癌症 cancer - PubMed 文献(第 3 页)
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癌症 的 PubMed 搜索结果(第 3 页)
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Cancer's craving for sugar: an opportunity for clinical exploitation. 癌症对糖的渴望：临床利用的机会
More than 80 years ago, Otto Warburg described the phenomenon whereby cancer cells avidly take up glucose and produce lactic acid under aerobic conditions, a process subsequently referred to as the Warburg effect or aerobic glycolysis. The exact molecular mechanisms underlying cancers reliance on glycolysis remains unclear, but is likely a combination of an epigenetic response to the hypoxic tumour environment in combination with direct oncogenic stimulation. The aim of the current manuscript is to review the normal process of glycolysis and highlight the alterations that occur with malignant transformation, to consider the potential advantages of glycolytic respiration for cancer cell survival, and finally to explore areas where altered glucose metabolism can be exploited for clinical benefit.
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The Intratumoral Heterogeneity of Cancer Metabolism. 癌症代谢的瘤内异质性
Cancer is one of the deadliest diseases in the world, especially within the past few decades, causing over half a million deaths a year in the USA only [1]. Despite recent advances made in the field of cancer biology and the therapies that have been developed, it is clear that more advances are necessary for us to classify cancer as curable. The logical question that arises is simple: Why, despite all the technologies and medical innovations of our time, has a cure eluded us? This chapter will shed light on one of cancer’s most impactful attributes: its heterogeneity and, more specifically, the intratumoral heterogeneity of cancer metabolism. Simply put, what makes cancer one of the deadliest known diseases is its ability to change and adapt. Cancer cells’ rapid evolution, coupled with their irrepressible ability to divide, gives them the advantage over our immune systems. In this chapter, we will delve into the complexities of this adaptability and the vital role that metabolism plays in the rise and progression of this heterogeneity.
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Mapping cutaneous field carcinogenesis of nonmelanoma skin cancer using mesoscopic imaging of pro-inflammation cues. 利用促炎症线索的介观成像绘制非黑色素瘤皮肤癌的皮肤区域癌变图谱
Nonmelanoma skin cancers remain the most widely diagnosed types of cancers globally. Thus, for optimal patient management, it has become imperative that we focus our efforts on the detection and monitoring of cutaneous field carcinogenesis. The concept of field cancerization (or field carcinogenesis), introduced by Slaughter in 1953 in the context of oral cancer, suggests that invasive cancer may emerge from a molecularly and genetically altered field affecting a substantial area of underlying tissue including the skin. A carcinogenic field alteration, present in precancerous tissue over a relatively large area, is not easily detected by routine visualization. Conventional dermoscopy and microscopy imaging are often limited in assessing the entire carcinogenic landscape. Recent efforts have suggested the use of noninvasive mesoscopic (between microscopic and macroscopic) optical imaging methods that can detect chronic inflammatory features to identify pre-cancerous and cancerous angiogenic changes in tissue microenvironments. This concise review covers major types of mesoscopic optical imaging modalities capable of assessing pro-inflammatory cues by quantifying blood haemoglobin parameters and hemodynamics. Importantly, these imaging modalities demonstrate the ability to detect angiogenesis and inflammation associated with actinically damaged skin. Representative experimental preclinical and human clinical studies using these imaging methods provide biological and clinical relevance to cutaneous field carcinogenesis in altered tissue microenvironments in the apparently normal epidermis and dermis. Overall, mesoscopic optical imaging modalities assessing chronic inflammatory hyperemia can enhance the understanding of cutaneous field carcinogenesis, offer a window of intervention and monitoring for actinic keratoses and nonmelanoma skin cancers and maximise currently available treatment options.
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Neoplastic "Black Ops": cancer's subversive tactics in overcoming host defenses. 肿瘤的“黑色行动”：癌症克服宿主防御的颠覆性策略
Metastatic cancer is usually an incurable disease. Cancers have a broad repertoire of subversive tactics to defeat the immune system. They mimic self, they down-regulate MHC molecules so that T cells are blind to their presence, they interfere with antigen presentation, and they produce factors that can kill T cells or paralyze their response to antigens. Furthermore, the same powerful machinery designed to prevent harmful autoimmune responses is also acting to protect cancers. In particular, cancer is protected with the help of so-called regulatory immune cells. These unique subsets of cells, represented by almost every immune cell type, function to control responses of effector immune cells. In this review, we will discuss the evidence that cancer actively promotes cross-talk of regulatory immune cells to evade immunosurveillance. We will also discuss the role of a newly described cell type, regulatory B cells, by emphasizing their importance in suppression of antitumor immune responses. Thus, cancer not only directly suppresses immune function, but also recruits components of the immune system to become traitors and protect the tumor from immune attack.
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Biomarkers for early identification of recurrences in HPV-driven oropharyngeal cancer. 用于早期识别HPV驱动口咽癌复发的生物标志物
One of the major concerns in oncology lies in the ability to detect recurrences at their earliest stage to increase the likelihood of cure following second line, or salvage, therapy. Although human papillomavirus (HPV)-driven oropharyngeal cancers have a good prognosis, 20-25% of patients will recur within 5 years of treatment and a significant portion will die from their disease. In recent years, great effort has been put toward evaluating the potential clinical utility of HPV-related biomarkers for early diagnosis of recurrent disease. Indeed, following completion of treatment, detection of HPV-DNA in oral rinses or blood and serologic assays against HPV oncoproteins could be helpful to track residual disease or recurrence. Several recent studies have reported promising findings, thus potentially paving the way for the use of biomarkers in the management of HPV-OPC. In this review, we evaluate and discuss the current knowledge on this topic and provide some directions for future research.
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Clonal evolution and therapy resistance in the era of precision cancer medicine: evolutionary trajectories in pediatric cancer. 精准癌症医学时代的克隆进化与治疗耐药：儿童癌症的进化轨迹
Pediatric cancers exhibit complex evolutionary dynamics driven by genetic instability, clonal selection, epigenetic reprogramming, and microenvironmental interactions. Tumor evolution is typically characterized by branching phylogenies, where subclones with unique genetic profiles emerge at different locations and time points. Partly as a result of this diversity, advanced cancers often develop resistance to multiple therapies, complicating treatment strategies. This review explores recurrent themes in clonal evolution across childhood cancers as well as evolution-inspired strategies to counter treatment resistance. A model of dynamic decision making is suggested to accommodate emerging methods for monitoring shifts in a cancer's clonal landscape and the widening repertoire of precision drugs. A larger drug toolbox will allow for more sophisticated evolutionary stratagems to cure or stabilize cancer, using methods such as adaptive therapy, extinction therapy, and reflexive control therapies. However, there are also inherent limits in predicting and controlling cancer evolution- emphasizing the need for early detection, particularly in the setting of predicting relapse, which disproportionately contributes to cancer related mortality in childhood. Understanding the evolutionary trajectories of pediatric cancers can inform more effective, personalized treatment protocols, ultimately enhancing survival rates and quality of life for young patients.
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Distinct mechanisms of cell in breast cancer and their clinical implication. 乳腺癌中细胞的不同机制及其临床意义
Breast cancer is a heterogeneous disease affecting women globally. Despite significant advancements in therapeutic interventions in recent years, breast cancer remains a leading cause of cancer-related morbidity in women. Breast cancer's diverse molecular subtypes and escalating complexities in targeted therapies underscore the imperative need to explore novel therapeutic targets. The obstruction of apoptosis and the suppression of cell death are hallmarks of malignant tumors. Cell death, a pivotal regulatory event during tumorigenesis, includes apoptosis, anoikis, autophagy, necroptosis, ferroptosis, pyroptosis, and cuproptosis. This review systematically dissects the molecular underpinnings of cell death pathways in breast cancer, offering novel mechanistic insights and therapeutic opportunities to inform clinical management strategies.
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Aneuploid Circulating Tumor-Derived Endothelial Cell (CTEC): A Novel Versatile Player in Tumor Neovascularization and Cancer Metastasis. 非整倍体循环肿瘤来源内皮细胞（CTEC）：肿瘤新生血管形成和癌症转移中的新型多面手
Hematogenous and lymphogenous cancer metastases are significantly impacted by tumor neovascularization, which predominantly consists of blood vessel-relevant angiogenesis, vasculogenesis, vasculogenic mimicry, and lymphatic vessel-related lymphangiogenesis. Among the endothelial cells that make up the lining of tumor vasculature, a majority of them are tumor-derived endothelial cells (TECs), exhibiting cytogenetic abnormalities of aneuploid chromosomes. Aneuploid TECs are generated from "cancerization of stromal endothelial cells" and "endothelialization of carcinoma cells" in the hypoxic tumor microenvironment. Both processes crucially engage the hypoxia-triggered epithelial-to-mesenchymal transition (EMT) and endothelial-to-mesenchymal transition (EndoMT). Compared to the cancerization process, endothelialization of cancer cells, which comprises the fusion of tumor cells with endothelial cells and transdifferentiation of cancer cells into TECs, is the dominant pathway. Tumor-derived endothelial cells, possessing the dual properties of cancerous malignancy and endothelial vascularization ability, are thus the endothelialized cancer cells. Circulating tumor-derived endothelial cells (CTECs) are TECs shed into the peripheral circulation. Aneuploid CD31 CTECs, together with their counterpart CD31 circulating tumor cells (CTCs), constitute a unique pair of cellular circulating tumor biomarkers. This review discusses a proposed cascaded framework that focuses on the origins of TECs and CTECs in the hypoxic tumor microenvironment and their clinical implications for tumorigenesis, neovascularization, disease progression, and cancer metastasis. Aneuploid CTECs, harboring hybridized properties of malignancy, vascularization and motility, may serve as a unique target for developing a novel metastasis blockade cancer therapy.
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Biology and chemoprevention of lung cancer. 肺癌的生物学与化学预防
Advances in cell and molecular biology have increased our understanding of the multiple events that lead to the development of lung cancer. The field cancerization theory suggests that multiple genetic abnormalities occur throughout the respiratory epithelium as a result of long-term carcinogen exposure. Because of this diffuse injury throughout the lung, systemic therapy that could halt or reverse the development of cancerous changes may be effective in preventing lung cancer. This article summarizes the chemoprevention agents that have been used in clinical trials to prevent lung cancer of the head and neck. Biomarkers that have been suggested as intermediate end points in evaluating the effectiveness of chemoprevention agents are also discussed.
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Could field cancerization be interpreted as a biochemical anomaly amplification due to transformed cells? 区域癌化能否被解释为转化细胞导致的生化异常放大？
Field cancerization is a concept used to explain cellular and molecular alterations in tissue associated to neoplasia and cancer. This effect was proposed by Slaughter in order to explain the development of multiple primary tumors and locally recurrent cancer. The particular changes associated with this effect, in each type of cancer, have been detected even at distances greater than 10cm off the tumor, in areas classified as normal by histopathological studies. Early detection of lung, colon, and ovary cancer has been reported by the use of Partial Wave Microscopy Spectroscopy (PWS) and has been explained in terms of the field cancerization effect. Until now, field cancerization has been studied as a field effect and we hypothesize that it can be understood as an amplifying effect of biochemical abnormalities in cells, which leads us to ask the question: Could field cancerization be interpreted as a biochemical anomaly amplification due to transformed cells? We propose this question because the biochemical changes due to field cancerization alter the dynamics of molecules and cells in abnormal tissues in comparison to normal ones, these alterations modify the interaction of intracellular and extracellular medium, as well as cellular movement. We hypothesize that field cancerization when interpreted as an amplification effect can be used for the early detection of cancer by measuring the change of cell dynamics.