Effective drug delivery is essential for cancer treatment. Drug delivery systems, which can be tailored to targeted transport and integrated tumor therapy, are vital in improving the efficiency of cancer treatment. Peptides play a significant role in various biological and physiological functions and offer high design flexibility, excellent biocompatibility, adjustable morphology, and biodegradability, making them promising candidates for drug delivery. This paper reviews peptide-mediated drug delivery systems, focusing on self-assembled peptides and peptide–drug conjugates. It discusses the mechanisms and structural control of self-assembled peptides, the varieties and roles of peptide–drug conjugates, and strategies to augment peptide stability. The review concludes by addressing challenges and future directions.

The secretory carrier-associated membrane proteins (SCAMPs) are associated with the development of multiple human cancers. The role of SCAMPs in acute myeloid leukemia (AML), however, remains to be identified. In the present study, we explored expression patterns and prognostic value of SCAMPs and network analysis of SCAMPs-related signaling pathways in AML using Oncomine, GEPIA, cBioPortal, LinkedOmics, DAVID and Metascape databases. Genetic alteration analysis revealed that the mutation rate of SCAMP genes was below 1% (9/1272) in AML, and there was no significant correlation between SCAMPs gene mutation and AML prognosis. However, the SCAMP2/5 mRNA levels were significantly higher in AML patients than in healthy controls. Moreover, high mRNA expressions of SCAMP2/4/5 were associated with poor overall survival, which might be due to that SCAMP2/4/5 and their co-expressed genes were associated with multiple pathways related to tumorigenesis and progression, including human T-cell leukemia virus 1 infection, acute myeloid leukemia, mTOR and NF-kappa B signaling pathways. These results suggest that SCAMP2/4/5 are potential prognostic markers for AML, and that SCAMP2 and SCAMP5 individually or in combination may be used as diagnostic markers for AML.

Background: The treatment of myeloid sarcoma (MS) is challenging and has not markedly improved patient prognosis. The introduction of venetoclax (VEN) has changed the treatment of MS, and venetoclax-based therapy has been described as very promising in several case reports. Methods: In this retrospective study, we analyzed the treatment outcomes of 14 patients with MS treated with venetoclax-based therapy at The First Affiliated Hospital of Xiamen University from January 2020 to October 2023 Results: The cohort consisted of 7 (50%) women and 7 (50%) men with an average age of 37.5 years. Four patients (28.6%) had isolated MS de novo, 2 (14.2%) were diagnosed synchronously with AML, and 8 (57.2%) had isolated extramedullary relapse. The most common sites for MS in our cohort were the skin and lung, followed by the spinal canal, soft tissue, bone and kidney. Five patients were affected at more than three sites. Nine patients received VEN in combination with azacytidine, and 5 patients received VEN in combination with other agents. The median number of venetoclax therapies administered was 2 cycles (range: 1–10 cycles). A response was observed in all patients included in the study, with 8 patients (57.2%) achieving a CR and 3 patients (21.4%) achieving a PR, corresponding to an ORR (including CR and PR) of 78.6%. The median follow-up time for all patients was 13 months (range 1–44 months), and the 1 year OS for all patients was 67.7%. Conclusions: Venetoclax-based therapy shows excellent efficacy and safety in MS patients in the “real world” at a single institution, and a corresponding prospective study is needed to verify this conclusion.

High-grade B-cell lymphoma with concurrent MYC and BCL2/BCL6 rearrangements (HGBL-DHL) is a challenging disease resistant to front-line immunochemotherapies, which urgently requires novel therapeutic approaches. Herein, combination of chidamide and anlotinib demonstrated potential synergistic anti-lymphoma effects against HGBL-DHL. The cooperative effect of cell proliferation inhibition, apoptosis induction, and cell cycle arrest were demonstrated in cell lines through Cell Counting Kit-8, Annexin V/PI staining, and PI staining respectively. Moreover, in an HGBL-DHL-xenografted mouse model, the combination therapy markedly reduced tumor burden without inducing fatal toxicity. Mechanistically, chidamide suppressed HDAC3, while anlotinib inhibited VEGFR2, both leading to down-regulation of the PI3K/AKT signaling cascade. This dual suppression occurred as a result of their synergistic interaction. Downstream targets of the PI3K/AKT signaling pathway including proliferation-associated protein c-Myc, anti-apoptotic proteins BCL2 and MCL1, and cell cycle-associated protein cyclin A2 were all synergistically down-regulated, which coincided with the phenotypic outcomes. Collectively, our preclinical findings underscored the synergistic activity of chidamide and anlotinib combination against HGBL-DHL, warranting further clinical evaluation of this regimen for treating this challenging entity.

Transformed follicular lymphoma (t-FL) is a heterogeneous, aggressive B-cell malignancy with unfavorable clinical outcomes, while there is no standard and effective treatment available for t-FL. In this study, we investigated the preclinical anti-lymphoma efficacies and potential mechanism of action for a novel therapeutic strategy, combining the DGKα inhibitor ritanserin with chiauranib, a new orally bioavailable multi-target kinase inhibitor, in t-FL models. This combination therapy exhibited synergistic cytotoxicity against t-FL cells and primary B lymphoma cells, evidenced by cooperatively inducing loss of cell viability and promoting cell apoptosis. Moreover, the combination of ritanserin with chiauranib resulted in significant suppression of tumor burden in xenograft models. The synergistic lethality of ritanserin and chiauranib in t-FL was associated with the synergistic effect of these two medications on the inhibition of their respective targets. Of importance, the combined treatment was dual blockade of PI3K/AKT/mTOR and RAF/MEK/ERK pathways as well as vertical targeting of DGKα. Besides, downregulating the levels of c-Myc, BCL-xL and MCL-1 also contributed to the synergistic effects of the combined regimen on t-FL. Taken together, these findings suggest that the synergy between the DGKα inhibitor ritanserin and multi-targeted inhibitor chiauranib might represent a promising option for the treatment of t-FL.