Molecular and Cellular Oncology最新文献_第2页

The Role of V-ATPase ATP6V0D1 Subunit in Chemoresistance and Ellipticine-Induced Cytoplasmic Vacuolation in Neuroblastoma Cells. v - atp酶ATP6V0D1亚基在神经母细胞瘤细胞化疗耐药和椭圆素诱导的细胞质空泡化中的作用。

IF 2.6

Molecular and Cellular Oncology Pub Date : 2025-06-17 eCollection Date: 2025-01-01 DOI: 10.1080/23723556.2025.2518774

M Rychla, J Hrabeta, P Jencova, N Podhorska, T Eckschlager

{"title":"The Role of V-ATPase ATP6V0D1 Subunit in Chemoresistance and Ellipticine-Induced Cytoplasmic Vacuolation in Neuroblastoma Cells.","authors":"M Rychla, J Hrabeta, P Jencova, N Podhorska, T Eckschlager","doi":"10.1080/23723556.2025.2518774","DOIUrl":"10.1080/23723556.2025.2518774","url":null,"abstract":"Drug resistance remains a major obstacle in neuroblastoma treatment. Lysosomal sequestration, facilitated by the V-ATPase proton pump, is one of the mechanisms of chemoresistance. Overexpression of the ATP6V0D1 subunit of V-ATPase, previously reported in various cancers, was also observed in ellipticine-resistant neuroblastoma cells in our study. Neuroblastoma cells also exhibited increased lysosomal capacity and vacuolation after ellipticine treatment. Knockdown of ATP6V0D1, but not ATP6V1H, enhanced ellipticine sensitivity, suppressed proliferation and migration, decreased lysosomal uptake, and induced G2/M arrest in neuroblastoma cell lines. Notably, inhibiting another V-ATPase subunit, ATP6V1H, had no effect, highlighting the specific role of ATP6V0D1 in drug resistance. Ellipticine-induced vacuolation, identified as endoplasmic reticulum swelling, lacked evidence of paraptosis. ATP6V0D1 knockdown suppressed this phenomenon, whereas ATP6V1H silencing did not. Our findings underscore the importance of ATP6V0D1 in neuroblastoma and suggest potential therapeutic strategies targeting V-ATPase for overcoming drug resistance.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"12 1","pages":"2518774"},"PeriodicalIF":2.6,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12184147/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144477147","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

GSTP1 knockdown induces metabolic changes affecting energy production and lipid balance in pancreatic cancer cells. GSTP1敲低诱导代谢变化，影响胰腺癌细胞的能量产生和脂质平衡。

IF 2.6

Molecular and Cellular Oncology Pub Date : 2025-06-14 eCollection Date: 2025-01-01 DOI: 10.1080/23723556.2025.2518773

Jenna N Duttenhefner, Katie M Reindl

{"title":"GSTP1 knockdown induces metabolic changes affecting energy production and lipid balance in pancreatic cancer cells.","authors":"Jenna N Duttenhefner, Katie M Reindl","doi":"10.1080/23723556.2025.2518773","DOIUrl":"10.1080/23723556.2025.2518773","url":null,"abstract":"Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer with limited treatment options, underscoring the need for novel therapeutic targets. Metabolic reprogramming is a hallmark of PDAC, enabling tumor cells to sustain rapid proliferation and survive under nutrient-deprived conditions. While glutathione S-transferase pi 1 (GSTP1) is a known regulator of redox homeostasis in PDAC, its role in metabolic adaptation remains unclear. Here, we show that GSTP1 knockdown disrupts PDAC metabolism, leading to downregulation of key metabolic enzymes (ALDH7A1, CPT1A, SLC2A3, PGM1), ATP depletion, mitochondrial dysfunction, and phospholipid remodeling. Phospholipid remodeling, including an increase in phosphatidylcholine (PC) levels, further suggests a compensatory response to metabolic stress. Importantly, GSTP1 knockdown led to elevated lipid peroxidation, increasing 4-hydroxynonenal (4-HNE) accumulation. Treatment with the antioxidant N-acetyl cysteine (NAC) partially restored metabolic gene expression, reinforcing GSTP1's role in the interplay between redox regulation and metabolism in PDAC. By disrupting multiple metabolic pathways, GSTP1 depletion creates potential therapeutic vulnerabilities that could be targeted through metabolic and oxidative stress-inducing therapies to enhance treatment efficacy.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"12 1","pages":"2518773"},"PeriodicalIF":2.6,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12169041/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144310462","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

Increased MLH1, MGMT, and p16INK4a methylation levels in colon mucosa potentially useful as early risk marker of colon cancer. 结肠粘膜中MLH1、MGMT和p16INK4a甲基化水平升高，可能是结肠癌的早期风险标志物。

IF 2.6

Molecular and Cellular Oncology Pub Date : 2025-05-10 eCollection Date: 2025-01-01 DOI: 10.1080/23723556.2025.2503069

Yvonne Wettergren, Peter Rolny, Helena Lindegren, Elisabeth Odin, Victoria Rotter Sopasakis, Simon Keane, Katarina Ejeskär

{"title":"Increased MLH1, MGMT, and p16INK4a methylation levels in colon mucosa potentially useful as early risk marker of colon cancer.","authors":"Yvonne Wettergren, Peter Rolny, Helena Lindegren, Elisabeth Odin, Victoria Rotter Sopasakis, Simon Keane, Katarina Ejeskär","doi":"10.1080/23723556.2025.2503069","DOIUrl":"https://doi.org/10.1080/23723556.2025.2503069","url":null,"abstract":"The genes MutL Homolog 1 (MLH1), O6-methylguanine-DNA methyltransferase (MGMT), and cyclin-dependent kinase inhibitor p16INK4a are commonly downregulated by hypermethylation in colorectal cancer. Long interspersed nucleotide element 1 (LINE-1) can be used as marker for global hypomethylation. This study compared MLH1, MGMT, p16INK4a, and LINE-1 methylation with gene expression in colon tumors, matched non-cancerous mucosa, and control mucosa to identify signs of premalignancy. Tissues were obtained from 20 colon cancer patients and 40 controls. CpG site methylation was quantified by pyrosequencing, expression by qPCR, and MSI/KRAS status by fragment analysis and droplet digital PCR. MLH1, MGMT, and p16INK4a methylation was increasingly higher in control mucosa, non-cancerous mucosa, and tumors. MLH1 expression was lower in tumors compared to non-cancerous mucosa but higher compared to control mucosa. Tumoral LINE-1 methylation correlated negatively with MLH1 (r = -0.51, p = .021) and p16INK4a (r = -0.55, p = .012) methylation, but positively (r = 0.74, p = .0002) with MLH1 expression. A p16INK4a SNP (rs3814960 C>T) was associated with methylation, expression, and MSI/KRAS status. Aberrant methylation of tumor suppressor genes in colon mucosa could be an early cancer risk marker. Control mucosa is a more reliable reference than non-cancerous mucosa when identifying premalignant changes. Extended studies will evaluate the possible association between rs3814960 and cancer susceptibility. Trial registration: NCT03072641.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"12 1","pages":"2503069"},"PeriodicalIF":2.6,"publicationDate":"2025-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12068326/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144052226","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

CHK1 inhibition overcomes gemcitabine resistance in non-small cell lung cancer cell A549. CHK1抑制在非小细胞肺癌细胞A549中克服吉西他滨耐药

IF 2.6

Molecular and Cellular Oncology Pub Date : 2025-04-09 eCollection Date: 2025-01-01 DOI: 10.1080/23723556.2025.2488537

Zhi-Yin Ke, Tian Fu, Xue-Chun Wang, Xuan Ma, Hai-Han Yin, Wen-Xuan Wang, Yong-Jun Liu, Ai-Ling Liang

{"title":"CHK1 inhibition overcomes gemcitabine resistance in non-small cell lung cancer cell A549.","authors":"Zhi-Yin Ke, Tian Fu, Xue-Chun Wang, Xuan Ma, Hai-Han Yin, Wen-Xuan Wang, Yong-Jun Liu, Ai-Ling Liang","doi":"10.1080/23723556.2025.2488537","DOIUrl":"https://doi.org/10.1080/23723556.2025.2488537","url":null,"abstract":"The purpose of the study is mainly to investigate anti proliferation of non-small cell lung cancer A549 cells and its mechanism by inhibition of CHK1 expression combined with gemcitabine. The mRNA and protein levels of genes were analyzed by RT-qPCR and Western blot, respectively. Cell viability was detected by CCK-8 assay and clone formation assay. The detection of the cell cycle was used by Annexin V/7-amino-actinomycin D apoptosis detection kit. Analysis of DNA damage was done by immunofluorescence and alkaline comet assay. The results showed that inhibition of CHK1 and gemcitabine combination significantly reduced the proliferation ability of the two cell lines. We also revealed the degradation of full-length PARP and reduced Bcl-2/Bax ratio on increased apoptosis. Inhibition of CHK1 expression leads to DNA damage, induces phosphorylation of γ-H2AX, and affects the repair of homologous recombination ability through Rad51. Mechanistically, gemcitabine increased phosphorylation-ATR and phosphorylation-CHK1, indicating activation of the DNA repair system and ATR-CHK1-CDC25A pathway. Inhibition of CHK1 resulted in increased synthesis of CDK2/Cyclin A2 and CDK2/Cyclin E1 complexes, and more cells entered the subsequent cell cycle, leading to S phase arrest and mitotic catastrophe. We identified inhibition of CHK1 as a potential treatment for NSCLC and confirmed that inhibition of this kinase could overcome acquired gemcitabine resistance.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"12 1","pages":"2488537"},"PeriodicalIF":2.6,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11988257/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144031300","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

The immunopeptidome of colon cancer cells treated with topoisomerase inhibiting drug reveals differential as well as common endogenous protein sampling and display of MHC I-associated peptides. 拓扑异构酶抑制药物处理的结肠癌细胞的免疫肽球显示了不同的以及共同的内源性蛋白质采样和MHC i相关肽的显示。

IF 2.6

Molecular and Cellular Oncology Pub Date : 2025-03-03 eCollection Date: 2025-01-01 DOI: 10.1080/23723556.2025.2471640

Deepa Bedi, Mohammed Hassan, Alehegne Yirsaw, Biba Vikas, Pran Datta, Temesgen Samuel

{"title":"The immunopeptidome of colon cancer cells treated with topoisomerase inhibiting drug reveals differential as well as common endogenous protein sampling and display of MHC I-associated peptides.","authors":"Deepa Bedi, Mohammed Hassan, Alehegne Yirsaw, Biba Vikas, Pran Datta, Temesgen Samuel","doi":"10.1080/23723556.2025.2471640","DOIUrl":"10.1080/23723556.2025.2471640","url":null,"abstract":"Immunotherapy options for microsatellite stable (MSS) colorectal cancer are currently very limited. The lack of detectably unique or altered immunogens in the tumor microenvironment may be a factor. Radiation and chemotherapy may enhance immunotherapy by increasing cancer cell visibility through Major Histocompatibility Complex I (MHC I) expression. To investigate this, we treated MSS and microsatellite-instable (MSI) colon cancer cells with a topoisomerase inhibitor and analyzed MHC I-associated peptides. Treatment increased peptide numbers by 5% in RKO (MSI) cells and 83% in SW620 (MSS) cells, with 40-50% of peptides being exclusive to treatment. Additionally, clustering analysis revealed a set of peptides with uniquely conserved residues displayed only in treated MSS SW620 cells. Gene Ontology analysis of MHC I-displayed proteins revealed a treatment-induced increase in extracellular vesicle- and nuclear-derived proteins, alongside reduced cytosolic protein sampling. Overall, we present evidence for treatment-inducible differential display of peptides, some of which may affect interactions and functions of immune cells. Given the multitude of factors that modulate the effects of increased MHC I expression and associated peptides, further studies are needed to elucidate the pathophysiological implications of these changes.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"12 1","pages":"2471640"},"PeriodicalIF":2.6,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11881837/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143574152","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

METTL14-mediated m6A modification upregulates HOXB13 expression to activate NF-κB and exacerbate cervical cancer progression. METTL14 介导的 m6A 修饰会上调 HOXB13 的表达，从而激活 NF-κB 并加剧宫颈癌的进展。

IF 2.6

Molecular and Cellular Oncology Pub Date : 2024-11-11 eCollection Date: 2024-01-01 DOI: 10.1080/23723556.2024.2423986

Qian Li, Na Zhao, Xuejing Ding, Jufen Zhao

{"title":"METTL14-mediated m6A modification upregulates HOXB13 expression to activate NF-κB and exacerbate cervical cancer progression.","authors":"Qian Li, Na Zhao, Xuejing Ding, Jufen Zhao","doi":"10.1080/23723556.2024.2423986","DOIUrl":"https://doi.org/10.1080/23723556.2024.2423986","url":null,"abstract":"Cervical cancer (CC) is one of the common malignant tumors in women, and the incidence rate is located in the second place of female tumors. As a major RNA N6-methyladenosine (m6A) methyltransferase, methyltransferase-like 14 (METTL14) is involved in tumor progression by catalyzing methylation modifications in mRNAs. However, the molecular mechanism of METTL14-mediated m6A modification in CC remains not fully revealed. The expression of METTL14 was detected by RT-qPCR and western blot. Cell function was assayed by cell counting kit-8 (CCK-8) assay and flow cytometry analysis. Methylated RNA immunoprecipitation (MeRIP) was used to confirm the relationship between METTL14 and homeobox B13 (HOXB13). In our study, we found that the level of METTL14 was elevated in CC tissues and cells compared with their controls. The inhibition of METTL14 significantly impaired cell proliferation and the epithelial-mesenchymal transition (EMT) process, while also induced apoptosis in HeLa and C33A cells. Furthermore, our findings indicated that homeobox B13 (HOXB13) was a target of METTL14, which positively regulated the expression of HOXB13 in an m6A-dependent manner. Rescue experiments indicated that overexpression of HOXB13 effectively reversed the tumor suppression induced by METTL14 knockdown. Finally, we confirmed that METTL14-modified HOXB13 exerted an oncogenic effect through activation of the nuclear factor kappa B (NF-κB) pathway. In conclusion, our data demonstrated that the m6A modification of HOXB13, mediated by METTL14, facilitated the advancement of CC through targeting the NF-κB pathway, which may be a potential molecular target for the treatment of CC.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"11 1","pages":"2423986"},"PeriodicalIF":2.6,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11556271/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142629584","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

An antibody-drug conjugate for endometrioid carcinoma based on the expression of cell adhesion molecule 1. 基于细胞粘附分子 1 表达的子宫内膜样癌抗体-药物共轭物。

IF 2.6

Molecular and Cellular Oncology Pub Date : 2024-09-05 eCollection Date: 2024-01-01 DOI: 10.1080/23723556.2024.2399379

Man Hagiyama, Azusa Yoneshige, Tomoyuki Otani, Akihiro Wada, Fuka Takeuchi, Yuji Shoya, Takao Inoue, Akihiko Ito

{"title":"An antibody-drug conjugate for endometrioid carcinoma based on the expression of cell adhesion molecule 1.","authors":"Man Hagiyama, Azusa Yoneshige, Tomoyuki Otani, Akihiro Wada, Fuka Takeuchi, Yuji Shoya, Takao Inoue, Akihiko Ito","doi":"10.1080/23723556.2024.2399379","DOIUrl":"https://doi.org/10.1080/23723556.2024.2399379","url":null,"abstract":"Cell adhesion molecule 1 (CADM1), an immunoglobulin superfamily member, is expressed in endometrial glandular cells highly during the proliferative phase but lowly during the secretory phase. Previously, a CADM1-targeting antibody-drug conjugate (ADC) was generated, in which a humanized anti-CADM1 ectodomain antibody h3E1 was linked with monomethyl auristatin E (h3E1-MMAE ADC). The present study aimed at probing whether this ADC could be useful for the treatment of endometrial neoplasm. Firstly, immunohistochemistry for CADM1 was conducted on proliferative-phase endometrium (n = 13), endometrial hyperplasia (n = 35), and endometrioid carcinoma at various stages (n = 166). CADM1 immunostaining intensity was highest in atypical endometrial hyperplasia and endometrioid carcinoma confined within the endometrium and was decreased stepwise as the carcinoma stage progressed. Next, h3E1-MMAE ADC was examined for its cytotoxicity in vitro using human endometrial adenocarcinoma cell lines expressing CADM1; HEC-1B, HEC-50B, JHUM-3, and OMC-2. The ADC killed these cells in a dose-dependent manner with half maximal inhibitory concentration (IC50) of 12.02 nM for HEC-1B and 2.04 nM for HEC-50B. Collectively, h3E1-MMAE ADC may serve as a noninvasive alternative to simple hysterectomy in the treatment of endometrioid carcinoma confined within the endometrium.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"11 1","pages":"2399379"},"PeriodicalIF":2.6,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11382700/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142297421","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

The SIRT7-nucleolus connection in cancer: ARF enters the fray. 癌症中 SIRT7 与核仁的联系：ARF 加入战局

IF 2.6

Molecular and Cellular Oncology Pub Date : 2024-07-17 eCollection Date: 2024-01-01 DOI: 10.1080/23723556.2024.2381287

Shahriar Tarighi, Poonam Kumari, Alejandro Vaquero, Thomas Braun, Alessandro Ianni

引用次数: 0

Amino acid deprivation in cancer cells with compensatory autophagy induction increases sensitivity to autophagy inhibitors. 癌细胞中氨基酸匮乏与自噬代偿诱导可增加对自噬抑制剂的敏感性。

IF 2.6

Molecular and Cellular Oncology Pub Date : 2024-07-14 eCollection Date: 2024-01-01 DOI: 10.1080/23723556.2024.2377404

Takahito Fukui, Manami Yabumoto, Misuzu Nishida, Shiori Hirokawa, Riho Sato, Taichi Kurisu, Miyu Nakai, Md Abul Hassan, Koji Kishimoto

{"title":"Amino acid deprivation in cancer cells with compensatory autophagy induction increases sensitivity to autophagy inhibitors.","authors":"Takahito Fukui, Manami Yabumoto, Misuzu Nishida, Shiori Hirokawa, Riho Sato, Taichi Kurisu, Miyu Nakai, Md Abul Hassan, Koji Kishimoto","doi":"10.1080/23723556.2024.2377404","DOIUrl":"10.1080/23723556.2024.2377404","url":null,"abstract":"Inhibition of autophagy is an important strategy in cancer therapy. However, prolonged inhibition of certain autophagies in established cancer cells may increase therapeutic resistance, though the underlying mechanisms of its induction and enhancement remain unclear. This study sought to elucidate the mechanisms of therapeutic resistance through repeated autophagy inhibition and amino acid deprivation (AD) in an in vitro model of in vivo chronic nutrient deprivation associated with cancer cell treatment. In the human cervical cancer cell line HeLa and human breast cancer cell line MCF-7, initial extracellular AD induced the immediate expression of endosomal microautophagy (eMI). However, repeated inhibition of eMI with U18666A and extracellular AD induced macroautophagy (MA) to compensate for reduced eMI, simultaneously decreasing cytotoxicity. Here, hyperphosphorylated JNK was transformed into a hypophosphorylated state, suggesting conversion of the cell death signal to a survival signal. In a nutrient medium, cell death could not be induced by MA inhibition. However, since LAT1 inhibitors induce intracellular AD, combining them with MA and eMI inhibitors successfully promoted cell death in resistant cells. Our study identified a novel therapeuic approach for promoting cell death and addressing therapeutic resistance in cancers under autophagy-inhibitor treatment.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"11 1","pages":"2377404"},"PeriodicalIF":2.6,"publicationDate":"2024-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11253891/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141634856","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

Selection forces underlying aneuploidy patterns in cancer. 癌症非整倍体模式背后的选择力量。

IF 2.6

Molecular and Cellular Oncology Pub Date : 2024-06-24 eCollection Date: 2024-01-01 DOI: 10.1080/23723556.2024.2369388

Tamara C Klockner, Christopher S Campbell

{"title":"Selection forces underlying aneuploidy patterns in cancer.","authors":"Tamara C Klockner, Christopher S Campbell","doi":"10.1080/23723556.2024.2369388","DOIUrl":"10.1080/23723556.2024.2369388","url":null,"abstract":"Aneuploidy, the presence of an aberrant number of chromosomes, has been associated with tumorigenesis for over a century. More recently, advances in karyotyping techniques have revealed its high prevalence in cancer: About 90% of solid tumors and 50-70% of hematopoietic cancers exhibit chromosome gains or losses. When analyzed at the level of specific chromosomes, there are strong patterns that are observed in cancer karyotypes both pan-cancer and for specific cancer types. These specific aneuploidy patterns correlate strongly with outcomes for tumor initiation, progression, metastasis formation, immune evasion and resistance to therapeutic treatment. Despite their prominence, understanding the basis underlying aneuploidy patterns in cancer has been challenging. Advances in genetic engineering and bioinformatic analyses now offer insights into the genetic determinants of aneuploidy pattern selection. Overall, there is substantial evidence that expression changes of particular genes can act as the positive selective forces for adaptation through aneuploidy. Recent findings suggest that multiple genes contribute to the selection of specific aneuploid chromosomes in cancer; however, further research is necessary to identify the most impactful driver genes. Determining the genetic basis and accompanying vulnerabilities of specific aneuploidy patterns is an essential step in selectively targeting these hallmarks of tumors.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"11 1","pages":"2369388"},"PeriodicalIF":2.6,"publicationDate":"2024-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11197905/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141451814","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