癌症 cancer - PubMed 文献(第 4 页)
PubMed 共收录约 5,709,791 篇相关文献，本站只列出其中相关度最高的前 50 篇（共 5 页）；要看全部结果、按影响因子 / 分区 / 年份筛选，请前往完整搜索。
本页是「癌症（cancer）」PubMed 检索结果的第 4 页，列出第 31–40 篇相关文献；主题介绍见第 1 页。
癌症 的 PubMed 搜索结果(第 4 页)
-
{"_":"A dose-finding trial with a novel ingenol derivative (ingenol disoxate: LEO 43204) for field treatment of actinic keratosis on full face or 250 cm on the chest.","sup":["2"]} {"_":"一项新型巨大戟醇衍生物（巨大戟醇二异辛酸酯：LEO 43204）用于全面部或胸部250 cm区域光化性角化病区域治疗的剂量探索试验。","sup":["2"]}
Actinic keratoses (AKs) may progress to squamous cell carcinoma and can occur in cancerized fields as sub-clinical and clinically visible lesions. Ingenol disoxate gel is a topical field therapy for AK. This Phase I/II trial aimed to assess the safety and efficacy of ingenol disoxate on full face or chest in patients with AKs. Part 1 was a phase-I, open-label, dose-escalation trial investigating the maximum tolerated dose of ingenol disoxate. Part 2 was a phase-II, randomized, double-blind, vehicle-controlled trial; patients were randomized 1:1:1:1 to ingenol disoxate 0.018%, 0.012%, 0.006% gel or vehicle for 2 consecutive days. Reduction in AK count from baseline at Week 8 was significantly higher than with vehicle for all doses of ingenol disoxate gel (0.018%, 79.0%; 0.012%, 73.4%; 0.006%, 69.7%; vehicle; 42.3%; p < .001). Local skin responses peaked at Day 3 for all doses, rapidly declined, and reached mild levels at Week 2. Most adverse events were mild or moderate in intensity, and were most commonly application site pain/pruritus. Ingenol disoxate gel is efficacious and well tolerated as field treatment for AKs on the full face or chest. Clinical Trial No.: NCT01922050.
-
The value of genomics in dissecting the RAS-network and in guiding therapeutics for RAS-driven cancers. 基因组学在解析RAS网络和指导RAS驱动癌症治疗中的价值
The rise in genomic knowledge over the past decade has revealed the molecular etiology of many diseases, and has identified intricate signaling network activity in human cancers. Genomics provides the opportunity to determine genome structure and capture the activity of thousands of molecular events concurrently, which is important for deciphering highly complex genetic diseases such as cancer. In this review, we focus on genomic efforts directed towards one of cancer's most frequently mutated networks, the RAS pathway. Genomic tools such as gene expression signatures and assessment of mutations across the RAS network enable the capture of RAS signaling complexity. Due to this high level of interaction and cross-talk within the network, efforts to target RAS signaling in the clinic have generally failed, and we currently lack the ability to directly inhibit the RAS protein with high efficacy. We propose that the use of gene expression data can identify effective treatments that broadly inhibit the RAS network as this approach measures pathway activity independent of mutation status or any single mechanism of activation. Here, we review the genomic studies that map the complexity of the RAS network in cancer, and that show how genomic measurements of RAS pathway activation can identify effective RAS inhibition strategies. We also address the challenges and future directions for treating RAS-driven tumors. In summary, genomic assessment of RAS signaling provides a level of complexity necessary to accurately map the network that matches the intricacy of RAS pathway interactions in cancer.
-
[The influence of Qi-lan granulates on the variation of proliferating cell nuclear antigen during the course of SD rat tongue carcinogenesis]. [芪蓝颗粒对SD大鼠舌癌变过程中增殖细胞核抗原变化的影响]
To study the cancer blocking effect of the Qi-lan granulates in SD rats. A total of 150 SD rats were divided into five groups A,B,C,D,E. Rats in group A, B, C, D were fed with 0.002% 4NQO dissolved in drinking water to induce tongue carcinogenesis in rats. Different concentration of the herb Qi-lan granulates was given to the rats of group B, C, D during oral carcinogenesis. Group A was model group, group E was normal group. The rats were sacrificed at 9, 18, 27 and 36 weeks respectively from the beginning of the experiment. The samples were collected for histophology and PCNA immunohistochemistry. The date was analyzed by Chi-square test and Kruskal-Wallis test using SPSS13.0 software package. The overall canceration rate of group B (14.29%), C (3.57%), D (14.29%) was significantly lower than group A (39.29%) (P<0.05), the effect of Qi-lan granulates in group C was the best. Immunohistochemistry result showed that 6 cases of normal oral mucosa in group A had positive expression of PCNA. In 11 cases of dysplasia, 8 had positive express of PCNA, 11 rats with oral cancerous tissues had positive expression of PCNA.In group A, the expression of PCNA was normal tissue<dysplasia tissue<tongue cancer tissue (P<0.05). The expression rate of PCNA in tongue dysplasia from rats in group A(8/11) was significantly higher than the other group B (6/15), C (4/14) and D(3/13) (P<0.05). But in cancer tissues, the expression of PCNA in group A was not significantly different from group B,C and D (P>0.05). In general, the expression of PCNA in group A was significantly higher than the Qi-lan granulates group, the difference was statistically significant (P<0.05). The expression of PCNA in group E was negative. Qi-lan granulates have significant inhibitory effect on tongue cancer, through blocking cell proliferation.
-
Comprehensive Evaluation of Multi-Omics Clustering Algorithms for Cancer Molecular Subtyping. 多组学聚类算法用于癌症分子分型的综合评估
As a highly heterogeneous and complex disease, the identification of cancer's molecular subtypes is crucial for accurate diagnosis and personalized treatment. The integration of multi-omics data enables a comprehensive interpretation of the molecular characteristics of cancer at various biological levels. In recent years, an increasing number of multi-omics clustering algorithms for cancer molecular subtyping have been proposed. However, the absence of a definitive gold standard makes it challenging to evaluate and compare these methods effectively. In this study, we developed a general framework for the comprehensive evaluation of multi-omics clustering algorithms and introduced an innovative metric, the accuracy-weighted average index, which simultaneously considers both clustering performance and clinical relevance. Using this framework, we performed a thorough evaluation and comparison of 11 state-of-the-art multi-omics clustering algorithms, including deep learning-based methods. By integrating the accuracy-weighted average index with computational efficiency, our analysis reveals that PIntMF demonstrates the best overall performance, making it a promising tool for molecular subtyping across a wide range of cancers.
-
Pathophysiological dynamics of human ovarian surface epithelial cells in epithelial ovarian carcinogenesis. 人卵巢表面上皮细胞在上皮性卵巢癌变中的病理生理动力学
Epithelial ovarian cancer is responsible for almost half of all the deaths from female genital tract tumors. Major impediments to the clinical treatment of this disease are the relatively asymptomatic progression and a lack of knowledge regarding defined precursor or malignant lesions. Most epithelial ovarian cancers are thought to arise from the transformation of ovarian surface epithelial cells, a single continuous layer of flat-to-cuboidal mesothelial cells surrounding the ovary. To improve our understanding of the pathogenesis of epithelial ovarian cancer, it is necessary to study the biological characteristics of normal ovarian surface epithelial cells. However, this approach has been hampered by the inability to purify and culture such human cells. During the past decade, procedures to isolate and culture human ovarian surface epithelial cells have been developed, and, subsequently, using viral oncogenes, several immortalized cells have been established. This new experimental system is being employed to improve our understanding of the genetic changes leading to the initiation of epithelial ovarian cancer and to identify events in the cancer's development. This review mainly describes the biological dynamics of ovarian surface epithelial cells in the pathogenesis of epithelial ovarian cancer, focusing on humans and excluding small animal models.
-
A genetic explanation of Slaughter's concept of field cancerization: evidence and clinical implications. Slaughter区域癌化概念的遗传学解释：证据与临床意义
The concept of "field cancerization" was first introduced by Slaughter et al. [D. P, Slaughter et al., Cancer (Phila.), 6: 963-968, 1953] in 1953 when studying the presence of histologically abnormal tissue surrounding oral squamous cell carcinoma. It was proposed to explain the development of multiple primary tumors and locally recurrent cancer. Organ systems in which field cancerization has been described since then are: head and neck (oral cavity, oropharynx, and larynx), lung, vulva, esophagus, cervix, breast, skin, colon, and bladder. Recent molecular findings support the carcinogenesis model in which the development of a field with genetically altered cells plays a central role. In the initial phase, a stem cell acquires genetic alterations and forms a "patch," a clonal unit of altered daughter cells. These patches can be recognized on the basis of mutations in TP53, and have been reported for head and neck, lung, skin, and breast cancer. The conversion of a patch into an expanding field is the next logical and critical step in epithelial carcinogenesis. Additional genetic alterations are required for this step, and by virtue of its growth advantage, a proliferating field gradually displaces the normal mucosa. In the mucosa of the head and neck, as well as the esophagus, such fields have been detected with dimensions of >7 cm in diameter, whereas they are usually not detected by routine diagnostic techniques. Ultimately, clonal divergence leads to the development of one or more tumors within a contiguous field of preneoplastic cells. An important clinical implication is that fields often remain after surgery of the primary tumor and may lead to new cancers, designated presently by clinicians as "a second primary tumor" or "local recurrence," depending on the exact site and time interval. In conclusion, the development of an expanding preneoplastic field appears to be a critical step in epithelial carcinogenesis with important clinical consequences. Diagnosis and treatment of epithelial cancers should not only be focused on the tumor but also on the field from which it developed.
-
Current perspectives in prostate cancer vaccines. 前列腺癌疫苗的当前展望
The use of vaccines as a potential therapeutic modality for the treatment of cancer has been extensively studied. Recent advances include identification and characterization of tumor-associated antigens, novel vaccine delivery systems, and the combination of vaccines with immune stimulants and other therapeutic modalities. Immunotherapy as a modality for treatment of prostate cancer has received significant attention. There are several characteristics of prostate cancer that make it an ideal target for immunotherapy. Prostate cancer's relative indolence allows sufficient time to generate immune responses, which may take weeks or months to mount. In addition, prostate cancer-associated antigens direct the immune response to prostate cancer cells, thus sparing normal vital tissue. This review focuses on promising new vaccines and novel perspectives in the treatment of prostate cancer.
-
Multifocal Primary Prostate Cancer Exhibits High Degree of Genomic Heterogeneity. 多灶性原发性前列腺癌表现出高度的基因组异质性
Most primary prostate cancers are multifocal with individual tumors harboring different aggressiveness; however, the genomic heterogeneity among these tumors is poorly understood. To better understand the biological basis for clinical variability among different lesions, we sought to comprehensively characterize the heterogeneity of somatic gene mutations in multifocal prostate cancer. High-coverage whole-exome sequencing of 153 frozen tissue samples, taken from two to three distinct tumor foci and one non-cancerous area from each of 41 patients, covering a total of 89 tumor foci. State-of-the-art bioinformatics tools for mutation calling and copy number determination from whole-exome sequencing data. We found a very high degree of interfocal heterogeneity among tumors, that is, 76% of pairwise-compared tumor foci from the same prostatectomy specimen had no point mutations in common and DNA copy number changes were rarely shared across cancer foci. The few point mutations shared across tumor foci were seldom in cancer-critical genes. In this first large genomic heterogeneity study of primary prostate cancer, we observe that different tumor foci within the same patient are genetically distinct, only rarely sharing any somatic gene mutations, including those in cancer driver genes. This heterogeneity affects how genomics-based management of prostate cancer can be implemented, as information from all tumor foci is necessary to draw valid conclusions about the cancer's genomic alterations. Most primary prostate cancers consist of multiple tumors within the same organ, but little is known about their relationships. We have compared the sets of gene mutations among such tumors and found that they only exceptionally have any in common. This will influence treatment decisions in the future as each tumor's mutations will render it unique and have to be considered to gain the best treatment results.
-
Cholesterol metabolism in pancreatic cancer and associated therapeutic strategies. 胰腺癌中的胆固醇代谢及相关治疗策略
Pancreatic cancer remains one of the most lethal cancers due to late diagnosis and high chemoresistance. Despite recent progression in the development of chemotherapies, immunotherapies, and potential nanoparticles-based approaches, the success rate of therapeutic response is limited which is further compounded by cancer drug resistance. Understanding of emerging biological and molecular pathways causative of pancreatic cancer's aggressive and chemoresistance is vital to improve the effectiveness of existing therapeutics and to develop new therapies. One such under-investigated and relatively less explored area of research is documenting the effect that lipids, specifically cholesterol, and its metabolism, impose on pancreatic cancer. Dysregulated cholesterol metabolism has a profound role in supporting cellular proliferation, survival, and promoting chemoresistance and this has been well established in various other cancers. Thus, we aimed to provide an in-depth review focusing on the significance of cholesterol metabolism in pancreatic cancer and relevant genes at play, molecular processes contributing to cellular cholesterol homeostasis, and current research efforts to develop new cholesterol-targeting therapeutics. We highlight the caveats, weigh in different experimental therapeutic strategies, and provide possible suggestions for future research highlighting cholesterol's importance as a therapeutic target against pancreatic cancer resistance and cancer progression.
-
Forkhead box-O transcription factor: critical conductors of cancer's fate. 叉头框O转录因子：癌症命运的关键指挥者
Cells have evolved elaborated mechanisms to coordinate the cellular answer of either survival or apoptosis. Recent concepts of human carcinogenesis have suggested disturbances in these cellular relays as a potential link to cellular dedifferentiation and uncontrolled proliferation. Forkhead box-O transcription factors (FOXOs) play an important role in tumour suppression by regulating the expression of genes involved in stress resistance, DNA damage repair, cell cycle arrest and apoptosis. The specific regulation of FOXO function is tightly controlled by posttranslational modifications such as phosphorylation, acetylation and ubiquitination. Loss of FOXO function has recently been identified in several human cancers. In this review, we will give an overview about recent progress in the understanding of function and regulation of FOXOs, as well as their role in carcinogenesis. Furthermore, we will discuss a potential clinical use of FOXOs by therapeutically restoring their tumour suppressive properties.