Integrative Cancer Therapies最新文献

Objective: The internet has become a preferred source for obtaining information about diagnostic and treatment methods related to health issues. This study aims to investigate whether aerobic exercise videos on the YouTube platform are an excellent source for lung cancer patients.

Methods: The keywords, "lung cancer and exercise," "lung cancer and physical activity," and "lung cancer and rehabilitation" were used to identify videos on YouTube on 27 to 28 May 2023. We recorded the characteristics of the videos, including the number of views, duration, days since upload, and the number of likes and dislikes. The Global Quality Scale and the modified DISCERN questionnaire were used to assess the quality and reliability of videos.

Results: 150 videos were evaluated. 12 of 150 videos met the eligibility criteria. Lung cancer and aerobic exercise in rehabilitation videos were most commonly uploaded by health organizations and patients. Videos had a median of 3300 views. We assessed videos for user-focused video quality using the DISCERN instrument and found that the average total score was 3 (range 2-5). Inter-observer agreement was 0.89 and 0.91 for DISCERN and GQS scored, respectively.

Significance of results: The results show that YouTube can be a preferred, easy, and inexpensive way to access aerobic exercise modalities, which are the basic rehabilitation steps for lung cancer patients. Experts recommend increasing the number of high-quality videos explaining the exercises. To fill this gap, healthcare professionals and organizations can take an active role in planning, producing, or ensuring reliable content. Collaborations with medical institutions and physiotherapists could further ensure that patients have access to accurate and effective exercise guidance, ultimately improving rehabilitation outcomes.

Purpose: Chemotherapy-induced peripheral neuropathy (CIPN) worsens the quality of life for people with cancer. Massage therapy involves neuromuscular modulations and can potentially reduce CIPN symptoms. We examined the immediate improvements in CIPN-related pain and neuropathy following massage therapy among patients with CIPN.

Methods: In a retrospective cohort, we assessed patients who received 1 massage therapy session for CIPN symptom relief during or after chemotherapy at a National Cancer Institute-Designated Comprehensive Cancer Center from October 2017 to September 2022. We measured the severity of pain and neuropathy before and after massage therapy with a 4-item verbal rating scale (VRS) or a 0 to 10 numerical rating scale (NRS). We converted NRS to VRS scores and examined the pre-post differences in symptom severity using the Wilcoxon rank test.

Results: Among 23 patients (median [range] age 64 [4-85] years, female 74%, White 70%), one session of massage therapy decreased the percentage of patients reporting moderate-to-severe pain from 81% at baseline to 0% (none) post-massage; percentage of patients reporting neuropathy also reduced from 77% at baseline to 12% following treatment. The pre-post differences were statistically significant for both pain (mean: -1.6, 95% confidence interval [CI] -1.9 to -1.2; P = .001) and neuropathy scores (mean: -1.2, 95%CI -1.4 to -0.9; P < .0001).

Conclusion: Among cancer patients with CIPN, one session of massage therapy was associated with immediate neuropathy and CIPN pain relief reported by patients following treatment. However, this preliminary finding requires further rigorous verifications in future randomized controlled clinical trials.

In this study, we investigated the synergistic effect of co-administration of osimertinib and HAD-B1 using gefitinib-resistant non-small cell lung cancer cells, HCC827-GR. HAD-B1 is composed of 4 natural drugs, Panax Notoginseng Radix, Panax ginseng C. A. Meyer, Cordyceps militaris, and Boswellia carterii Birdwood, and has been reported to have therapeutic effects on patients with advanced non-small cell lung cancer in several studies. Resistance to gefitinib in HCC827 cells was acquired through MET activity. Co-treatment with osimertinib and HAD-B1 reduced the cell viability of HCC827-GR cells. In addition, phosphorylation of MET and ERK were effectively suppressed for HCC827-GR cells. And, compared to when osimertinib and HAD-B1 were administered alone, cell proliferation was significantly inhibited and apoptosis was effectively induced when osimertinib and HAD-B1 were co-administered to HCC827-GR cells. We found that the synergistic effect of osimertinib and HAD-B1 combination therapy resulted in cancer cell death and cell cycle arrest by targeting the ERK and mTOR signaling pathways. In conclusion, this study confirmed that the combination of osimertinib, a third-generation anticancer drug, and HAD-B1, a natural anticancer drug, had a potentially synergistic effect on non-small cell lung cancer resistant to EGFR-targeted anticancer drugs.

Triple-negative breast cancer (TNBC) is the most aggressive type of breast cancer, with a high incidence of metastasis and chemoresistance. Epithelial-mesenchymal transition (EMT) is one of the molecular mechanisms that has been linked to the promotion of metastasis, and it can be promoted by several activators including the NF-κB signaling pathway. As a result, targeting EMT may be a potential strategy for treating TNBC. Pinostrobin is one of the important flavonoids found in the rhizome and rootlet of Boesenbergia rotunda (L.) Mansf. (fingerroot) that exhibits anticancer activities. However, the precise mechanism underlying the anticancer effect of pinostrobin on breast cancer remains unclear, and additional evidence is needed. In this study, the MCF-7 and MDA-MB-231 breast cancer cells were treated with various concentrations of pinostrobin. To determine the effect of pinostrobin on cell viability, an MTT assay was performed. Wound healing and Transwell chamber assays were conducted to examine the effect of pinostrobin on migration ability. RT-PCR was used to detect the expression of mRNA involved in NF-κB and EMT signaling pathways. The results revealed that low concentrations of pinostrobin did not affect cell viability, while higher concentrations produced an inhibitory effect on the viability of both cell lines. Pinostrobin also impeded migration and suppressed the expression of N-cadherin, a mesenchymal marker. Molecular docking analysis also suggested that the pinostrobin may target N-cadherin with higher binding affinity than IKK complex and NF-κB p65. These findings indicate that pinostrobin may serve as a potential treatment for TNBC.

Colon cancer is one of the most prevalent cancers worldwide and the second leading cause of cancer-related deaths. The goal of the present study was to investigate the role of Prodigiosin (PG) in promoting programed cell death in irradiated Caco-2 colon cancer cells. We examined the extent to which PG disrupts the BCL-2/caspase-3 and PPAR-γ signaling pathways and affects apoptosis in these cancer cells. The inflammatory markers COX2, PGE2, NO, TNFα, and the inflammosome NLRP-3, MAPK in addition to prooxidant/antioxidant balance is also under investigation. Caco-2 cells were irradiated with gamma rays (6 Gy) either with or without PG and the results revealed that, PG established IC50 equivalent to 357.27 μgl/ml in Caco-2 cells. The flowcytometric analysis (Annexin V), BCL-2 and caspase-3 showed that PG induces apoptosis for Caco-2 cells. Furthermore, the PG + gamma irradiated (R) group of Caco-2 cells showed significant down regulation in proliferation and inflammatory cascade induction followed by changes in redox tone (expressed by increase in SOD and GSH activities and decrease in MDA concentration), resulted in reduction of tumor growth. It could be concluded that PG has an anti-proliferative action on Caco-2 cells because of its capability to enhance apoptosis in addition to its capability to enhance response of Caco-2 cells to gamma radiation. Based on our findings in the present study we were able to demonstrate that the oxidative status as well as inflammatory responses are grave for determining the longevity, life span and reactivity of Caco-2 colon cancer cells upon exposure to PG unaccompanied or accompanied by gamma radiation. Prodigiosin might represent a valuable key in contesting development of drug resistance of cancer cells and it could raise the radio-sensitivity of cells when PG delivered in combination with radiation exposures.

Purpose: Hepatocellular carcinoma (HCC) poses a significant global health burden with limited therapeutic options. Traditional Chinese medicine (TCM), particularly Yangyin Fuzheng Jiedu Prescription (YFJP), has shown promise in improving patient outcomes, but its mechanisms are poorly understood. This study aimed to elucidate the key components and mechanisms of YFJP in treating HCC using an integrative approach combining network pharmacology, molecular docking, and experimental validation.

Patients and methods: We analyzed data from 1021 HCC patients (481 treated with YFJP and 540 with Western medicine alone) using propensity score matching to minimize bias. Network pharmacology identified key components and targets of YFJP, with a focus on Jiedu Prescription (JDP). Molecular docking and dynamics simulations validated the binding affinity between core components and targets. GO and KEGG analyses elucidated biological functions and pathways. In vivo experiments using a tumor-bearing mouse model further validated the mechanisms.

Results: YFJP significantly improved overall survival (P < .0001) and increased CD4⁺T and CD8⁺T cell counts (P < .05) in HCC patients compared to the control group. Network pharmacology analysis identified JDP as the core component of YFJP, with quercetin, luteolin, and apigenin as the key active compounds. GO and KEGG pathway analyses revealed that JDP modulates HCC through the regulation of cell death, immune response, and the JAK-STAT signaling pathway. In vivo experiments demonstrated that JDP increases the proportion of CD8⁺T cells in the tumor microenvironment and inhibits apoptosis by downregulating the IL-6/STAT3 pathway. Molecular docking and dynamics simulations further confirmed the strong binding affinity of JDP's key compounds to STAT3, supporting their role in modulating this pathway.

Conclusion: YFJP, particularly its core component JDP, enhances anti-tumor immunity and improves survival in HCC patients by modulating the IL-6/STAT3 pathway. These findings highlight YFJP as a promising adjuvant therapy for HCC, offering a multi-target approach to enhance anti-tumor immunity.