Medical Oncology最新文献

{"title":"The effect of compression therapies and therapeutic modalities on lymphedema secondary to cancer: a rapid review and evidence map.","authors":"M L McNeely, S M Shallwani, M M Al Onazi, F Lurie","doi":"10.1007/s12032-024-02447-w","DOIUrl":"10.1007/s12032-024-02447-w","url":null,"abstract":"<p><p>The identification of effective therapeutic modalities to manage lymphedema secondary to cancer is a high priority among patients and clinicians. Complex decongestive therapy (CDT) remains a fundamental intervention for individuals with lymphedema; however, interventions involving modalities such as low level laser therapy, specially designed compression systems, and compression pumps may be helpful to improve outcomes and reduce costs of care. We conducted a rapid review of the literature examining compression therapies and therapeutic modalities in the treatment of lymphedema secondary to cancer. A search of the electronic databases from June 2018 to October 2023 was performed including MEDLINE, EMBASE, and CINAHL. The electronic search yielded 438 potentially relevant citations with 40 randomized controlled trials included in the review, and 30 in the mapping process. Ninety-three percent (n = 37) of the trials included participants with a diagnosis of breast cancer. Across all categories and domains, all but two trials were rated as having 'some concerns' or a 'high risk of bias'. Intervention effects ranged from clinically insignificant to large effects on lymphedema volume. Evidence mapping suggests potential for benefit from (1) compression garments for the prevention of lymphedema, (2) interventions added to CDT in the intensive reduction phase, and (3) nighttime compression and compression pump treatments in the maintenance phase. A multi-centre collaborative research approach is needed to support the conduct of high-quality large-scale trials to inform the optimal type, timing, and combination of compression therapies and therapeutic modalities in the treatment of lymphedema secondary to cancer.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11486789/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142469605","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Personalized oncology in pheochromocytomas and paragangliomas: integrating genetic analysis with machine learning.","authors":"Abida, Abdullah R Alzahrani, Hayaa M Alhuthali, Afnan Alkathiri, Ruba Omar M Almaghrabi, Jawaher Mohammad Alshehri, Syed Mohammed Basheeruddin Asdaq, Mohd Imran","doi":"10.1007/s12032-024-02532-0","DOIUrl":"10.1007/s12032-024-02532-0","url":null,"abstract":"<p><p>Pheochromocytomas and paragangliomas (PCCs/PGLs) are uncommon neuroendocrine tumors with a significant genetic tendency. Approximately 35-40% of these tumors are associated with genetic factors. The present study performed a thorough analysis using publicly accessible genetic and clinical data from the Cancer Genome Atlas (TCGA) to examine the involvement of six genes, namely GBP1, KIF13B, GPT, CSDE1, CEP164, and CLCA1, in the development of PCCs/PGLs. By employing multi-omics data, this study investigates the relationship between mutational patterns and the prognosis of tumors, focusing on the possibility of tailoring treatment methods to individual patients. The study utilizes Mutect2 to detect somatic mutations with high confidence in whole-exome sequencing data from PCCG samples. The study uncovers mild effects on protein function caused by particular mutations, including GBP1 (p.Cys12Tyr), KIF13B (p.Arg847Gly), and GPT (p.Gln50Arg). A random forest classifier uses mutational profiles to predict potential drug recommendations, proposing a focused therapy strategy. This study thoroughly analyzes the genetic mutations found in PCCs/PGLs, highlighting the significance of precision medicine in developing specific treatments for these uncommon types of cancer. This study aims to improve the understanding of the development of tumors and identify personalized treatment approaches by combining genetic data with machine learning analyses.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142469597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulation of the tumor microenvironment in non-muscle-invasive bladder cancer by OncoTherad® (MRB-CFI-1) nanoimmunotherapy: effects on tumor-associated macrophages, tumor-infiltrating lymphocytes, and monoamine oxidases.","authors":"Gabriela Cardoso de Arruda Camargo, Gabriela Oliveira, Bruna Nayara Silva Santos, Isadora Manzato Roberto, Monaliza Ávila, Bianca Ribeiro de Souza, João Carlos Cardoso Alonso, Nelson Durán, Wagner José Fávaro","doi":"10.1007/s12032-024-02533-z","DOIUrl":"10.1007/s12032-024-02533-z","url":null,"abstract":"<p><p>Non-muscle-invasive bladder cancer (NMIBC) presents management challenges due to its high recurrence rate and a complex tumor microenvironment (TME). This study investigated the effects of OncoTherad® (MRB-CFI1) nanoimmunotherapy on the TME of BCG-unresponsive NMIBC, focusing on alterations in monoamine oxidases (MAO-A and MAO-B) and immune markers: CD163, FOXP3, CD8, and CX3CR1. A comparative analysis of immunoreactivities was made before and after OncoTherad® treatment and an immune score (IS) was established to evaluate the correlation between immunological changes and clinical outcomes. Forty bladder biopsies of twenty patients were divided into 2 groups (n = 20/group): 1 (pre-treatment biopsies); and 2 (post-treatment biopsies). Our results showed stable MAO-A levels but a significant (p < 0.05) decrease in MAO-B immunoreactivity after treatment, suggesting OncoTherad®'s efficacy in targeting the tumor-promoting and immunosuppressive functions of MAO-B. Significant (p < 0.05) reductions in CD163 and FOXP3 immunoreactivities were seen in post-treatment biopsies, indicating a decreased presence of M2 macrophages and Tregs. Corroborating with these results, we observed reductions in tumor histological grading, focality and size, factors that collectively enhanced recurrence-free survival (RFS) and pathological complete response (PCR). Moreover, elevated IFN-γ immunoreactivities in treated biopsies correlated with increased counts of CD8⁺ T cells and higher CX3CR1 expression, underscoring OncoTherad®'s enhancement of cytotoxic T cell functionality and overall antitumor immunity. The IS revealed improvements in immune responses post-treatment, with higher scores associated with better RFS and PCR outcomes. These findings validate OncoTherad®'s capability to modify the bladder cancer microenvironment favorably, promoting effective immune surveillance and response.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142469594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DNA fragmentation factor 40-based therapeutic approaches for cancer: a review article.","authors":"Faezeh Masaeli, Saba Omoomi, Fatemeh Shafiee","doi":"10.1007/s12032-024-02511-5","DOIUrl":"10.1007/s12032-024-02511-5","url":null,"abstract":"<p><p>DNA Fragmentation Factor (DFF) is a heterodimer protein involved in DNA fragmentation during apoptosis, which acts as a trigger downstream of caspase-3 activation. DFF40 catalytically active homo-oligomers break down chromosomal DNA. Previous scientific investigations have revealed a link between DFF40 expression changes and various cancers. DFF40 deletion or down-regulation has been observed in some cancers. Consequently, therapeutic strategies involving the DFF40 molecule compensating led to an increased rate of cancer cell apoptosis. In this review article, we aimed to introduce cancers with low expression of this protein first. The second part of this paper focuses on studies that utilized exogenous DFF40 protein produced by recombinant DNA technology and surveyed during in vitro and in vivo tests. Finally, compensation for diminished expression of the mentioned protein via gene therapy-based techniques to make up for this apoptotic molecule's low expression is the topic of the last part of this review article.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142469584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"M1 macrophages deliver CASC19 via exosomes to inhibit the proliferation and migration of colon cancer cells.","authors":"Shuo Teng, Jiang Ge, Yi Yang, Zilu Cui, Li Min, Wenkun Li, Guodong Yang, Kuiliang Liu, Jing Wu","doi":"10.1007/s12032-024-02444-z","DOIUrl":"10.1007/s12032-024-02444-z","url":null,"abstract":"<p><p>Colorectal cancer (CRC) continues to be one of the leading causes of cancer-related death worldwide. Exosomes have been established to play an important role in intercellular communication and that long non-coding RNA (lncRNA) CASC19 is enriched within M1 macrophage-derived exosomes (M1-exo). However, the biological functions and underlying molecular mechanisms of exosomal CASC19 from macrophages on CRC remain unknown. Cell proliferation and migration were evaluated by MTS and transwell assays. The exosomes were characterized by western blot, nanoparticle tracking analysis (NTA) and electron microscope imaging. The expression levels of CASC19 and its putative target miR-410-3p were quantified by reverse-transcription polymerase chain reaction (RT-qPCR). The interaction between CASC19 and miR-410-3p was detected by the pull-down assay. We found that the non-contact inhibition of M1 macrophages on the proliferation of colon cancer cells is largely dependent on the CASC19 released from M1 exosomes. M1 exosomes successfully delivered CASC19 to colon cancer cells, exerting an inhibitory effect on cell proliferation and migration. The exosomes secreted by M1 cells with CASC19 knockdown showed less inhibition effect on cell proliferation and migration. Mechanically, CASC19 exerted an inhibitory effect on colon cancer cells by sponging miR-410-3p via tube morphogenesis and TGF-β signaling pathway. We first proved that CASC19 in M1 macrophages is delivered into colon cancer cells via exosomes, exerting an inhibitory effect on their proliferation and migration by sponging miR-410-3p. The study may provide mechanistic insights into the roles of lncRNAs in CRC progression and a potential therapeutic target for the treatment of CRC.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142469593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Revolutionizing cancer treatment: an in-depth exploration of CAR-T cell therapies.","authors":"Gurpreet Kandav, Akash Chandel","doi":"10.1007/s12032-024-02491-6","DOIUrl":"10.1007/s12032-024-02491-6","url":null,"abstract":"<p><p>Cancer is a leading cause of fatality worldwide. Due to the heterogeneity of cancer cells the effectiveness of various conventional cancer treatment techniques is constrained. Thus, researchers are diligently investigating therapeutic approaches like immunotherapy for effective tumor managements. Immunotherapy harnesses the inherent potential of patient's immune system to achieve desired outcomes. Within the realm of immunotherapy, CAR-T (Chimeric Antigen Receptor T) cells, emerges as a revolutionary innovation for cancer therapy. The process of CAR-T cell therapy entails extracting the patient's T cells, altering them with customized receptors designed to specifically recognize and eradicate the tumor cells, and then reinfusing the altered cells into the patient's body. Although there has been significant progress with CAR-T cell therapy in certain cases of specific B-cell leukemia and lymphoma, its effectiveness is hindered in hematological and solid tumors due to the challenges such as severe toxicities, restricted tumor infiltration, cytokine release syndrome and antigen escape. Overcoming these obstacles requires innovative approaches to design more effective CAR-T cells, which require a competent and diverse team to develop and implement. This comprehensive review addresses numerous therapeutic issues and provides a strategic solution while providing a deep understanding of the structural intricacies and production processes of CAR-T cells. In addition, this review explores the practical aspects of CAR-T cell therapy in clinical settings.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142469602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glycolytic pathway analysis and gene expression profiles of combination of aloe vera and paclitaxel on non-small cell lung cancer and breast cancer.","authors":"Tuğba Kul Köprülü, Jülide Balkan, Bahar Gezer, Burçin Erkal Çam","doi":"10.1007/s12032-024-02506-2","DOIUrl":"10.1007/s12032-024-02506-2","url":null,"abstract":"<p><p>The purpose of this study is to enhance the effectiveness of known anticancer medications using natural compounds. The study investigated the impact of combining AVE with PAX on non-small cell lung cancer (A549) and breast cancer (MCF7). In this study, A549 and MCF7 cells were treated with PAX (5 μM), AVE (24 μg/mL), and a combination of PAX and AVE (5 μM + 24 μg/mL). The glucose consumption rates of the cells were determined by extracellular acidification rate (ECAR) thanks to the SeaHorse XFe24 instrument. In addition, gene expression profiles were determined by performing Total RNA sequencing with the Novaseq 6000 instrument. Finally, the expressions of GAPDH, BAX, and BCL-2 genes involved in the apoptotic pathway were detected by RT-qPCR. The combined application of PAX and AVE reduced the ECAR value in both cell lines. According to the RT-qPCR results, the expression level of the apoptotic gene BAX increased in both cell lines (p < 0.05). Total RNA sequencing revealed that the combination effects of PAX and AVE play a role in the ribosome mechanism, thereby affecting the protein translation system in MCF7 while apoptosis and cell cycle have come to the forefront in A549.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142469588","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polydatin inhibits histone deacetylase 1 and shows an anti-angiogenic action in head and neck squamous cell carcinoma.","authors":"Aadil Manzoor Baba, Altaf Ahmad Shah, Imren Bayil, Satyabrata Nayak, Ritis Kumar Shyanti, Najma Nissa, Mansha Muzaffar, Mohammad Amin Hajam, Rezwan Akhtar, Bashir Ahmad Malla, Salman Akhtar, Rana P Singh, Nazir Ahmad Dar","doi":"10.1007/s12032-024-02490-7","DOIUrl":"10.1007/s12032-024-02490-7","url":null,"abstract":"<p><p>Polydatin, a natural derivative of resveratrol, has shown many anticancer properties. However, the underlying mechanisms of its anticancer properties including its effect on the epigenetic landscape are not well understood. Here, we explored the effect of polydatin on histone deacetylase 1 (HDAC1) activity. We used in silico approaches to assess the possible binding of polydatin to the active site pockets of HDAC1 and in vitro approaches to test the potential effects of the interaction on its enzymatic activity. As compared to SAHA, an approved drug, the polydatin showed stronger and stable binding to the HDAC1. The binding energy, conformational changes, formation of extra hydrogen bonding, and other interactions within and outside the active site all favour largely stable and strong polydatin binding to the enzyme. Further, the ADME and toxicity prediction values are encouraging for the evaluation of polydatin as a drug. The laboratory leg of the study substantiated that the polydatin binding was strong and stable enough to inhibit HDAC1 activity in UMS-CC-22B cells as demonstrated by an increase in H3K9 acetylation. In addition, polydatin treated cells showed attenuated proliferation. The in vitro tube formation and migration by HUVEC and UM-SCC-22B cells were inhibited by polydatin. The decreased tube formation due to HDAC1 inhibition is possibly due to up-regulation of the anti-angiogenic gene - TSP1 in UM-SCC-22B cells. As compared to SAHA, more promising results were shown both in its computational calculations and on the cell physiology features. Stronger and stable binding, more anti-proliferative and anti-angiogenic potential were observed with respect to polydatin. Further, the cell death was more pronounced with SAHA treatment. Therefore, polydatin might be a better anticancer drug and can have a potential to replace SAHA in combinational therapeutic regimen.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142469600","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Treating endometrial hyperplasia (EH) post-tamoxifen treatment in breast cancer survivors: what are our options?","authors":"Sagar Raut, Nanki Bakshi, Bharti Sharma","doi":"10.1007/s12032-024-02522-2","DOIUrl":"10.1007/s12032-024-02522-2","url":null,"abstract":"<p><p>Tamoxifen is known to raise the risk of endometrial hyperplasia and cancer. There is virtually limited literature on how to handle Tamoxifen-induced endometrial hyperplasia (EH) in a breast cancer survivor. Levonorgestrel-releasing intrauterine system (LNG-IUS) has been explored as preventive strategies, but its impact on breast cancer recurrence especially in Progesterone receptor (PR)-positive patient is not clear. Aromatase Inhibitors (AIs) have shown beneficial results in EH after tamoxifen and their role should be explored in further trials.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142469609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical research on triple-negative breast cancer that targets the PIK3CA pathway.","authors":"Kadri Altundag","doi":"10.1007/s12032-024-02493-4","DOIUrl":"10.1007/s12032-024-02493-4","url":null,"abstract":"","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142469579","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}