癌症耐药(英文)最新文献_第2页

Cancer-associated fibroblast cell surface markers as potential biomarkers or therapeutic targets in lung cancer. 作为肺癌潜在生物标记物或治疗靶点的癌症相关成纤维细胞表面标记物。

IF 4.6

癌症耐药(英文) Pub Date : 2024-09-10 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2024.55

Samaneh Tokhanbigli, Mehra Haghi, Kamal Dua, Brian Gregory George Oliver

{"title":"Cancer-associated fibroblast cell surface markers as potential biomarkers or therapeutic targets in lung cancer.","authors":"Samaneh Tokhanbigli, Mehra Haghi, Kamal Dua, Brian Gregory George Oliver","doi":"10.20517/cdr.2024.55","DOIUrl":"https://doi.org/10.20517/cdr.2024.55","url":null,"abstract":"Cancer-associated fibroblasts (CAFs) are the vital constituent of the tumor microenvironment, and in communication with other cells, they contribute to tumor progression and metastasis. Fibroblasts are the proposed origin of CAFs, which are mediated by pro-inflammatory cytokines and the recruitment of immune cells akin to wound healing. Although various studies have identified different subpopulations of CAFs in lung cancer, the heterogeneity of CAFs, particularly in lung cancer, and their potential as a therapeutic target remain largely unknown. Notwithstanding CAFs were previously thought to have predominantly tumor-promoting features, their pro- or anti-tumorigenic properties may depend on various conditions and cell origins. The absence of distinct markers to identify CAF subpopulations presents obstacles to the successful therapeutic targeting and treatment of CAFs in cancer. Human clinical and animal studies targeting CAFs have shown that targeting CAFs exacerbates the disease progression, suggesting that subpopulations of CAFs may exert opposing functions in cancer progression. Therefore, it is essential to pinpoint specific markers capable of characterizing these subpopulations and revealing their mechanisms of function. The cell-specific surface markers of CAFs will serve as an initial step in investigating precise CAF subpopulations and their role in diagnosing and targeting therapy against cancer-promoting CAF subsets in lung cancer.","PeriodicalId":70759,"journal":{"name":"癌症耐药(英文)","volume":"7 ","pages":"32"},"PeriodicalIF":4.6,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11472577/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142482158","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Research progress on the role and mechanism of circular RNA in drug resistance of head and neck squamous cell carcinoma. 环状 RNA 在头颈部鳞状细胞癌耐药性中的作用和机制的研究进展。

IF 4.6

癌症耐药(英文) Pub Date : 2024-09-02 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2024.57

Hongli Zeng, Junshang Ge, Yi Meng, Qian Wang, Mei Yang, Zhaoyang Zeng, Wei Xiong, Xuyu Zu

引用次数: 0

The role of circRNAs and miRNAs in drug resistance and targeted therapy responses in breast cancer. circRNA 和 miRNA 在乳腺癌耐药性和靶向治疗反应中的作用。

IF 4.6

癌症耐药(英文) Pub Date : 2024-08-20 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2024.62

Meilan Zhang, Zhaokuan Zheng, Shouliang Wang, Ruihan Liu, Mengli Zhang, Zhiyun Guo, Hao Wang, Weige Tan

引用次数: 0

The uniqueness of ABCB5 as a full transporter ABCB5FL and a half-transporter-like ABCB5β. ABCB5 作为全转运体 ABCB5FL 和半转运体类 ABCB5β 的独特性。

IF 4.6

癌症耐药(英文) Pub Date : 2024-08-07 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2024.56

Louise Gerard, Jean-Pierre Gillet

{"title":"The uniqueness of ABCB5 as a full transporter ABCB5FL and a half-transporter-like ABCB5β.","authors":"Louise Gerard, Jean-Pierre Gillet","doi":"10.20517/cdr.2024.56","DOIUrl":"https://doi.org/10.20517/cdr.2024.56","url":null,"abstract":"The ABCB5 gene encodes several isoforms, including two transporters (i.e., ABCB5FL, ABCB5β) and several soluble proteins, such as ABCB5α which has been hypothesized to have a regulatory function. ABCB5FL is a full ABC transporter and is expressed in the testis and prostate, whereas ABCB5β is an atypical half-transporter with a ubiquitous expression pattern. ABCB5β has been shown to mark cancer stem cells in several cancer types. In addition, ABCB5β and ABCB5FL have been shown to play a role in tumorigenesis and multidrug resistance. However, ABCB5β shares its entire protein sequence with ABCB5FL, making them difficult to distinguish. It cannot be excluded that some biological effects described for one transporter may be mediated by the other isoform. Therefore, it is difficult to interpret the available data and some controversies remain regarding their function in cancer cells. In this review, we discuss the data collected on ABCB5 isoforms over the last 20 years and propose a common ground on which we can build further to unravel the pathophysiological roles of ABCB5 transporters.","PeriodicalId":70759,"journal":{"name":"癌症耐药(英文)","volume":"7 ","pages":"29"},"PeriodicalIF":4.6,"publicationDate":"2024-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11391348/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142302166","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Unraveling the complexity of drug resistance mechanisms to SINE, T cell-engaging therapies and CELMoDs in multiple myeloma: a comprehensive review. 揭示多发性骨髓瘤中SINE、T细胞激活疗法和CELMoDs耐药机制的复杂性：综述。

IF 4.6

癌症耐药(英文) Pub Date : 2024-06-26 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2024.39

Jacqueline Schütt, Kerstin Brinkert, Andrzej Plis, Tino Schenk, Annamaria Brioli

引用次数: 0

Inhibition of glutaminolysis alone and in combination with HDAC inhibitor has anti-myeloma therapeutic effects. 单独或与 HDAC 抑制剂联合抑制谷氨酰胺分解具有抗骨髓瘤治疗效果。

IF 4.6

癌症耐药(英文) Pub Date : 2024-06-24 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2024.35

Seiichi Okabe, Yuko Tanaka, Mitsuru Moriyama, Akihiko Gotoh

{"title":"Inhibition of glutaminolysis alone and in combination with HDAC inhibitor has anti-myeloma therapeutic effects.","authors":"Seiichi Okabe, Yuko Tanaka, Mitsuru Moriyama, Akihiko Gotoh","doi":"10.20517/cdr.2024.35","DOIUrl":"https://doi.org/10.20517/cdr.2024.35","url":null,"abstract":"Aim: This study aimed to investigate drug candidates and their efficacy in treating refractory multiple myeloma (MM) despite significant therapeutic advances and the introduction of novel agents. Our study focused on how myeloma cells mediate the metabolic pathways essential for survival. Therefore, we examined the role of glutaminolysis in this process. Methods: We investigated the role of glutaminolysis in myeloma cell growth. In addition, we analyzed the ability of CB-839 (telaglenastat), a glutaminase (GLS) inhibitor, to suppress myeloma cell proliferation and enhance the sensitivity to histone deacetylase (HDAC) inhibitors. Results: Glutamate deprivation significantly reduced MM cell proliferation. We observed an upregulation of GLS1 expression in MM cell lines compared to that in normal controls. CB-839 inhibits MM cell proliferation in a dose-dependent manner, resulting in enhanced cytotoxicity. Additionally, intracellular α-ketoglutarate and nicotinamide adenine dinucleotide phosphate levels decreased after CB-839 administration. Combining panobinostat with CB-839 resulted in enhanced cytotoxicity and increased caspase 3/7 activity. Cells transfected with GLS shRNA exhibited reduced cell viability and elevated sub-G1 phase according to cell cycle analysis results. Compared to control cells, these cells also showed increased sensitivity to panobinostat. Conclusion: Glutaminolysis contributes to the viability of MM cells, and the GLS inhibitor CB-839 has been proven to be an effective treatment for enhancing the cytotoxic effect of HDAC inhibition. These results are clinically relevant and suggest that CB-839 is a potential therapeutic candidate for patients with MM.","PeriodicalId":70759,"journal":{"name":"癌症耐药(英文)","volume":"7 ","pages":"25"},"PeriodicalIF":4.6,"publicationDate":"2024-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11267151/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141762996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Recent advanced lipid-based nanomedicines for overcoming cancer resistance. 用于克服癌症抗药性的最新先进脂基纳米药物。

IF 4.6

癌症耐药(英文) Pub Date : 2024-06-21 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2024.19

Piroonrat Dechbumroong, Runjing Hu, Wisawat Keaswejjareansuk, Katawut Namdee, Xing-Jie Liang

{"title":"Recent advanced lipid-based nanomedicines for overcoming cancer resistance.","authors":"Piroonrat Dechbumroong, Runjing Hu, Wisawat Keaswejjareansuk, Katawut Namdee, Xing-Jie Liang","doi":"10.20517/cdr.2024.19","DOIUrl":"https://doi.org/10.20517/cdr.2024.19","url":null,"abstract":"The increasing prevalence of cancer drug resistance not only critically limits the efficiency of traditional therapies but also causes relapses or recurrences of cancer. Consequently, there remains an urgent need to address the intricate landscape of drug resistance beyond traditional cancer therapies. Recently, nanotechnology has played an important role in the field of various drug delivery systems for the treatment of cancer, especially therapy-resistant cancer. Among advanced nanomedicine technologies, lipid-based nanomaterials have emerged as effective drug carriers for cancer treatment, significantly improving therapeutic effects. Due to their biocompatibility, simplicity of preparation, and potential for functionalization, lipid-based nanomaterials are considered powerful competitors for resistant cancer. In this review, an overview of lipid-based nanomaterials for addressing cancer resistance is discussed. We summarize the recent progress in overcoming drug resistance in cancer by these lipid-based nanomaterials, and highlight their potential in future applications to reverse cancer resistance.","PeriodicalId":70759,"journal":{"name":"癌症耐药(英文)","volume":"7 ","pages":"24"},"PeriodicalIF":4.6,"publicationDate":"2024-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11267154/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141762997","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Emerging role of MYB transcription factors in cancer drug resistance. MYB 转录因子在癌症抗药性中的新作用。

癌症耐药(英文) Pub Date : 2024-04-30 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2023.158

Bernhard Biersack, Michael Höpfner

{"title":"Emerging role of MYB transcription factors in cancer drug resistance.","authors":"Bernhard Biersack, Michael Höpfner","doi":"10.20517/cdr.2023.158","DOIUrl":"10.20517/cdr.2023.158","url":null,"abstract":"Decades ago, the viral myeloblastosis oncogene v-myb was identified as a gene responsible for the development of avian leukemia. However, the relevance of MYB proteins for human cancer diseases, in particular for solid tumors, remained basically unrecognized for a very long time. The human family of MYB transcription factors comprises MYB (c-MYB), MYBL2 (b-MYB), and MYBL1 (a-MYB), which are overexpressed in several cancers and are associated with cancer progression and resistance to anticancer drugs. In addition to overexpression, the presence of activated MYB-fusion proteins as tumor drivers was described in certain cancers. The identification of anticancer drug resistance mediated by MYB proteins and their underlying mechanisms are of great importance in understanding failures of current therapies and establishing new and more efficient therapy regimens. In addition, new drug candidates targeting MYB transcription factor activity and signaling have emerged as a promising class of potential anticancer therapeutics that could tackle MYB-dependent drug-resistant cancers in a more selective way. This review describes the correlation of MYB transcription factors with the formation and persistence of cancer resistance to various approved and investigational anticancer drugs.","PeriodicalId":70759,"journal":{"name":"癌症耐药(英文)","volume":"7 ","pages":"15"},"PeriodicalIF":0.0,"publicationDate":"2024-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11149108/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141247867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

HER3-targeted therapy: the mechanism of drug resistance and the development of anticancer drugs. HER3靶向疗法：耐药机制与抗癌药物的开发。

癌症耐药(英文) Pub Date : 2024-04-29 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2024.11

Huilan Zeng, Wei Wang, Lin Zhang, Zhenghong Lin

{"title":"HER3-targeted therapy: the mechanism of drug resistance and the development of anticancer drugs.","authors":"Huilan Zeng, Wei Wang, Lin Zhang, Zhenghong Lin","doi":"10.20517/cdr.2024.11","DOIUrl":"10.20517/cdr.2024.11","url":null,"abstract":"Human epidermal growth factor receptor 3 (HER3), which is part of the HER family, is aberrantly expressed in various human cancers. Since HER3 only has weak tyrosine kinase activity, when HER3 ligand neuregulin 1 (NRG1) or neuregulin 2 (NRG2) appears, activated HER3 contributes to cancer development and drug resistance by forming heterodimers with other receptors, mainly including epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER2). Inhibition of HER3 and its downstream signaling, including PI3K/AKT, MEK/MAPK, JAK/STAT, and Src kinase, is believed to be necessary to conquer drug resistance and improve treatment efficiency. Until now, despite multiple anti-HER3 antibodies undergoing preclinical and clinical studies, none of the HER3-targeted therapies are licensed for utilization in clinical cancer treatment because of their safety and efficacy. Therefore, the development of HER3-targeted drugs possessing safety, tolerability, and sensitivity is crucial for clinical cancer treatment. This review summarizes the progress of the mechanism of HER3 in drug resistance, the HER3-targeted therapies that are conducted in preclinical and clinical trials, and some emerging molecules that could be used as future designed drugs for HER3, aiming to provide insights for future research and development of anticancer drugs targeting HER3.","PeriodicalId":70759,"journal":{"name":"癌症耐药(英文)","volume":"7 ","pages":"14"},"PeriodicalIF":0.0,"publicationDate":"2024-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11149107/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141247868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Dysregulation of calcium homeostasis in cancer and its role in chemoresistance. 癌症中的钙平衡失调及其在化疗抗药性中的作用。

癌症耐药(英文) Pub Date : 2024-03-15 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2023.145

Neema Kumari, Narasimha Pullaguri, Subha Narayan Rath, Ashish Bajaj, Vikas Sahu, Kranti Kiran Reddy Ealla

{"title":"Dysregulation of calcium homeostasis in cancer and its role in chemoresistance.","authors":"Neema Kumari, Narasimha Pullaguri, Subha Narayan Rath, Ashish Bajaj, Vikas Sahu, Kranti Kiran Reddy Ealla","doi":"10.20517/cdr.2023.145","DOIUrl":"10.20517/cdr.2023.145","url":null,"abstract":"Globally, cancer, as a major public health concern, poses a severe threat to people's well-being. Advanced and specialized therapies can now cure the majority of people with early-stage cancer. However, emerging resistance to traditional and novel chemotherapeutic drugs remains a serious issue in clinical medicine. Chemoresistance often leads to cancer recurrence, metastasis, and increased mortality, accounting for 90% of chemotherapy failures. Thus, it is important to understand the molecular mechanisms of chemoresistance and find novel therapeutic approaches for cancer treatment. Among the several factors responsible for chemoresistance, calcium (Ca2+) dysregulation plays a significant role in cancer progression and chemoresistance. Therefore, targeting this derailed Ca2+ signalling for cancer therapy has become an emerging research area. Of note, the Ca2+ signal and its proteins are a multifaceted and potent tool by which cells achieve specific outcomes. Depending on cell survival needs, Ca2+ is either upregulated or downregulated in both chemosensitive and chemoresistant cancer cells. Consequently, the appropriate treatment should be selected based on Ca2+ signalling dysregulation. This review discusses the role of Ca2+ in cancer cells and the targeting of Ca2+ channels, pumps, and exchangers. Furthermore, we have emphasised the role of Ca2+ in chemoresistance and therapeutic strategies. In conclusion, targeting Ca2+ signalling is a multifaceted process. Methods such as site-specific drug delivery, target-based drug-designing, and targeting two or more Ca2+ proteins simultaneously may be explored; however, further clinical studies are essential to validate Ca2+ blockers' anti-cancer efficacy.","PeriodicalId":70759,"journal":{"name":"癌症耐药(英文)","volume":"7 ","pages":"11"},"PeriodicalIF":0.0,"publicationDate":"2024-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10951838/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140178025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0