RESUMO
Small extracellular (EV) particles known as exosomes are released by a variety of cell types, including immune system cells, stem cells, and tumor cells. They are regarded as a subgroup of EVs and have a diameter that ranges from 30 to 150 nm. Proteins, lipids, nucleic acids (including RNA and DNA), and different bioactive compounds are among the wide range of biomolecules that make up the cargo of exosomes. Exosomes are crucial for intercellular communication because they let cells share information and signaling chemicals. They are involved in various physiological and pathological processes, including immune responses, tissue regeneration, cancer progression, and neurodegenerative diseases. In conclusion, it is essential to continue research into exosome-based cancer medicines to advance understanding, improve treatment plans, create personalized tactics, ensure safety, and speed up clinical translation.
Assuntos
Neoplasias Colorretais , Exossomos , Vesículas Extracelulares , MicroRNAs , Humanos , MicroRNAs/genética , MicroRNAs/uso terapêutico , MicroRNAs/metabolismo , Exossomos/genética , Exossomos/metabolismo , Transdução de Sinais , Comunicação Celular , Neoplasias Colorretais/diagnóstico , Neoplasias Colorretais/genética , Neoplasias Colorretais/terapia , Vesículas Extracelulares/metabolismoRESUMO
Pulmonary injury is one of the key restricting factors for the therapy of malignancies with chemotherapy or following radiotherapy for chest cancers. The lung is a sensitive organ to some severely toxic antitumor drugs, consisting of bleomycin and alkylating agents. Furthermore, treatment with radiotherapy may drive acute and late adverse impacts on the lung. The major consequences of radiotherapy and chemotherapy in the lung are pneumonitis and fibrosis. Pneumonitis may arise some months to a few years behind cancer therapy. However, fibrosis is a long-term effect that appears years after chemo/or radiotherapy. Several mechanisms such as oxidative stress and severe immune reactions are implicated in the progression of pulmonary fibrosis. Epithelial-mesenchymal transition (EMT) is offered as a pivotal mechanism for lung fibrosis behind chemotherapy and radiotherapy. It seems that pulmonary fibrosis is the main consequence of EMT after chemo/radiotherapy. Several biological processes, consisting of the liberation of pro-inflammatory and pro-fibrosis molecules, oxidative stress, upregulation of nuclear factor of κB and Akt, epigenetic changes, and some others, may participate in EMT and pulmonary fibrosis behind cancer therapy. In this review, we aim to discuss how chemotherapy or radiotherapy may promote EMT and lung fibrosis. Furthermore, we review potential targets and effective agents to suppress EMT and lung fibrosis after cancer therapy.
Assuntos
Quimiorradioterapia , Transição Epitelial-Mesenquimal , Fibrose Pulmonar , Humanos , Transição Epitelial-Mesenquimal/efeitos dos fármacos , Fibrose Pulmonar/induzido quimicamente , Fibrose Pulmonar/metabolismo , Fibrose Pulmonar/patologia , Fibrose Pulmonar/etiologia , Quimiorradioterapia/efeitos adversos , Animais , Estresse Oxidativo/efeitos dos fármacos , Lesão Pulmonar/etiologia , Lesão Pulmonar/patologia , Lesão Pulmonar/induzido quimicamente , Lesão Pulmonar/metabolismoRESUMO
The majority of cancer cases are colorectal cancer, which is also the second largest cause of cancer-related deaths worldwide. Metastasis is the leading cause of death for patients with colorectal cancer. Metastatic colorectal cancer incidence are on the rise due to a tiny percentage of tumors developing resistant to medicines despite advances in treatment tactics. Cutting-edge targeted medications are now the go-to option for customized and all-encompassing CRC care. Specifically, multitarget kinase inhibitors, antivascular endothelial growth factors, and epidermal growth factor receptors are widely used in clinical practice for CRC-targeted treatments. Rare targets in metastatic colorectal cancer are becoming more well-known due to developments in precision diagnostics and the extensive use of second-generation sequencing technology. These targets include the KRAS mutation, the BRAF V600E mutation, the HER2 overexpression/amplification, and the MSI-H/dMMR. Incorporating certain medications into clinical trials has significantly increased patient survival rates, opening new avenues and bringing fresh viewpoints for treating metastatic colorectal cancer. These focused therapies change how cancer is treated, giving patients new hope and better results. These markers can significantly transform and individualize therapy regimens. They could open the door to precisely customized and more effective medicines, improving patient outcomes and quality of life. The fast-growing body of knowledge regarding the molecular biology of colorectal cancer and the latest developments in gene sequencing and molecular diagnostics are directly responsible for this advancement.
Assuntos
Neoplasias do Colo , Neoplasias Colorretais , Humanos , Medicina Molecular , Qualidade de Vida , Neoplasias Colorretais/tratamento farmacológico , Neoplasias Colorretais/genética , Resistência a MedicamentosRESUMO
PURPOSE: The use of perineural dexamethasone as an adjuvant drug to peripheral nerve block for postoperative pain is controversial. This systematic review aimed to determine the effectiveness of adding dexamethasone to lidocaine in upper limb nerve blocks. DESIGN: Systematic review. METHODS: This review used a comprehensive search strategy to retrieve relevant published randomized trial articles that fulfilled the inclusion and exclusion criteria, without time limits, (until December 2023) that assessed the effects of a combination of dexamethasone to lidocaine in upper limb nerve blocks. The databases used for the electronic literature search included PubMed, Embase, and Clinical Trials.gov, dbGaP, Cochrane library, and Google Scholar. There was no language, gender, or age limitation. This systematic review is reported in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analysis statement. FINDINGS: Of 3,926 articles identified by the initial search, 8 studies that met our inclusion criteria. All articles were original research studies. All eight articles were clinical trials. The sample size in the selected studies ranged from 30 to 90 people. Studies demonstrated that combining dexamethasone with lidocaine significantly improved the quality of peripheral nerve blocks, increased the analgesia period, and decreased analgesic consumption. CONCLUSIONS: This review supported that the combination of dexamethasone (dose of 4 to 10 mg) and lidocaine (concentration of 1.5% to 2%) for upper limb block was more effective and beneficial without any side effects. However, further clinical trials in this regard with more data, various regions, and larger sample sizes to support our hypothesis are recommended.
RESUMO
Oropharyngeal cancer, a subset of head and neck cancer, is increasingly recognized as a unique clinical entity primarily influenced by high-risk human papillomavirus (HPV) infections, particularly HPV-16. This review delves into the viral life cycle of HPV-16 and its interactions with host cells, with a specific focus on the crucial roles played by the viral oncoproteins E6 and E7. These oncoproteins drive cellular proliferation by targeting critical tumor suppressor proteins like p53 and Rb, resulting in uncontrolled cell growth and genomic instability. Furthermore, the significance of epigenetic modifications induced by HPV-16 and their implications is important for cancer progression. This comprehensive review provides valuable insights into the intricate molecular landscape of HPV-induced oropharyngeal cancer, shedding light on the development of targeted therapies and preventive strategies for this emerging global health concern. Video Abstract.
Assuntos
Neoplasias de Cabeça e Pescoço , Proteínas Oncogênicas Virais , Neoplasias Orofaríngeas , Infecções por Papillomavirus , Humanos , Papillomavirus Humano 16/genética , Papillomavirus Humano 16/metabolismo , Proteínas Oncogênicas Virais/metabolismo , Neoplasias Orofaríngeas/patologia , Proteínas E7 de Papillomavirus/genética , Infecções por Papillomavirus/complicações , Infecções por Papillomavirus/genética , Infecções por Papillomavirus/patologiaRESUMO
MicroRNAs (miRNAs) have been linked to abnormal expression and regulation in a number of diseases, including cancer. Recent studies have concentrated on miRNA Let-7e's significance in precision medicine for cancer screening and diagnosis as well as its prognostic and therapeutic potential. Differential let-7e levels in bodily fluids have the possibility to enable early detection of cancer utilizing less-invasive techniques, reducing biopsy-related risks. Although Let-7e miRNAs have been described as tumor suppressors, it is crucial to note that there exists proof to support their oncogenic activity in vitro and in in vivo. Let-7e's significance in chemo- and radiation treatment decisions has also been demonstrated. Let-7e can also prevent the synthesis of proinflammatory cytokines in a number of degenerative disorders, including musculoskeletal and neurological conditions. For the first time, an overview of the significance of let-7e in the prevention, detection, and therapy of cancer and other conditions has been given in the current review. Additionally, we focused on the specific molecular processes that underlie the actions of let-7e, more particularly, on malignant cells.
Assuntos
MicroRNAs , Neoplasias , Humanos , MicroRNAs/genética , MicroRNAs/metabolismo , Prognóstico , Neoplasias/genéticaRESUMO
Since cancer is one of the world's top causes of death, early diagnosis is critical to improving patient outcomes. Artificial intelligence (AI) has become a viable technique for cancer diagnosis by using machine learning algorithms to examine large volumes of data for accurate and efficient diagnosis. AI has the potential to alter the way cancer is detected fundamentally. Still, it has several disadvantages, such as requiring a large amount of data, technological limitations, and ethical concerns. This overview looks at the possibilities and restrictions of AI in cancer detection, as well as current applications and possible future developments. We can better understand how to use AI to improve patient outcomes and reduce cancer mortality rates by looking at its potential for cancer detection.
Assuntos
Inteligência Artificial , Neoplasias , Humanos , Neoplasias/diagnóstico , AlgoritmosRESUMO
It is becoming more and more apparent that many of the genetic alterations associated with cancer are located in areas that do not encode proteins. lncRNAs are a class of RNAs that do not code for proteins but play a crucial role in maintaining cell function and regulating various cellular processes. By doing this, they have recently introduced what may be a brand-new and essential layer of biological control. These have more than 200 nucleotides and are linked to several diseases; as a result, they have become potential tools for therapeutic intervention. Emerging technologies suggest the presence of mutations on genomic loci that give rise to lncRNAs rather than proteins in a disease as complex as cancer. These lncRNAs play essential parts in gene regulation, which impacts several cellular homeostasis processes, including proliferation, survival, migration, and genomic stability. The leading cause of death in the world today is cancer. Delays in diagnosis and a lack of standard and efficient treatments are the leading causes of the high death rate. Clinically, surgery is frequently used successfully to remove cancers that have not spread, but it is less successful in treating metastatic cancer, which has a drastically lower chance of survival. Chemotherapeutic drugs are a typical therapy to treat the cancer that has spread to other organs. Drug resistance to chemotherapy, however, presents a significant challenge to achieving positive outcomes and is frequently the cause of treatment failure. A substantial barrier to progress in medical oncology is cancer drug resistance. Resistance can develop clinically either before or after cancer treatment. According to this study, lncRNAs influence drug resistance through several different methods. LncRNAs often impact drug resistance by controlling the expression of a few intermediary regulatory variables rather than by directly affecting drug resistance. Additionally, lncRNAs have a variety of roles in cancer medication resistance. Most lncRNAs induce drug resistance when overexpressed; however, other lncRNAs have inhibitory effects. This study provides an overview of the current understanding of lncRNAs, relevance to cancer, and potential therapeutic applications.
Assuntos
Neoplasias , RNA Longo não Codificante , Humanos , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo , Neoplasias/tratamento farmacológico , Neoplasias/genética , Neoplasias/patologia , Resistencia a Medicamentos Antineoplásicos/genética , Transdução de Sinais/genéticaRESUMO
Exosomes are nanometric membrane vesicles of late endosomal origin that are released by most, if not all, cell types as a sophisticated means of intercellular communication. They play an essential role in the movement of materials and information between cells, transport a variety of proteins, lipids, RNA, and other vital data, and over time, they become an essential part of the drug delivery system and a marker for the early detection of many diseases. Dendritic cells have generated interest in cancer immunotherapy due to their ability to initiate and modify effective immune responses. Apart from their cytokine release and direct interactions with other cell types, DCs also emit nanovesicles, such as exosomes, that contribute to their overall activity. Numerous studies have demonstrated exosomes to mediate and regulate immune responses against cancers. Dendritic cell-derived exosomes (DCs) have attracted a lot of attention as immunotherapeutic anti-cancer treatments since it was found that they contain functional MHC-peptide complexes along with a variety of other immune-stimulating components that together enable immune cell-dependent tumor rejection. By enhancing tumor and immunosuppressive immune cells or changing a pro-inflammatory milieu to inhibit tumor advancement, exosomes generated from dendritic cells can initiate and support tumor growth. This study reviewed the immunogenicity of dendritic cell-derived exosomes and strategies for expanding their immunogenic potential as novel and effective anti-cancer therapies.
Assuntos
Exossomos , Neoplasias , Humanos , Exossomos/genética , Células Dendríticas , Neoplasias/patologia , Imunidade , ImunoterapiaRESUMO
In the immunological surveillance against cancer, natural killer (NK) cells are essential effectors that help eradicate altered cells. The complex interactions that occur between NK cells and the tumor microenvironment (TME) are thoroughly examined in this review. The review examines how cytokine stimulation affects NK cell activation, focusing on the dynamic modulation of NK cell function within the TME. It looks at NK cell-related biomarkers such as PD-1/PD-L1, methylation HOXA9 (Homeobox A9), Stroma AReactive Invasion Front Areas (SARIFA), and NKG2A/HLA-E, providing critical information about prognosis and treatment outcomes. The changing landscape of immunotherapies-including checkpoint inhibitors, CAR-NK cells, and cytokine-based interventions-is examined in the context of enhancing NK cell activity. The review highlights the potential pathways for precision medicine going forward, focusing on customized immunotherapies based on unique biomarker profiles and investigating combination medicines to produce more robust anti-tumor responses.
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Neoplasias , Microambiente Tumoral , Humanos , Vigilância Imunológica , Células Matadoras Naturais , Neoplasias/patologia , Citocinas/metabolismoRESUMO
Treatment with chimeric antigen receptor (CAR) T cells indicated remarkable clinical responses with liquid cancers such as hematological malignancies; however, their therapeutic efficacy faced with many challenges in solid tumors due to severe toxicities, antigen evasion, restricted and limited tumor tissue trafficking and infiltration, and, more importantly, immunosuppressive tumor microenvironment (TME) factors that impair the CAR T-cell function adds support survival of cancer stem cells (CSCs), responsible for tumor recurrence and resistance to current cancer therapies. Therefore, in-depth identification of TME and development of more potent CAR platform targeting CSCs may overcome the raised challenges, as presented in this review. We also discuss recent stemness-based innovations in CAR T-cell production and engineering to improve their efficacy in vivo, and finally, we propose solutions and strategies such as oncolytic virus-based therapy and combination therapy to revive the function of CAR T-cell therapy, especially in TME of solid tumors in future.