DECR1 overexpression, leading to decreased intracellular PUFA content and promoting resistance to sorafenib-induced ferroptosis in HCC. Our results indicated the pivotal role of lipid metabolism-related and liver-specific HNF4A-AS1 in inhibiting sorafenib resistance by promoting ferroptosis and suggesting that HNF4A-AS1 might be a potential target for HCC.

In addition, the combination treatment led to the suppression of c-Myc, particularly in JHH-7 cells. Taken together, combining Sor with PGV-1 promotes better efficacy than Sor alone to inhibit HCC cell proliferation, and further evaluation of the efficacy and safety of adding PGV-1 to Sor in HCC therapy is worthwhile as a potential combination treatment option.

But the cause of hypoglycemia may not always be identified. In cases where the cause is not understood, other treatment options for hypoglycemia, such as increasing caloric intake, intravenous glucose administration, high-dose steroids, glucagon, and octreotide, should be considered.

The primary objective of this study is to evaluate the potential of deinoxanthin as a protective agent against the nephrotoxic side effects of sorafenib in HCC. Our study identified the potential synergistic effects of sorafenib and deinoxanthin on nephrotoxicity in rats with hepatocellular carcinoma.

Circ_0001944 is a putative target for reversing sorafenib resistance in HCC. Our findings are expected to provide new targets and new directions for sorafenib sensitization in the treatment of HCC.

A heightened receptivity was noted toward particular chemotherapy drugs, encompassing gemcitabine, vincristine, paclitaxel, gefitinib, and sorafenib, within this high-risk group. Conversely, a superior reaction to cisplatin was distinctly evident among those marked by low MSC scores... The five-gene MSC prognostic model demonstrates substantial efficacy in prognosticating clinical outcomes and gauging responsiveness to chemotherapy and immunotherapy regimens. The genes ZNF165, MXRA7, CEMIP, ARL4C, and CERCAM are underscored as promising candidates warranting further exploration for anti-MSC therapeutic strategies, thereby offering novel insights for personalized treatment approaches in BC.

Sorafenib is a targeted therapy for unresectable canine HCC...Differentially expressed genes (DEGs) between canine HCC and normal liver were explored based on previously reported molecular-targeted agents for human tumours. PARP3, DNMT1, FGF19, FGF23, and RET DEGs were upregulated, whereas KIT, FGFR2, and FGF21 DEGs were downregulated.

P1, N=32, Active, not recruiting, M.D. Anderson Cancer Center | Recruiting --> Active, not recruiting | N=54 --> 32

P3, N=648, Active, not recruiting, Chia Tai Tianqing Pharmaceutical Group Co., Ltd. | Not yet recruiting --> Active, not recruiting | Trial completion date: Dec 2024 --> Dec 2026 | Trial primary completion date: Jun 2024 --> Dec 2026

The antitumor activities of the derivatives against sorafenib were compared. Of the 20 synthesized compounds, compound 16 demonstrated potential as a potent anti-HCC drug candidate through downregulation of interleukin 6 which reduces inflammation and tumorigenesis with a strong binding interaction and bioavailability.

In conclusion, our findings suggest that miR-22-3p inhibits HCC progression by regulating the expression of STK26 and ATG4B, potentially through autophagy inhibition, thereby increasing sensitivity to sorafenib treatment. This offers a new therapeutic approach for effective HCC.

Pan-cancer analysis found HIF1A expression was decreased in several tumors, and chemosensitivity analysis revealed that HIF1A was associated with sensitivity of several anti-tumor drugs, such as Sorafenib, Navitoclax, and Venetoclax. Our findings provide evidence for identifying high-risk population and facilitating individualized treatment in TCL patients with SE.

In conclusion, HBV infection increases resistance to both sorafenib and lenvatinib in hepatoma cells by influencing the cell cycle regulatory genes and critical signaling pathways. However, the resistance mechanisms likely differ between the two medications.

Restoring miR-122 levels has shown promising therapeutic potential, increasing sensitivity to treatments like sorafenib...Given its context-dependent functions, miR-122 could serve as a potential therapeutic target, where restoring or inhibiting its expression may help in treating HCC and BC, respectively. The dual roles of miR-122 underscore its significance in cancer biology and its potential in precision medicine.

Sorafenib is increasingly significant after allo-HSCT maintenance, offering a promising option for high-risk AML cases. In this case, the patient achieved long-term remission with minimal side effects.

Hsa_circ_0088036 promoted HCC tumorigenesis and chemotherapy resistance by activating the PI3K/Akt and Notch pathways through regulating miR-140-3p/KIF2A signaling. Thus, hsa_circ_0088036 may be a potential therapeutic target in chemotherapy-resistant HCC.

We established an 11-gene prognostic model that effectively stratifies liver cancer patients based on differentially expressed genes between tumor and adjacent non-tumor cells clustered by scRNA-seq data. The two risk groups had significantly different molecular characteristics. We identified 14 drugs that might be effective for high-risk HCC patients. Our study provides novel insights into tumor cell characteristics, aiding in research on tumor development and treatment.

In HCC cells, knockdown of DHFR or treatment with pralatrexate enhanced the sensitivity of HCC cells to molecularly targeted agents, such as sorafenib, regorafenib, lenvatinib, cabozantinib, or anlotinib...Therefore, pralatrexate upregulates the sensitivity of HCC cells to molecularly targeted drugs. These results expand our understanding of folate metabolism and HCC and can help provide more options for HCC treatment.

Univariate and multivariate Cox regression analyses revealed that PDHA1 expression was an independent prognostic indicator for HCC patients, and the nomogram incorporating PDHA1 expression exhibited excellent predictive capacity. Furthermore, PDHA1 expression was positively linked to the sensitivity of 5-fluorouracil, gemcitabine, paclitaxel, and sorafenib, and the molecular docking analysis demonstrated their excellent binding affinity.

Additionally, a higher MBGS expression score was associated with lack of significant improvement in overall survival or progression-free survival in the atezolizumab-bevacizumab arm vs. the sorafenib arm in the IMbrave150 cohort. We have developed a molecular signature that could serve as a companion diagnostic and uses bulk or spatial transcriptomic data to identify a unique subclass of liver tumors. This subgroup of liver cancer patients derive limited benefit from the current standard of care and are expected to benefit from specialized directed therapies that are on the horizon.

Our findings verify the therapeutic effects of targeting LIF in SFN-resistance, uncover the potential mechanism for the increased sensitivity to SFN and sought to elucidate how this intervention might contribute to overcoming SFN resistance. KLTI is a promising immunomodulatory drug by regulating LIF and macrophage-NK cell interaction, which could be a potential combination partner for HCC treatment.

We report three patients with histiocytic disorders harboring novel alterations who had sustained responses to off-label kinase inhibitors specific to their histiocytic disorder. Pathogenic variants outside of the MAPK pathway, including variants of unknown significant, may be targeted with readily available small molecules.

P1, N=29, Completed, National Cancer Institute (NCI) | Active, not recruiting --> Completed | Trial completion date: May 2025 --> Mar 2024

Notably, nanoassemblies composed of linoleic acid-conjugated camptothecin and sorafenib demonstrated stability and sustained release of their payloads...This combinatory platform effectively overcame therapeutic resistance and demonstrated sustained tumor inhibition in hepatocellular carcinoma-bearing mouse models. This new self-assembling cytotoxic nanotherapeutic strategy has potential applications for the development of other injectable nanomedicines.

The docking study showed that compounds 22 and 29 had docking scores similar to those of Erlotinib and Sorafenib, co-crystallized ligands, for the EGFR and VEGFR-2 proteins. The experiments on lipophilicity showed that the new pyrimidines had a consistent result. This group of compounds has better biological activity in all the biological systems studied with low lipophilicity.

Sorafenib, Temozolomide, U-73122, and LOXO-101 effectively eliminate cancer cells. Inhibiting the pathways regulated by TrkB receptor combined with Temozolomide action, led to successful gliomas elimination. Those results might serve as basis for modern targeted treatment development.

We sought to investigate the utility of AFP response across first-line sorafenib (1L SOR) and later-line checkpoint inhibitor (CPI) therapies...Early AFP response with 1L SOR and any subsequent CPI was associated with longer OS and TOT, and early AFP progression was associated with shorter OS and TOT. These data support utilizing longitudinal AFP changes as a surrogate endpoint in HCC systemic therapy.

Among five genes, ALB, ESR1 and SRC tend to be core genes because of probable status as potential targets for sorafenib...Regulating the expression of TanIIA-related gene signatures (ALB, SRC and ESR1), and inhibiting the SRC/MAPK/ERK signaling axis might potentially contribute to the TanIIA treatment of HCC. And the three gene signatures could be identified for predicting the prognosis of HCC, which may provide novel biomarkers for HCC treatment.

Our study demonstrated that sorafenib-induced EVs, enriched with specific tumor-suppressor ncRNAs, can effectively inhibit the aggressive BC characteristics in vitro and in vivo. Our findings indicate an alternative way to enrich EVs with specific tumor-suppressor ncRNAs by treating the cells with an anticancer drug and support the development of new potential experimental molecular approaches to target the aggressive properties of cancer cells.