Advances in Cancer Research最新文献_第4页

Assessment of thiol/disulfide homeostasis for prognostic follow-up of cholangiocarcinoma patients 胆管癌患者预后随访中硫醇/二硫稳态的评估

2区医学

Advances in Cancer Research Pub Date : 2023-01-01 DOI: 10.53388/2023623009

Z. Guleken, H. Bulut, Kürşat Rahmi Serin, M. Büyük, E. Ulukaya

引用次数: 0

Tumor heterogeneity: An oncogenic driver of PDAC progression and therapy resistance under stress conditions. 肿瘤异质性：压力条件下 PDAC 进展和耐药性的致癌驱动因素。

2区医学

Advances in Cancer Research Pub Date : 2023-01-01 Epub Date: 2023-04-21 DOI: 10.1016/bs.acr.2023.02.005

António M Palma, Vignesh Vudatha, Maria Leonor Peixoto, Esha Madan

{"title":"Tumor heterogeneity: An oncogenic driver of PDAC progression and therapy resistance under stress conditions.","authors":"António M Palma, Vignesh Vudatha, Maria Leonor Peixoto, Esha Madan","doi":"10.1016/bs.acr.2023.02.005","DOIUrl":"10.1016/bs.acr.2023.02.005","url":null,"abstract":"Pancreatic ductal adenocarcinoma (PDAC) is a clinically challenging disease usually diagnosed at advanced or metastasized stage. By this year end, there are an expected increase in 62,210 new cases and 49,830 deaths in the United States, with 90% corresponding to PDAC subtype alone. Despite advances in cancer therapy, one of the major challenges combating PDAC remains tumor heterogeneity between PDAC patients and within the primary and metastatic lesions of the same patient. This review describes the PDAC subtypes based on the genomic, transcriptional, epigenetic, and metabolic signatures observed among patients and within individual tumors. Recent studies in tumor biology suggest PDAC heterogeneity as a major driver of disease progression under conditions of stress including hypoxia and nutrient deprivation, leading to metabolic reprogramming. We therefore advance our understanding in identifying the underlying mechanisms that interfere with the crosstalk between the extracellular matrix components and tumor cells that define the mechanics of tumor growth and metastasis. The bilateral interaction between the heterogeneous tumor microenvironment and PDAC cells serves as another important contributor that characterizes the tumor-promoting or tumor-suppressing phenotypes providing an opportunity for an effective treatment regime. Furthermore, we highlight the dynamic reciprocating interplay between the stromal and immune cells that impact immune surveillance or immune evasion response and contribute towards a complex process of tumorigenesis. In summary, the review encapsulates the existing knowledge of the currently applied treatments for PDAC with emphasis on tumor heterogeneity, manifesting at multiple levels, impacting disease progression and therapy resistance under stress.","PeriodicalId":50875,"journal":{"name":"Advances in Cancer Research","volume":"159 ","pages":"203-249"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9653442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The epigenome and the many facets of cancer drug tolerance. 表观基因组和癌症药物耐受性的许多方面。

2区医学

Advances in Cancer Research Pub Date : 2023-01-01 DOI: 10.1016/bs.acr.2022.12.002

Paul C Moore, Kurt W Henderson, Marie Classon

{"title":"The epigenome and the many facets of cancer drug tolerance.","authors":"Paul C Moore, Kurt W Henderson, Marie Classon","doi":"10.1016/bs.acr.2022.12.002","DOIUrl":"https://doi.org/10.1016/bs.acr.2022.12.002","url":null,"abstract":"The use of chemotherapeutic agents and the development of new cancer therapies over the past few decades has consequently led to the emergence of myriad therapeutic resistance mechanisms. Once thought to be explicitly driven by genetics, the coupling of reversible sensitivity and absence of pre-existing mutations in some tumors opened the way for discovery of drug-tolerant persisters (DTPs): slow-cycling subpopulations of tumor cells that exhibit reversible sensitivity to therapy. These cells confer multi-drug tolerance, to targeted and chemotherapies alike, until the residual disease can establish a stable, drug-resistant state. The DTP state can exploit a multitude of distinct, yet interlaced, mechanisms to survive otherwise lethal drug exposures. Here, we categorize these multi-faceted defense mechanisms into unique Hallmarks of Cancer Drug Tolerance. At the highest level, these are comprised of heterogeneity, signaling plasticity, differentiation, proliferation/metabolism, stress management, genomic integrity, crosstalk with the tumor microenvironment, immune escape, and epigenetic regulatory mechanisms. Of these, epigenetics was both one of the first proposed means of non-genetic resistance and one of the first discovered. As we describe in this review, epigenetic regulatory factors are involved in most facets of DTP biology, positioning this hallmark as an overarching mediator of drug tolerance and a potential avenue to novel therapies.","PeriodicalId":50875,"journal":{"name":"Advances in Cancer Research","volume":"158 ","pages":"1-39"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9335657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Deciphering epithelial-to-mesenchymal transition in pancreatic cancer. 解密胰腺癌上皮细胞向间质转化的过程。

2区医学

Advances in Cancer Research Pub Date : 2023-01-01 Epub Date: 2023-03-23 DOI: 10.1016/bs.acr.2023.02.008

Creighton Friend, Parash Parajuli, Mohammed S Razzaque, Azeddine Atfi

引用次数: 0

Measuring the multifaceted roles of mucin-domain glycoproteins in cancer. 测量粘蛋白结构域糖蛋白在癌症中的多方面作用。

2区医学

Advances in Cancer Research Pub Date : 2023-01-01 Epub Date: 2022-10-08 DOI: 10.1016/bs.acr.2022.09.001

Nicholas M Riley, Ru M Wen, Carolyn R Bertozzi, James D Brooks, Sharon J Pitteri

引用次数: 0

Clinical evidence of neoadjuvant immunotherapy for resectable locally advanced esophageal carcinoma: A systematic review 新辅助免疫治疗可切除局部晚期食管癌的临床证据:一项系统综述

2区医学

Advances in Cancer Research Pub Date : 2023-01-01 DOI: 10.53388/2023623013

Zikun Wu, Chong Xiao, Xue-Ke Li, Feng-Ming You

{"title":"Clinical evidence of neoadjuvant immunotherapy for resectable locally advanced esophageal carcinoma: A systematic review","authors":"Zikun Wu, Chong Xiao, Xue-Ke Li, Feng-Ming You","doi":"10.53388/2023623013","DOIUrl":"https://doi.org/10.53388/2023623013","url":null,"abstract":"Background: Immune checkpoint inhibitors (ICIs) as the neoadjuvant therapy for resectable locally advanced esophageal carcinoma (rlaEC) remains challenging given the poor reports of efficacy and safety. This study aimed to summarize reliable evidence for the preoperative neoadjuvant immunotherapy of rlaEC by analyzing all the published clinical trials on the ICIs as the neoadjuvant therapy for rlaEC. Methods: PubMed, Cochrane Library, Embase and ClinicalTrials.gov were searched from inception until June 1st, 2023, for available reports to perform a meta-analysis. The primary endpoints were R0 resection, objective response rate (ORR), pathological complete response (pCR) and major pathological response (MPR), as well as treatment-related adverse events (AEs) and postoperative complications. The Stata 14.0 software was employed to estimate pooled effect size. Results: A total of 18 single-arm clinical trials involving 625 patients met the inclusion criteria. Meta-analysis showed that, among these patients with rlaEC, the pooled R0 resection rate was 97.0% (95% CI: 94.0% – 99.0%), the pooled ORR was 70.0% (95% CI: 64.0% – 76.0%), the pooled pCR and MPR rate were 34.0% (95 % CI: 29.0% – 39.0%) and 56.0% (95% CI: 47.0% – 65.0%) respectively. The incidence of main treatment-related AEs and postoperative complications was about 6% – 45% and 8% – 19% respectively. Conclusions: Patients with rlaEC were tolerated to neoadjuvant immunotherapy and it might be beneficial to improve efficacy. But this meta-analysis had limitations and the conclusions still needed to be validated by more rigorous phase III randomized controlled clinical trials.","PeriodicalId":50875,"journal":{"name":"Advances in Cancer Research","volume":"25 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74723479","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cancer and diet: significance of diet in a patient whose life expectancy was 4 to 5 months 癌症与饮食:饮食对预期寿命为4至5个月的患者的意义

2区医学

Advances in Cancer Research Pub Date : 2023-01-01 DOI: 10.53388/2023623002

José Ramón Toro López

引用次数: 0

The biology of E-selectin ligands in leukemogenesis. e -选择素配体在白血病发生中的生物学作用。

2区医学

Advances in Cancer Research Pub Date : 2023-01-01 DOI: 10.1016/bs.acr.2022.07.001

Evan Ales, Robert Sackstein

{"title":"The biology of E-selectin ligands in leukemogenesis.","authors":"Evan Ales, Robert Sackstein","doi":"10.1016/bs.acr.2022.07.001","DOIUrl":"https://doi.org/10.1016/bs.acr.2022.07.001","url":null,"abstract":"Both the cascade whereby a blood-borne cell enters a tissue and the anchoring of hematopoietic stem/progenitor cells (HSPCs) within bone marrow critically pivots on cell-cell interactions mediated by E-selectin binding to its canonical carbohydrate ligand, the tetrasaccharide termed \"sialylated Lewis X\" (sLeX). E-selectin, a member of the selectin class of adhesion molecules that is exclusively expressed by vascular endothelium, engages sLeX-bearing glycoconjugates that adorn mature leukocytes and HSPCs, as well as malignant cells, thereby permitting these cells to extravasate into various tissues. E-selectin expression is induced on microvascular endothelial cells within inflammatory loci at all tissues. However, conspicuously, E-selectin is constitutively expressed within microvessels in skin and marrow and, additionally, is inducibly expressed at these sites. Within the marrow, E-selectin receptor/ligand interactions promote lodgment of HSPCs and their malignant counterparts within hematopoietic growth-promoting microenvironments, collectively known as \"vascular niches\". Indeed, E-selectin receptor/ligand interactions have been reported to regulate both hematopoietic stem, and leukemic, cell proliferative dynamics. As such, signaling induced via engagement of E-selectin ligands is gaining interest as a critical mediator of homeostatic and malignant hematopoiesis, and this review will present current perspectives on the glycoconjugates mediating E-selectin receptor/ligand interactions and their currently defined role(s) in leukemogenesis.","PeriodicalId":50875,"journal":{"name":"Advances in Cancer Research","volume":"157 ","pages":"229-250"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9735209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Collaborative Spirit Drives the Field of Tumor Glycobiology: A Preface to Special Volume on Cancer Glycobiology. 协作精神推动肿瘤糖生物学领域：癌症糖生物学特刊序言。

2区医学

Advances in Cancer Research Pub Date : 2023-01-01 DOI: 10.1016/S0065-230X(23)00010-6

Charles J Dimitroff, Karen L Abbott

引用次数: 0

The epigenetic regulation of cancer cell recovery from therapy exposure and its implications as a novel therapeutic strategy for preventing disease recurrence. 癌症细胞从治疗暴露中恢复的表观遗传调控及其作为预防疾病复发的新治疗策略的意义。

2区医学

Advances in Cancer Research Pub Date : 2023-01-01 DOI: 10.1016/bs.acr.2022.11.001

Christiana O Appiah, Manjulata Singh, Lauren May, Ishita Bakshi, Ashish Vaidyanathan, Paul Dent, Gordon Ginder, Steven Grant, Harry Bear, Joseph Landry

{"title":"The epigenetic regulation of cancer cell recovery from therapy exposure and its implications as a novel therapeutic strategy for preventing disease recurrence.","authors":"Christiana O Appiah, Manjulata Singh, Lauren May, Ishita Bakshi, Ashish Vaidyanathan, Paul Dent, Gordon Ginder, Steven Grant, Harry Bear, Joseph Landry","doi":"10.1016/bs.acr.2022.11.001","DOIUrl":"https://doi.org/10.1016/bs.acr.2022.11.001","url":null,"abstract":"The ultimate goal of cancer therapy is the elimination of disease from patients. Most directly, this occurs through therapy-induced cell death. Therapy-induced growth arrest can also be a desirable outcome, if prolonged. Unfortunately, therapy-induced growth arrest is rarely durable and the recovering cell population can contribute to cancer recurrence. Consequently, therapeutic strategies that eliminate residual cancer cells reduce opportunities for recurrence. Recovery can occur through diverse mechanisms including quiescence or diapause, exit from senescence, suppression of apoptosis, cytoprotective autophagy, and reductive divisions resulting from polyploidy. Epigenetic regulation of the genome represents a fundamental regulatory mechanism integral to cancer-specific biology, including the recovery from therapy. Epigenetic pathways are particularly attractive therapeutic targets because they are reversible, without changes in DNA, and are catalyzed by druggable enzymes. Previous use of epigenetic-targeting therapies in combination with cancer therapeutics has not been widely successful because of either unacceptable toxicity or limited efficacy. The use of epigenetic-targeting therapies after a significant interval following initial cancer therapy could potentially reduce the toxicity of combination strategies, and possibly exploit essential epigenetic states following therapy exposure. This review examines the feasibility of targeting epigenetic mechanisms using a sequential approach to eliminate residual therapy-arrested populations, that might possibly prevent recovery and disease recurrence.","PeriodicalId":50875,"journal":{"name":"Advances in Cancer Research","volume":"158 ","pages":"337-385"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9335662","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1