癌症 cancer - PubMed 文献(第 2 页)
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癌症 的 PubMed 搜索结果(第 2 页)
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Uncovering cancer's secrets: could liquid biopsies and artificial intelligence hold the answers? 揭开癌症的秘密：液体活检和人工智能能找到答案吗？
Tweetable abstract How are #liquidbiopsies and #AI pushing us closer to the goal of early cancer detection for all? Plus, what more needs to be done to truly deciphers cancer's secrets? Find out in this editorial by @JadeParkerB.
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A Guide to Extrachromosomal DNA: Cancer's Dynamic Circular Genome. 染色体外DNA指南：癌症的动态环状基因组
Focal amplifications of oncogenes are important cancer drivers. They can occur on chromosomes or in the context of circular extrachromosomal DNA (ecDNA). Many key features of ecDNAs were described in the 1960s to 1980s, including their "unstable" nature and their ability to confer drug resistance. With the benefit of new technologies, our understanding of ecDNAs has advanced dramatically in the last decade, both in breadth and in depth, including the remarkable discovery that ecDNAs are present in 17% of all cancers and are associated with worse patient outcomes. In this study, we present a guide to ecDNA tools and biology. Focal amplifications on ecDNAs are commonly found in cancer and are associated with poor patient outcomes and distinct biology. In this review, we provide a guide to ecDNA biology and available tools as well as our perspective on this rapidly evolving field.
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Liquid biopsy: an essential tool for metastatic breast cancer's follow-up. 液体活检：转移性乳腺癌症随访的重要工具
Breast cancer is the most common malignancy in women worldwide. While personalized treatment options are obstructed by the limitations of conventional biopsy follow-up, the liquid biopsy could detect the tumor's characteristics in order to reach a more targeted therapy for metastatic breast cancer patients. The aim of this article is to review the characteristics of the liquid biopsy in the follow-up of metastatic breast cancer patients. A comprehensive literature search was conducted using the PubMed literature to retrieve topic-related articles using keywords 'metastatic breast cancer,' 'liquid biopsy' and 'follow up.' A descriptive analysis was undertaken, and 29 original articles were retained. The study of blood biomarkers is being used in the monitoring and follow-up of metastatic breast cancer. It is used to determine the survival rate based on different biomarkers and monitor the response to treatment through the status of the tumor. This review describes the latest findings on breast cancer's circulating tumor cells, circulating cell-free DNA, circulating tumor DNA, proteomes, and extracellular vesicles (exosomes) in the plasma. Our literature review revealed that the liquid biopsy is capable of detecting breast cancer biomarkers in order to monitor breast cancer patients, improve their treatment choices and predict their prognosis more accurately.
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Tackling the complexity of cancer with generative models. 用生成模型处理癌症的复杂性
The Hallmarks of Cancer framework has played a seminal role in developing our understanding of cancer biology. By design, these hallmarks abstract cancer into a common set of functional capabilities. The hallmarks thus constitute an intentionally reductionist framework that has unified diverse observations and yielded valuable mechanistic insight, while leaving unresolved how these processes interact across scales. Complementary tools are therefore needed to capture cancer's inherently complex, multimodal, and multiscale nature. Here, we posit that generative models, built on the recent advances of artificial intelligence, are the key technology to capture this complexity and to thereby improve how we diagnose, understand, and intervene in cancer. Specifically, because of their ability to recognize complex patterns, process unstructured inputs, and synthesize multimodal inputs, generative models are poised to usher in a new era of biological discovery and clinical care. Ultimately, we envision a synergistic cycle wherein generative models of cancer and the Hallmarks of Cancer complement one another, the former driving hypothesis generation and discovery and the latter guiding the prioritization and development of new measurement tools.
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Metastatic prostate cancer mimicking a subdural hematoma: A case report and literature review. 模拟硬膜下血肿的转移性前列腺癌：一例病例报告及文献综述
Occurrences of metastatic prostate cancer imitating a subdural hematoma are limited to a small number of case reports, even though prostate cancer spreads to the dura more than other types of cancer. Here, we present the case of a 64 year-old male whose prostate carcinoma's metastasis mimicked a subdural hematoma, and he suffered a middle cerebral artery stroke. Prostate cancer's high rate of progression to the dura is disproportionate to its relatively low rate of brain metastasis. Furthermore, we explore the potential molecular implications of prostate cancer's propensity to spread to the dura.
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A membrane-specific tyrosinase chelate: the mitotic regulator? 一种膜特异性酪氨酸酶螯合物：有丝分裂调节因子？
Cancer's random, reversible, unstable transitions to "normal" structures imply their functional relation. Similar random, continuous, reversible oncogene "mutational transformation" also lacks a consistent hybrid. Positing cancer's "mutationally altered genotype" leads to medically foreign causes, qualities, inducers, suppressors, immune proteins, and viruses. Its random variation, however, opposes the functionally discrete, ordered, stable, irreversible hybrid variation and single-valued transforms of molecular genetics. There, "causal mutational operators" remain unspecified; only consistent single-valued DNA base and amino acid change, as "transform operand", are made explicit. A mitotically "blocked" (normal) and "unblocked" (malignant) stem cell "phenotype", operationally constructed from microscopic data, is therefore viewed within the homeostatic context of open-system enzyme-regulatory equilibrium. This functional, stochastic field distribution between "structurally bound" and "freely dividing" stem cell number discloses their putative regulatory mitotic-blocking factor. A tyrosinase complex, interacting by Cu2+-Fe2+ chelation with a proline hydroxylase divisional enzyme near stem cell ribosomes, maintains steady-state mitotic equilibrium. Based upon familiar medical, biochemical, and energy principles this confronts cancer's pigmentary-depigmentary signs, glycolytic metabolism, elevated serum tyrosinase, defective collagen production, exposed membrane binding sites, and tyrosine's recent growth control role.
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The status of ultrasound and color Doppler imaging for the early detection of ovarian carcinoma. 超声和彩色多普勒成像在卵巢癌早期检测中的地位
Noninvasive imaging techniques such as ultrasound and color doppler imaging have been evaluated during the last decade for their ability to detect organ-confined curable ovarian cancer. While sensitivities approaching 100% can be achieved by these techniques, their specificities and the frequent invasive procedures required to confirm the abnormal sonographic findings have led to caution regarding the widespread use of ultrasound screening for ovarian cancer. These data are reviewed, as well as the NIH Consensus Panel on ovarian cancer's recommendation that routine screening for ovarian carcinoma should not be carried out at this time. Hereditary ovarian cancer syndromes account for approximately 5-10% of the cases. Many of the genes responsible for these syndromes have recently been elucidated. Due to the significant increase in the risk of ovarian cancer in these families, many screening studies have focused on this patient population. Findings from these trials, as well as studies on the psychological impact of screening are presented.
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Is ingested inorganic arsenic a "threshold" carcinogen? 摄入的无机砷是一种“阈值”致癌物吗？
Ingested inorganic arsenic (As) is known to be a human carcinogen. An intriguing question is whether there is a threshold for the carcinogenic effects of As, i.e., is there a level below which it does not induce the development of cancer(s)? This Roundtable will discuss the United States Environmental Protection Agency's As risk assessment using the Taiwan data from different viewpoints. It will also consider the hypothesis that there is a threshold for As and data for or against this hypothesis. For example, some scientists believe that epidemiological data cannot answer this question, while others feel that different study designs and larger sampling will provide adequate data. Reasons for each position are given. This Roundtable discussion demonstrates the controversy surrounding the use of the Taiwan data for risk assessment.
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Finding cancer's weakest link. 发现癌症最薄弱的环节
The biological programs of vertebrates exhibit a remarkable degree of functional degeneracy, adaptive compensation and robustness, to preserve homeostasis and generate reproducible phenotypic outputs irrespective of variations in signal strength, noise and quality. Cancers are difficult to treat not only because they are so mechanistically diverse but also because they adapt or evolve in response to any pharmacological elective pressure we impose upon them. Hence, an ideal cancer drug target would exert a function both necessary for cancer cell survival and functionally non-redundant, rendering it impossible for tumor cells to compensate for, or evolve independence from, the inhibitory effect of any drug aimed at that target. In this review, we discuss the unique, non-degenerate and highly pleiotropic role played by Myc in coordinating, engaging and maintaining the diverse intracellular and extracellular programs required for cell proliferation in vivo. These properties make Myc a compelling candidate cancer drug target, at least in principle: an assertion recently reinforced by new in vivo genetic data.
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Revolutionizing cancer treatment: Navigating the intricate landscape of cellular signaling networks. 癌症治疗的革命性：驾驭细胞信号网络的复杂景观
Cancer progression and therapeutic resistance are propelled by the remarkable plasticity of signaling networks, which dynamically rewire under selective pressures to maintain proliferation, enable immune evasion and promote metastasis. Despite advances in precision oncology, the dynamic crosstalk between tumor cells, non-coding genomes and the microenvironment continues to undermine treatment efficacy. This call for submissions, Revolutionizing Cancer Treatment: Navigating the Intricate Landscape of Cellular Signaling Networks, seeks cutting-edge research that dissects these adaptive mechanisms through innovative technologies - from single-cell multi-omics and spatial transcriptomics to AI-powered network modeling. We welcome studies leveraging physiomimetic models (e.g., organoids, 3D-bioprinted ecosystems) to decode tumor heterogeneity, as well as translational work targeting emergent vulnerabilities at the intersection of epigenetics, metabolic reprogramming and stromal interactions. By integrating systems biology with computational and experimental approaches, this collection aims to catalyze the design of adaptive therapies that outmaneuver cancer's evolutionary resilience.