{"title":"Pancancer analysis of NDUFA4L2 with focused role in tumor progression and metastasis of colon adenocarcinoma.","authors":"Runlong Zhou, Zhe Sun, Ruijie Zhou, Mengyi Wang, Qing Zhuo, Xiaotong Deng, Zhenrong Wang, Yao Xu","doi":"10.1007/s12032-024-02531-1","DOIUrl":"10.1007/s12032-024-02531-1","url":null,"abstract":"<p><p>Colon adenocarcinoma (COAD) is a prevalent gastrointestinal malignant disease with a high mortality rate, and identification of novel prognostic biomarkers and therapeutic targets is urgently needed. Although NDUFA4L2 has high expressions in various tumors and affects tumor progression, its role in COAD remains unclear. The role of NDUFA4L2 in COAD was analyzed utilizing datasets available from public databases including The Cancer Genome Atlas, The Genotype-Tissue Expression (GTEx), Gene Expression Omnibus, Alabama Cancer Database (UALCAN), and The Human Protein Atlas databases. The prognostic value of NDUFA4L2 was determined using Kaplan-Meier analysis and Cox regression analysis. To investigate the possible mechanism underlying the role of NDUFA4L2 in COAD, Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and gene set enrichment analysis (GSEA) were employed. The correlation between NDUFA4L2 expression and immune cell infiltration levels was examined through single-sample gene set enrichment analysis (ssGSEA). The NDUFA4L2 expression levels in COAD patients and cell lines were validated through immunohistochemistry, immunofluorescence, qRT-PCR, and Western blot. Wound healing assay was also performed to evaluate the effect of NDUFA4L2 on COAD metastasis. Furthermore, the NDUFA4L2 mediated competing endogenous RNA (ceRNA) regulatory network was predicted and constructed through a variety of databases. The comprehensive pan-cancer analysis showed that NDUFA4L2 possesses diagnostic and prognostic value in many cancers, especially in COAD. GO-KEGG and GSEA analyses indicated that NDUFA4L2 was associated with multiple biological functions including epithelial-mesenchymal transition and adaptation to hypoxia. The ssGSEA analysis showed that NDUFA4L2 expression was associated with immune infiltration. In vitro experiments confirmed upregulation of NDUFA4L2 in COAD tissues and cell lines, and NDUFA4L2 overexpression significantly promoted migration of COAD cells. In addition, the C9orf139 /miR-194-3p axis was speculated as the possible upstream regulators of NDUFA4L2 in COAD. This study demonstrated that NDUFA4L2 upregulation was correlated with tumor progression, relapsed prognosis and aggressive migration of COAD, suggesting that NDUFA4L2 can act as an effective prognostic biomarker and a promising therapeutic target for COAD treatment.</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":"142469595","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}
Medical OncologyPub Date : 2024-10-14DOI: 10.1007/s12032-024-02457-8
Nicole L Stout, Marize Ibrahim, Jane Armer, Mary Vargo, Julia Rodrick, Jeanne Nourse, Brandy McKeown, Jessica C Griffin, Melissa B Aldrich
{"title":"Consensus statement on non-cancer-related risk factors for development of secondary lymphedema.","authors":"Nicole L Stout, Marize Ibrahim, Jane Armer, Mary Vargo, Julia Rodrick, Jeanne Nourse, Brandy McKeown, Jessica C Griffin, Melissa B Aldrich","doi":"10.1007/s12032-024-02457-8","DOIUrl":"10.1007/s12032-024-02457-8","url":null,"abstract":"<p><p>Non-cancer-related risk factors for secondary lymphedema were defined across four categories: co-morbidity, social determinants of health, behavioral factors, and environmental effectors. Based on rapid reviews of the literature and presentations at the ACS/LANA Lymphedema Summit, this working group categorized these risk factors according to the strength of evidence. Consensus agreement on level of evidence was achieved through one face-to-face working session and three follow-up virtual meetings. Findings elucidate strong evidence for co-morbidities, such as cardio/metabolic and vascular factors contributing to the risk for lymphedema. Evidence is low-to-moderate for social and behavioral factors and is lacking for environmental factors. Panel recommendations suggest a tailored approach to prospective surveillance when monitoring for secondary lymphedema that includes social determinants of health considering the growing awareness and evidence of these factors' influence on cancer and cancer-related morbidity.</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":"142469582","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":"PARP1 acetylation at K119 is essential in regulating the progression and proliferation of cervical cancer cells.","authors":"Li-Li Yang, Xue-Ke Zhang, Ying Cao, Li-Ya Shi, Shi-Ya Xie, Yan-Jie Yang, Shao-Jun Wu, Hong-Zhan Sun, Xue-Jun Tang, Dong-Lan Yuan, Dong Zhang, Xiao-Feng Xu, Qian Li, Xiao-Yan Ying","doi":"10.1007/s12032-024-02315-7","DOIUrl":"10.1007/s12032-024-02315-7","url":null,"abstract":"<p><p>Cervical cancer, CC, is one of the malignant cancers in women worldwide. Many studies about the genesis and progression of CC have been done at genomic, transcriptional, translational, and epigenetic levels. However, much less is done at post-translational modification (PTM) level. We first used pan-PTM antibodies to compare the pan PTM levels between clinical normal cervical tissues and CC tissues; we then sent the selected samples for label-free identification of acetylation sites. Next, we employed WT or K119A mutant PARP1-EGFP-STREPII plasmid transfection in Hela cells and examined various indexes including colony formation, wound healing, ROS generation, early apoptosis, and immunofluorescence and quantification of proliferation markers (Ki67, PCNA, and p-P53). Last, we examined the levels of multiple important kinases regulating cervical cancer progression. We found that pan-acetylation was the most downregulated in clinical CC samples, whereas the acetylation of PARP1, Poly(ADP-ribose) polymerase-1, was upregulated at K119. Next, we showed that PARP1-WT overexpression significantly suppressed the proliferation and progression in CC cell line Hela, while K119A overexpression didn't show any impact. Finally, PARP1-WT overexpression significantly decreased p-ERK1/2 while didn't affect the phosphorylation levels of other important kinases such as AKT, MTOR, and RPS6. This study discovered a new type of PTM of PARP1 in CC, and showed that PARP1 acetylation at K119 is essential in regulating the proliferation and progression of CC through ERK1/2. Further studies are required to investigate how PARP1 acetylation impact its function.</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":"142469596","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":"Targeting telomerase with MST-312 leads to downregulation of CCND1, MDM2, MYC, and HSP90AA1 and induce apoptosis in Jurkat cell line.","authors":"Atefeh Bahmei, Fatemeh Karimi, Seyed Moein Mahini, Hamed Irandoost, Parisa Tandel, Homa Niknam, Gholmhossein Tamaddon","doi":"10.1007/s12032-024-02412-7","DOIUrl":"10.1007/s12032-024-02412-7","url":null,"abstract":"<p><p>Acute lymphoblastic leukemia is a challenging disease to treat, especially in older adults who are most commonly diagnosed and have a high risk of relapse, even with current treatment options. MST-312, targets the RNA component of telomerase, inhibiting its activity and leading to growth arrest and telomere shortening in cancer cells. This study aimed to investigate the effects of MST-312 on apoptosis rates and the expression of telomerase target genes, CCND1, MDM2, MYC, and HSP90AA1, in Jurkat cell line. Jurkat cell line was cultured and treated with various concentrations of MST-312(0 µM, 0.5 µM, 1 µM, 2 µM, and 4 µM). The optimal concentration of MST-312 was determined using MTT assay. Flow cytometry was employed to evaluate the apoptosis induced by MST-312 treatment. The expression levels of the target genes were measured using real-time polymerase chain reaction before and after the treatment with MST-312. P-value < 0.05 was considered statistically significant. The percentages of apoptotic cells after 48 h, as determined by flow cytometry analysis, were 30.32%, 52.35%, 57.60%, and 68.82%, respectively, compared to the control group which was 4.6%. The expression levels of all genes, including CCND1, MDM2, MYC, and HSP90AA1, were decreased compared to the control group. The results showed that MST-312 induced dose- and time-dependent apoptosis and downregulated the expression of CCND1, MDM2, MYC, and HSP90AA1in Jurkat cell line.</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":"142469604","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}
Medical OncologyPub Date : 2024-10-14DOI: 10.1007/s12032-024-02474-7
Nicole L Stout, McKinzey Dierkes, Jill M Oliveri, Stanley Rockson, Electra D Paskett
{"title":"The influence of non-cancer-related risk factors on the development of cancer-related lymphedema: a rapid review.","authors":"Nicole L Stout, McKinzey Dierkes, Jill M Oliveri, Stanley Rockson, Electra D Paskett","doi":"10.1007/s12032-024-02474-7","DOIUrl":"10.1007/s12032-024-02474-7","url":null,"abstract":"<p><p>Extensive research supports an evidence-base for cancer treatment-related risk factors, including extent of lymph node dissection and use of radiotherapy, as contributing to secondary lymphedema. Additionally, comorbidities, such as higher body mass index, and vascular-related conditions are identified to further augment risk. While social determinants of health (SDOH) and socioeconomic factors are widely regarded as influencing an individual's healthcare outcomes, including cancer risk and survival, these factors have not been explored as risk factors for developing secondary lymphedema. A rapid literature review explored the current evidence for SDOH as risk factors for lymphedema. Studies that were published over the last 10 years and that specifically analyzed social factors as variables associated with lymphedema were included. Studies that only characterized the social determinants of the study population were not included. Forty-nine studies were identified through a rapid literature review, and 13 studies that expressly analyzed social determinants as risk factors for secondary lymphedema were reviewed and extracted. All studies were conducted in patients with breast cancer-related lymphedema. Social risk factors included race, educational level, insurance type, and income level. These are consistent with the socioeconomic inequalities related to cancer survival. SDOH may influence the risk of developing cancer treatment-related health conditions like secondary lymphedema. Research trials studying cancer treatment-related conditions should collect consistent and robust data across social, behavioral, environmental, and economic domains and should analyze these variables to understand their contribution to study endpoints. Risk prediction modeling could be a future pathway to better incorporate social determinants, along with medical and co-morbidity data, to holistically understand lymphedema risk.</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":"142469606","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}
Medical OncologyPub Date : 2024-10-14DOI: 10.1007/s12032-024-02520-4
Niher Tabassum Snigdha
{"title":"Letter to Editor \"Possible protective effect of rosuvastatin in chemotherapy‑induced cardiotoxicity in HER2-positive breast cancer patients: a randomized controlled trial\".","authors":"Niher Tabassum Snigdha","doi":"10.1007/s12032-024-02520-4","DOIUrl":"10.1007/s12032-024-02520-4","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":"142469591","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}
Medical OncologyPub Date : 2024-10-14DOI: 10.1007/s12032-024-02500-8
Steven Sorscher
{"title":"Personalized oncology, ethics and adherence to NCCN guidelines.","authors":"Steven Sorscher","doi":"10.1007/s12032-024-02500-8","DOIUrl":"10.1007/s12032-024-02500-8","url":null,"abstract":"<p><p>Successful personalized oncology today depends on clinicians taking advantage of the extensive, evidence-based information provided by the National Comprehensive Cancer Network (NCCN) Guidelines, which arguably represent the most important advance in cancer care occurring in the last many decades. Personalized oncology also demands that clinicians present guideline information to each patient in a thorough, comprehendible and unbiased manner. Finally, the patient's ability to process that information for shared decision-making about whether an intervention is consistent with their personal preferences, goals and values is perhaps the most important ingredient in truly personalized oncology care. Here, the ethics of sometimes transgressing from the NCCN guidelines with the aim of more personalized care is discussed.</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":"142469598","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":"Camptothecin and its derivatives: Advancements, mechanisms and clinical potential in cancer therapy.","authors":"Madhu Kamle, Shikha Pandhi, Sadhna Mishra, Sreejani Barua, Anju Kurian, Dipendra Kumar Mahato, Prasad Rasane, Dietrich Büsselberg, Pradeep Kumar, Daniela Calina, Javad Sharifi-Rad","doi":"10.1007/s12032-024-02527-x","DOIUrl":"10.1007/s12032-024-02527-x","url":null,"abstract":"<p><p>Camptothecin (CPT), an alkaloid isolated from the Camptotheca tree, has demonstrated significant anticancer properties in a range of malignancies. However, its therapeutic efficacy is limited by its hydrophobicity, poor bioavailability, and systemic toxicity. Derivatives, analogues, and nanoformulations of CPT have been synthesized to overcome these limitations. The aim of this review is to comprehensively analyze existing studies to evaluate the therapeutic efficacy, mechanistic aspects, and clinical potential of CPT and its modified forms, including derivatives, analogues, and nanoformulations, in cancer treatment. A comprehensive literature review was performed using PubMed/Medline, Scopus, and Web of Science databases; articles were selected based on specific inclusion criteria, and data were extracted on the pharmacological profile, clinical studies, and therapeutic efficacy of CPT and its different forms. Current evidence suggests that derivatives and analogues of CPT have improved water solubility, bioavailability, and reduced systemic toxicity compared to CPT. Nanoformulations further enhance targeted delivery and reduce off-target effects. Clinical trials indicate promising outcomes with enhanced survival rates and lower side effects. CPT and its modified forms hold significant promise as potent anticancer agents. Ongoing research and clinical trials are essential for establishing their long-term efficacy and safety; the evidence overwhelmingly supports further development and clinical testing of these compounds.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142391679","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}
Medical OncologyPub Date : 2024-10-08DOI: 10.1007/s12032-024-02509-z
Robert A Smith
{"title":"Progress in lymphedema.","authors":"Robert A Smith","doi":"10.1007/s12032-024-02509-z","DOIUrl":"10.1007/s12032-024-02509-z","url":null,"abstract":"<p><p>A century ago, the first description of secondary lymphedema resulting from mastectomy was published in the medical literature. For most of the remaining twentieth century, evidence about cancer treatment related lymphedema grew slowly, and mostly through clinicians who wished to understand its causes, natural-history, and post-treatment risks, as well as from clinicians involved with its treatment. In the late 1990s, there was growing recognition that there were large gaps in our understanding of predisposing and post-treatment risks of onset, the near and long-term prevalence of lymphedema, and how to educate patients. Moreover, there was no consensus on best practices for treating lymphedema, and how to ensure the quality of treatment. In 1998, with support from the Longaberger Company®, the American Cancer Society began a long-standing commitment to address enduring challenges associated with lymphedema. This commitment began with a landmark international workshop on lymphedema that was held in New York City in February 1998, millions of dollars in research funding, support to establish the Lymphology Association of North America (LANA), a second workshop convened in February 2011 on the prospective surveillance model for rehabilitation for women with breast cancer, and most recently, the 2023 Lymphedema Summit: Forward momentum; Future Steps in Lymphedema Management, co-sponsored with the LANA, Washington University School of Medicine in St. Louis, and the Stryker Corporation. This editorial introduces the papers and expert consensus statements from that Summit.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142391680","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":"Regulation of autophagy by non-coding RNAs in human glioblastoma.","authors":"Mehran Molavand, Niloufar Ebrahimnezhade, Arash Kiani, Bahman Yousefi, Ahmad Nazari, Maryam Majidinia","doi":"10.1007/s12032-024-02513-3","DOIUrl":"10.1007/s12032-024-02513-3","url":null,"abstract":"<p><p>Glioblastoma, a lethal form of brain cancer, poses substantial challenges in treatment due to its aggressive nature and resistance to standard therapies like radiation and chemotherapy. Autophagy has a crucial role in glioblastoma progression by supporting cellular homeostasis and promoting survival under stressful conditions. Non-coding RNAs (ncRNAs) play diverse biological roles including, gene regulation, chromatin remodeling, and the maintenance of cellular homeostasis. Emerging evidence reveals the intricate regulatory mechanisms of autophagy orchestrated by non-coding RNAs (ncRNAs) in glioblastoma. The diverse roles of these ncRNAs in regulating crucial autophagy-related pathways, including AMPK/mTOR signaling, the PI3K/AKT pathway, Beclin1, and other autophagy-triggering system regulation, sheds light on ncRNAs biological mechanisms in the proliferation, invasion, and therapy response of glioblastoma cells. Furthermore, the clinical implications of targeting ncRNA-regulated autophagy as a promising therapeutic strategy for glioblastoma treatment are in the spotlight of ongoing studies. In this review, we delve into our current understanding of how ncRNAs regulate autophagy in glioblastoma, with a specific focus on microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), and their intricate interplay with therapy response.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142391681","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}