Advances in Cancer Research最新文献_第5页

Preface. 前言。

2区医学

Advances in Cancer Research Pub Date : 2023-01-01 DOI: 10.1016/S0065-230X(23)00049-0

Luni Emdad, Azeddine Atfi, Rajan Gogna, Jose G Trevino, Paul B Fisher

引用次数: 0

In vivo models of pancreatic ductal adenocarcinoma. 胰腺导管腺癌体内模型。

2区医学

Advances in Cancer Research Pub Date : 2023-01-01 Epub Date: 2023-03-23 DOI: 10.1016/bs.acr.2023.02.002

Vignesh Vudatha, Kelly M Herremans, Devon C Freudenberger, Christopher Liu, Jose G Trevino

{"title":"In vivo models of pancreatic ductal adenocarcinoma.","authors":"Vignesh Vudatha, Kelly M Herremans, Devon C Freudenberger, Christopher Liu, Jose G Trevino","doi":"10.1016/bs.acr.2023.02.002","DOIUrl":"10.1016/bs.acr.2023.02.002","url":null,"abstract":"Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy with high mortality rate. Within the next decade, PDAC is projected to become the second leading cause of cancer-associated death in the United States. Understanding the pathophysiology of PDAC tumorigenesis and metastases is crucial toward developing new therapeutics. One of the challenges in cancer research is generating in vivo models that closely recapitulate the genomic, histological, and clinical characteristics of human tumors. An ideal model for PDAC not only captures the tumor and stromal environment of human disease, but also allows for mutational control and is easy to reproduce in terms of time and cost. In this review, we highlight evolution of in vivo models for PDAC including spontaneous tumors models (i.e., chemical induction, genetic modification, viral delivery), implantation models including patient derived xenografts (PDX), and humanized PDX. We discuss the implementation of each system and evaluate the benefits and shortcomings of these models. Overall, this review provides a broad overview of prior and current techniques of in vivo PDAC modeling and their associated challenges.","PeriodicalId":50875,"journal":{"name":"Advances in Cancer Research","volume":"159 ","pages":"75-112"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10000191","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

Setting sail: Maneuvering SHP2 activity and its effects in cancer. 扬帆起航：操纵SHP2活性及其在癌症中的作用。

2区医学

Advances in Cancer Research Pub Date : 2023-01-01 Epub Date: 2023-04-17 DOI: 10.1016/bs.acr.2023.03.003

Colin L Welsh, Sarah Allen, Lalima K Madan

{"title":"Setting sail: Maneuvering SHP2 activity and its effects in cancer.","authors":"Colin L Welsh, Sarah Allen, Lalima K Madan","doi":"10.1016/bs.acr.2023.03.003","DOIUrl":"10.1016/bs.acr.2023.03.003","url":null,"abstract":"Since the discovery of tyrosine phosphorylation being a critical modulator of cancer signaling, proteins regulating phosphotyrosine levels in cells have fast become targets of therapeutic intervention. The nonreceptor protein tyrosine phosphatase (PTP) coded by the PTPN11 gene \"SHP2\" integrates phosphotyrosine signaling from growth factor receptors into the RAS/RAF/ERK pathway and is centrally positioned in processes regulating cell development and oncogenic transformation. Dysregulation of SHP2 expression or activity is linked to tumorigenesis and developmental defects. Even as a compelling anti-cancer target, SHP2 was considered \"undruggable\" for a long time owing to its conserved catalytic PTP domain that evaded drug development. Recently, SHP2 has risen from the \"undruggable curse\" with the discovery of small molecules that manipulate its intrinsic allostery for effective inhibition. SHP2's unique domain arrangement and conformation(s) allow for a truly novel paradigm of inhibitor development relying on skillful targeting of noncatalytic sites on proteins. In this review we summarize the biological functions, signaling properties, structural attributes, allostery and inhibitors of SHP2.","PeriodicalId":50875,"journal":{"name":"Advances in Cancer Research","volume":"160 ","pages":"17-60"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10500121/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10625904","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Tumor microenvironment interactions with cancer stem cells in pancreatic ductal adenocarcinoma. 胰腺导管腺癌中肿瘤微环境与癌症干细胞的相互作用

2区医学

Advances in Cancer Research Pub Date : 2023-01-01 Epub Date: 2023-04-27 DOI: 10.1016/bs.acr.2023.02.007

António M Palma, Grace G Bushnell, Max S Wicha, Rajan Gogna

{"title":"Tumor microenvironment interactions with cancer stem cells in pancreatic ductal adenocarcinoma.","authors":"António M Palma, Grace G Bushnell, Max S Wicha, Rajan Gogna","doi":"10.1016/bs.acr.2023.02.007","DOIUrl":"10.1016/bs.acr.2023.02.007","url":null,"abstract":"Pancreatic ductal adenocarcinoma (PDAC) is the most common type of pancreatic cancer in the United States. Additionally, the low survival rate makes PDAC the third-leading cause of cancer-related mortality in the United States, and it is projected that by 2030, it will become the second-leading cause of cancer mortality. Several biological factors contribute to PDAC aggressiveness, and their understanding will narrow the gap from biology to clinical care of PDAC, leading to earlier diagnoses and the development of better treatment options. In this review, we describe the origins of PDAC highlighting the role of cancer stem cells (CSC). CSC, also known as tumor initiating cells, which exhibit a unique metabolism that allows them to maintain a highly plastic, quiescent, immune- and therapy-evasive state. However, CSCs can exit quiescence during proliferation and differentiation, with the capacity to form tumors while constituting a small population in tumor tissues. Tumorigenesis depends on the interactions between CSCs and other cellular and non-cellular components in the microenvironment. These interactions are fundamental to support CSC stemness and are maintained throughout tumor development and metastasis. PDAC is characterized by a massive desmoplastic reaction, which result from the deposition of high amounts of extracellular matrix components by stromal cells. Here we review how this generates a favorable environment for tumor growth by protecting tumor cells from immune responses and chemotherapy and inducing tumor cell proliferation and migration, leading to metastasis formation ultimately leading to death. We emphasize the interactions between CSCs and the tumor microenvironment leading to metastasis formation and posit that better understanding and targeting of these interactions will improve patient outcomes.","PeriodicalId":50875,"journal":{"name":"Advances in Cancer Research","volume":"159 ","pages":"343-372"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11218813/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9656740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Role of O-GlcNAcylation on cancer stem cells: Connecting nutrient sensing to cell plasticity. O-GlcNAcylation 在癌症干细胞中的作用：连接营养传感与细胞可塑性。

2区医学

Advances in Cancer Research Pub Date : 2023-01-01 Epub Date: 2022-07-28 DOI: 10.1016/bs.acr.2022.06.002

Giang Le Minh, Mauricio J Reginato

{"title":"Role of O-GlcNAcylation on cancer stem cells: Connecting nutrient sensing to cell plasticity.","authors":"Giang Le Minh, Mauricio J Reginato","doi":"10.1016/bs.acr.2022.06.002","DOIUrl":"10.1016/bs.acr.2022.06.002","url":null,"abstract":"Tumor growth and metastasis can be promoted by a small sub-population of cancer cells, termed cancer stem-like cells (CSCs). While CSCs possess capability in self-renewing and differentiating, the hierarchy of CSCs during tumor growth is highly plastic. This plasticity in CSCs fate and function can be regulated by signals from the tumor microenvironment. One emerging pathway in CSCs that connects the alteration in microenvironment and signaling network in cancer cells is the hexosamine biosynthetic pathway (HBP). The final product of HBP, UDP-N-acetylglucosamine (UDP-GlcNAc), is utilized for glycosylating of membrane and secreted proteins, but also nuclear and cytoplasmic proteins by the post-translational modification O-GlcNAcylation. O-GlcNAcylation and its enzyme, O-GlcNAc transferase (OGT), are upregulated in nearly all cancers and been linked to regulate many cancer cell phenotypes. Recent studies have begun to connect OGT and O-GlcNAcylation to regulation of CSCs. In this review, we will discuss the emerging role of OGT and O-GlcNAcylation in regulating fate and plasticity of CSCs, as well as the potential in targeting OGT/O-GlcNAcylation in CSCs.","PeriodicalId":50875,"journal":{"name":"Advances in Cancer Research","volume":"157 ","pages":"195-228"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9895886/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9292439","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Interplay between MAP kinases and tumor microenvironment: Opportunity for immunotherapy in pancreatic cancer. MAP 激酶与肿瘤微环境之间的相互作用：胰腺癌免疫疗法的机遇。

2区医学

Advances in Cancer Research Pub Date : 2023-01-01 Epub Date: 2023-03-10 DOI: 10.1016/bs.acr.2023.02.003

Sandeep Kumar, Sunil Kumar Singh, Piush Srivastava, Swathi Suresh, Basabi Rana, Ajay Rana

{"title":"Interplay between MAP kinases and tumor microenvironment: Opportunity for immunotherapy in pancreatic cancer.","authors":"Sandeep Kumar, Sunil Kumar Singh, Piush Srivastava, Swathi Suresh, Basabi Rana, Ajay Rana","doi":"10.1016/bs.acr.2023.02.003","DOIUrl":"10.1016/bs.acr.2023.02.003","url":null,"abstract":"Pancreatic Ductal Adenocarcinoma (PDAC), commonly called pancreatic cancer, is aggressive cancer usually detected at a late stage, limiting treatment options with modest clinical responses. It is projected that by 2030, PDAC will be the second most common cause of cancer-related mortality in the United States. Drug resistance in PDAC is common and significantly affects patients' overall survival (OS). Oncogenic KRAS mutations are nearly uniform in PDAC, affecting over 90% of patients. However, effective drugs directed to target prevalent KRAS mutants in pancreatic cancer are not in clinical practice. Accordingly, efforts are continued on identifying alternative druggable target(s) or approaches to improve patient outcomes with PDAC. In most PDAC cases, the KRAS mutations turn-on the RAF-MEK-MAPK pathways, leading to pancreatic tumorigenesis. The MAPK signaling cascade (MAP4K→MAP3K→MAP2K→MAPK) plays a central role in the pancreatic cancer tumor microenvironment (TME) and chemotherapy resistance. The immunosuppressive pancreatic cancer TME is another unfavorable factor affecting the therapeutic efficacy of chemotherapy and immunotherapy. The immune checkpoint proteins (ICPs), including CTLA-4, PD-1, PD-L1, and PD-L2, are critical players in T cell dysfunction and pancreatic tumor cell growth. Here, we review the activation of MAPKs, a molecular trait of KRAS mutations and their impact on pancreatic cancer TME, chemoresistance, and expression of ICPs that could influence the clinical outcomes in PDAC patients. Therefore, understanding the interplay between MAPK pathways and TME could help to design rational therapy combining immunotherapy and MAPK inhibitors for pancreatic cancer treatment.","PeriodicalId":50875,"journal":{"name":"Advances in Cancer Research","volume":"159 ","pages":"113-143"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9892361","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

Mechanical factors driving cancer progression. 推动癌症发展的机械因素。

2区医学

Advances in Cancer Research Pub Date : 2023-01-01 Epub Date: 2023-07-16 DOI: 10.1016/bs.acr.2023.06.002

Jessanne Y Lichtenberg, Sydnie Tran, Priscilla Y Hwang

引用次数: 0

Mass spectrometry based biomarkers for early detection of HCC using a glycoproteomic approach. 基于质谱的生物标志物，利用糖蛋白组学方法早期检测 HCC。

2区医学

Advances in Cancer Research Pub Date : 2023-01-01 Epub Date: 2022-09-06 DOI: 10.1016/bs.acr.2022.07.005

Yehia Mechref, Wenjing Peng, Sakshi Gautam, Parisa Ahmadi, Yu Lin, Jianhui Zhu, Jie Zhang, Suyu Liu, Amit G Singal, Neehar D Parikh, David M Lubman

引用次数: 0

Histone deacetylase inhibitors as sanguine epitherapeutics against the deadliest lung cancer. 组蛋白去乙酰化酶抑制剂治疗致命肺癌的疗效。

2区医学

Advances in Cancer Research Pub Date : 2023-01-01 DOI: 10.1016/bs.acr.2022.12.003

Shabir Ahmad Ganai, Basit Amin Shah, Manzoor Ahmad Yatoo

{"title":"Histone deacetylase inhibitors as sanguine epitherapeutics against the deadliest lung cancer.","authors":"Shabir Ahmad Ganai, Basit Amin Shah, Manzoor Ahmad Yatoo","doi":"10.1016/bs.acr.2022.12.003","DOIUrl":"https://doi.org/10.1016/bs.acr.2022.12.003","url":null,"abstract":"The back-breaking resistance mechanisms generated by lung cancer cells against epidermal growth factor receptor (EGFR), KRAS and Janus kinase 2 (JAK2) directed therapies strongly prioritizes the requirement of novel therapies which are perfectly tolerated, potentially cytotoxic and can reinstate the drug-sensitivity in lung cancer cells. Enzymatic proteins modifying the post-translational modifications of nucleosome-integrated histone substrates are appearing as current targets for defeating various malignancies. Histone deacetylases (HDACs) are hyperexpressed in diverse lung cancer types. Blocking the active pocket of these acetylation erasers through HDAC inhibitors (HDACi) has come out as an optimistic therapeutic recourse for annihilating lung cancer. This article in the beginning gives an overview about lung cancer statistics and predominant lung cancer types. Succeeding this, compendium about conventional therapies and their serious drawbacks has been provided. Then, connection of uncommon expression of classical HDACs in lung cancer onset and expansion has been detailed. Moreover, keeping the main theme in view this article deeply discusses HDACi in the context of aggressive lung cancer as single agents and spotlights various molecular targets suppressed or induced by these inhibitors for engendering cytotoxic effect. Most particularly, the raised pharmacological effects achieved on using these inhibitors in concerted form with other therapeutic molecules and the cancer-linked pathways altered by this procedure are described. The positive direction towards further heightening of efficacy and the pressing requirement of exhaustive clinical assessment has been proposed as a new focus point.","PeriodicalId":50875,"journal":{"name":"Advances in Cancer Research","volume":"158 ","pages":"163-198"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9335658","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

From ecology to oncology: To understand cancer stem cell dormancy, ask a Brine shrimp (Artemia). 从生态学到肿瘤学：要了解癌症干细胞休眠，请向卤水虾（Artemia）提问。

2区医学

Advances in Cancer Research Pub Date : 2023-01-01 Epub Date: 2023-01-10 DOI: 10.1016/bs.acr.2022.12.004

Christopher R Wood, Wen-Tao Wu, Yao-Shun Yang, Jin-Shu Yang, Yongmei Xi, Wei-Jun Yang

{"title":"From ecology to oncology: To understand cancer stem cell dormancy, ask a Brine shrimp (Artemia).","authors":"Christopher R Wood, Wen-Tao Wu, Yao-Shun Yang, Jin-Shu Yang, Yongmei Xi, Wei-Jun Yang","doi":"10.1016/bs.acr.2022.12.004","DOIUrl":"10.1016/bs.acr.2022.12.004","url":null,"abstract":"The brine shrimp (Artemia), releases embryos that can remain dormant for up to a decade. Molecular and cellular level controlling factors of dormancy in Artemia are now being recognized or applied as active controllers of dormancy (quiescence) in cancers. Most notably, the epigenetic regulation by SET domain-containing protein 4 (SETD4), is revealed as highly conserved and the primary control factor governing the maintenance of cellular dormancy from Artemia embryonic cells to cancer stem cells (CSCs). Conversely, DEK, has recently emerged as the primary factor in the control of dormancy exit/reactivation, in both cases. The latter has been now successfully applied to the reactivation of quiescent CSCs, negating their resistance to therapy and leading to their subsequent destruction in mouse models of breast cancer, without recurrence or metastasis potential. In this review, we introduce the many mechanisms of dormancy from Artemia ecology that have been translated into cancer biology, and herald Artemia's arrival on the model organism stage. We show how Artemia studies have unlocked the mechanisms of the maintenance and termination of cellular dormancy. We then discuss how the antagonistic balance of SETD4 and DEK fundamentally controls chromatin structure and consequently governs CSCs function, chemo/radiotherapy resistance, and dormancy in cancers. Many key stages from transcription factors to small RNAs, tRNA trafficking, molecular chaperones, ion channels, and links with various pathways and aspects of signaling are also noted, all of which link studies in Artemia to those of cancer on a molecular and/or cellular level. We particularly emphasize that the application of such emerging factors as SETD4 and DEK may open new and clear avenues for the treatment for various human cancers.","PeriodicalId":50875,"journal":{"name":"Advances in Cancer Research","volume":"158 ","pages":"199-231"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9335659","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