Tumor Biology最新文献_第5页

Medium and large alleles of the PGC gene are risk factors for gastric cancer. PGC基因中、大等位基因是胃癌发生的危险因素。

Tumor Biology Pub Date : 2023-01-01 DOI: 10.3233/TUB-220025

Josefina Yoaly Sánchez-López, Katia Carolina Vázquez-Ibarra, Andrea Marlene García-Muro, Azaria García-Ruvalcaba, Sergio Pacheco-Sotelo, Luis Carlos Díaz-Herrera, Marıa Eugenia Marin-Contreras

{"title":"Medium and large alleles of the PGC gene are risk factors for gastric cancer.","authors":"Josefina Yoaly Sánchez-López, Katia Carolina Vázquez-Ibarra, Andrea Marlene García-Muro, Azaria García-Ruvalcaba, Sergio Pacheco-Sotelo, Luis Carlos Díaz-Herrera, Marıa Eugenia Marin-Contreras","doi":"10.3233/TUB-220025","DOIUrl":"https://doi.org/10.3233/TUB-220025","url":null,"abstract":"Background: A 100-bp insertion/deletion polymorphism in the pepsinogen C gene has been associated with the risk of gastric cancer (GC).Objective: We analyzed the relationships of the 100-bp insertion/deletion polymorphism with GC, atrophic gastritis (AG), and intestinal metaplasia (IM) in the Mexican general population (MGP).Methods: We studied the genomic DNA of subjects with GC n = 80, AG and IM n = 60, controls n = 110, and the MGP n = 97. PGC gene insertion/deletion polymorphism was identified by means of PCR, capillary electrophoresis and GeneScan software.Results: Different allele sizes of PGC polymorphism were observed in the studied groups, from 266 bp to 499 bp, which were grouped for the analysis as short alleles of 266-399 bp, medium alleles of 400-433 bp and large alleles of 434-499 bp. Carriers of one or two medium alleles, had an increased risk of GC, with OR of 1.99 (CI95% 1.08-3.67 p = 0.026) compared to homozygotes (no medium/no medium).Conclusions: Previous studies have related PGC short alleles to risk for or protection against GC depending on the ethnic origin of the population. In our study, medium alleles were related to risk for GC. Further studies are required to establish the importance of this polymorphism in the origin of gastric neoplasia.","PeriodicalId":23364,"journal":{"name":"Tumor Biology","volume":"45 1","pages":"15-21"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9669165","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Oral Presentations' Abstracts. 口头报告的摘要。

Tumor Biology Pub Date : 2023-01-01 DOI: 10.3233/TUB-239003

引用次数: 0

Poster Presentations' Abstracts. 海报展示的摘要。

Tumor Biology Pub Date : 2023-01-01 DOI: 10.3233/TUB-239004

引用次数: 0

A statement regarding the mass retraction of Iranian papers in November 2016. 关于2016年11月伊朗报纸被大规模撤稿的声明。

Tumor Biology Pub Date : 2023-01-01 DOI: 10.3233/TUB-220031

Aram Mokarizadeh

引用次数: 0

Book of Abstracts. 摘要之书。

Tumor Biology Pub Date : 2023-01-01 DOI: 10.3233/TUB-239001

引用次数: 0

Bithiophene derivative induced apoptosis and suppression of Akt pathway in mouse leukemic model. 二噻吩衍生物诱导小鼠白血病模型细胞凋亡及抑制Akt通路。

Tumor Biology Pub Date : 2022-04-12 DOI: 10.3233/tub-211538

Ali Samy Algharib, G. Shanab, Abdel-Rahman B Abdel-Ghaffar, Mohamed A Ismail, R. H. Mohamed

{"title":"Bithiophene derivative induced apoptosis and suppression of Akt pathway in mouse leukemic model.","authors":"Ali Samy Algharib, G. Shanab, Abdel-Rahman B Abdel-Ghaffar, Mohamed A Ismail, R. H. Mohamed","doi":"10.3233/tub-211538","DOIUrl":"https://doi.org/10.3233/tub-211538","url":null,"abstract":"BACKGROUND\u0000Bithiophene derivatives show a promising anti-cancer potential. We previously showed that Bithienyl Fluorobenzamidine (BFB) has an anti-proliferative effect against several leukemia cell lines. Acute myeloid leukemia (AML) accounts for 18% of the total leukemia cases worldwide with heavier burden during the past 30 years. Therefore, the main aim remains the discovery of safe and effective medications.\u0000\u0000\u0000OBJECTIVE\u0000The current research aims to investigate the anti-cancer efficacy of BFB and its effect on the apoptosis in the 7,12-Dimethylbenz[a]anthracene (DMBA) induced AML in mice.\u0000\u0000\u0000METHODS\u0000AML was induced in mice by DMBA and then treated by 2 different doses of BFB. After BFB treatment, the hematological and histological pattern changes was examined. Furthermore, the molecular effect of BFB on apoptosis, cell cycle markers and Protein kinase B (Akt) pathway was examined using qPCR, Western blotting and ELISA.\u0000\u0000\u0000RESULTS\u0000BFB treatment ameliorates leukemia histological and hematological markers significantly, despite non-significant changes in normal mice. This improvement exhibits cell cycle arrest and apoptosis induction, represented by elevation of tp53/p53, p21/p21, Caspase3 and downregulation of ckk1/Cdk1 in the bone marrow, as well as Akt pathway suppression.\u0000\u0000\u0000CONCLUSIONS\u0000Our results establishes BFB as a promising therapeutic candidate against AML through cell cycle arrest, apoptosis induction and Akt pathway modulation.","PeriodicalId":23364,"journal":{"name":"Tumor Biology","volume":"13 1","pages":"53-67"},"PeriodicalIF":0.0,"publicationDate":"2022-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90837375","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Tumor-associated CD3- and CD8-positive immune cells in colorectal cancer: The additional prognostic value of CD8+-to-CD3+ ratio remains debatable. 结直肠癌肿瘤相关CD3-和CD8阳性免疫细胞:CD8+ / CD3+比值的额外预后价值仍有争议。

Tumor Biology Pub Date : 2022-04-07 DOI: 10.3233/tub-211571

Jussi Kasurinen, J. Hagström, T. Kaprio, Ines Beilmann-Lehtonen, C. Haglund, C. Böckelman

{"title":"Tumor-associated CD3- and CD8-positive immune cells in colorectal cancer: The additional prognostic value of CD8+-to-CD3+ ratio remains debatable.","authors":"Jussi Kasurinen, J. Hagström, T. Kaprio, Ines Beilmann-Lehtonen, C. Haglund, C. Böckelman","doi":"10.3233/tub-211571","DOIUrl":"https://doi.org/10.3233/tub-211571","url":null,"abstract":"BACKGROUND\u0000A large number of infiltrating CD3- and CD8-positive inflammatory cells indicates an improved survival in colorectal cancer (CRC), similar to many other cancers.\u0000\u0000\u0000OBJECTIVE\u0000We investigated the prognostic value of different combinations of CD3- and CD8-positive immune cells in CRC patients.\u0000\u0000\u0000METHODS\u0000The densities of CD3- and CD8-positive cells in intratumoral and stromal tissues were evaluated from 539 patients, for which we calculated a CD3 tumor-stroma index, a CD8 tumor-stroma index, and a CD3-CD8 tumor-stroma index.\u0000\u0000\u0000RESULTS\u0000High CD3 and CD8 tumor-stroma indices associated with stage I to II disease (p < 0.001 for both). The CD3 tumor-stroma index associated with a colonic tumor location (p = 0.006), while the CD8 tumor-stroma index associated with right-sided tumors (p < 0.001) and histological grade 3 tumors (p = 0.032). High intratumoral and stromal densities for CD3- and CD8-positive immune cells, the CD3 tumor-stroma index, the CD8 tumor-stroma index, and the CD3-CD8 tumor-stroma index all indicated a better DSS.\u0000\u0000\u0000CONCLUSIONS\u0000The CD3 tumor-stroma index carries a strong prognostic value in CRC, and none of the CD3 and CD8 combinations we analyzed proved superior.","PeriodicalId":23364,"journal":{"name":"Tumor Biology","volume":"343 1","pages":"37-52"},"PeriodicalIF":0.0,"publicationDate":"2022-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79585202","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 5

Vitamin B12 enhances the antitumor activity of 1,25-dihydroxyvitamin D3 via activation of caspases and targeting actin cytoskeleton. 维生素B12通过激活半胱天酶和靶向肌动蛋白细胞骨架增强1,25-二羟基维生素D3的抗肿瘤活性。

Tumor Biology Pub Date : 2022-01-01 DOI: 10.3233/TUB-211536

Manar F Atoum, Foad E Alzoughool, Zainab A Al-Mazaydeh, Majdoleen S Rammaha, Lubna H Tahtamouni

{"title":"Vitamin B12 enhances the antitumor activity of 1,25-dihydroxyvitamin D3 via activation of caspases and targeting actin cytoskeleton.","authors":"Manar F Atoum, Foad E Alzoughool, Zainab A Al-Mazaydeh, Majdoleen S Rammaha, Lubna H Tahtamouni","doi":"10.3233/TUB-211536","DOIUrl":"https://doi.org/10.3233/TUB-211536","url":null,"abstract":"Background: 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) is an effective anticancer agent, and when combined with other agents it shows superior activities. Vitamin B12 has been shown to contribute to increasing the effectiveness of anticancer drugs when used in combination. Thus, the current study aimed at investigating the anticancer potential of the combination of 1,25(OH)2D3 and vitamin B12.Methods: MTT assay was used to determine the cytotoxic activity of combining 1,25(OH)2D3 and vitamin B12 against six different cancer cell lines and one normal cell line. The surviving fraction after clonogenic assay was measured, and the effects of 1,25(OH)2D3/B12 combination on the activity of different caspases, cell adhesion, actin cytoskeleton, cell morphology, and percentage of polarized cells were evaluated.Results: Vitamin B12 did not cause cytotoxicity, however, it enhanced the cytotoxicity of 1,25(OH)2D3 against cancer cells. The cytotoxic effects of 1,25(OH)2D3 and its combination with vitamin B12 was not evident in the normal mammary MCF10A cell line indicating cancer cell-specificity. The cytotoxic effects of 1,25(OH)2D3/B12 combination occurred in a dose-dependent manner and was attributed to apoptosis induction which was mediated by caspase 4 and 8. Moreover, 1,25(OH)2D3/B12-treated cells showed enhanced inhibition of clonogenic tumor growth, reduced cell adhesion, reduced cell area, reduced percentage of cell polarization, and disorganized actin cytoskeleton resulting in reduced migratory phenotype when compared to cells treated with 1,25(OH)2D3 alone.Conclusion: 1,25(OH)2D3 and vitamin B12 exhibited synergistic anticancer effects against different cancer cell lines. The combination therapy of 1,25(OH)2D3 and vitamin B12 may provide a potential adjunctive treatment option for some cancer types.","PeriodicalId":23364,"journal":{"name":"Tumor Biology","volume":" ","pages":"17-35"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39935488","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 4

Role of colony-stimulating factor 1 in the neoplastic process of tenosynovial giant cell tumor. 集落刺激因子 1 在腱鞘巨细胞瘤肿瘤过程中的作用

Tumor Biology Pub Date : 2022-01-01 DOI: 10.3233/TUB-220005

William D Tap, John H Healey

{"title":"Role of colony-stimulating factor 1 in the neoplastic process of tenosynovial giant cell tumor.","authors":"William D Tap, John H Healey","doi":"10.3233/TUB-220005","DOIUrl":"10.3233/TUB-220005","url":null,"abstract":"Tenosynovial giant cell tumors (TGCTs) are rare, locally aggressive, mesenchymal neoplasms, most often arising from the synovium of joints, bursae, or tendon sheaths. Surgical resection is the first-line treatment, but recurrence is common, with resulting impairments in patients' mobility and quality of life. Developing and optimizing the role of systemic pharmacologic therapies in TGCT management requires an understanding of the underlying disease mechanisms. The colony-stimulating factor 1 receptor (CSF1R) has emerged as having an important role in the neoplastic processes underlying TGCT. Lesions appear to contain CSF1-expressing neoplastic cells derived from the synovial lining surrounded by non-neoplastic macrophages that express the CSF1R, with lesion growth stimulated by both autocrine effects causing proliferation of the neoplastic cells themselves and by paracrine effects resulting in recruitment of CSF1 R-bearing macrophages. Other signaling pathways with evidence for involvement in TGCT pathogenesis include programmed death ligand-1, matrix metalloproteinases, and the Casitas B-cell lymphoma family of ubiquitin ligases. While growing understanding of the pathways leading to TGCT has resulted in the development of both regulatory approved and investigational therapies, more detail on underlying disease mechanisms still needs to be elucidated in order to improve the choice of individualized therapies and to enhance treatment outcomes.","PeriodicalId":23364,"journal":{"name":"Tumor Biology","volume":"44 1","pages":"239-248"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11167812/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10355512","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

Induction of alternative NF-κB within TAg-induced basal mammary tumors in activation-resistant inhibitor of κ-B kinase (IKKα) mutant mice. 活化抵抗性κ b激酶抑制剂(IKKα)突变小鼠在标签诱导的基底乳腺肿瘤中诱导替代性NF-κB

Tumor Biology Pub Date : 2022-01-01 DOI: 10.3233/TUB-220006

Fares Ould-Brahim, Andrea Sau, David A Carr, Tianqi Jiang, M A Christine Pratt

{"title":"Induction of alternative NF-κB within TAg-induced basal mammary tumors in activation-resistant inhibitor of κ-B kinase (IKKα) mutant mice.","authors":"Fares Ould-Brahim, Andrea Sau, David A Carr, Tianqi Jiang, M A Christine Pratt","doi":"10.3233/TUB-220006","DOIUrl":"https://doi.org/10.3233/TUB-220006","url":null,"abstract":"Background: The alternative NF-κB pathway is activated by the NF-κB-inducing kinase (NIK) mediated phosphorylation of the inhibitor of κ-B kinase α (IKKα). IKKα then phosphorylates p100/NFKB2 to result in its processing to the active p52 subunit. Evidence suggests that basal breast cancers originate within a subpopulation of luminal progenitor cells which is expanded by signaling to IKKα.Objective: To determine the role of IKKα in the development of basal tumors.Methods: Kinase dead IkkαAA/AA mice were crossed with the C3(1)-TAg mouse model of basal mammary cancer. Tumor growth and tumor numbers in WT and IkkαAA/AA mice were assessed and immunopathology, p52 expression and stem/progenitor 3D colony forming assays were performed. Nik-/- mammary glands were isolated and mammary colonies were characterized.Results: While tumor growth was slower than in WT mice, IkkαAA/AA tumor numbers and pathology were indistinguishable from WT tumors. Both WT and IkkαAA/AA tumors expressed p52 except those IkkαAA/AA tumors where NIK, IKKαAA/AA and ErbB2 were undetectable. Colonies formed by WT and IkkαAA/AA mammary cells were nearly all luminal/acinar however, colony numbers and sizes derived from IkkαAA/AA cells were reduced. In contrast to IkkαAA/AA mice, virgin Nik-/- mammary glands were poorly developed and colonies were primarily derived from undifferentiated bipotent progenitor cells.Conclusions: C3(1)-TAg induced mammary tumors express p100/p52 even without functional IKKα. Therefore the development of basal-like mammary cancer does not strictly rely on IKKα activation. Signal-induced stabilization of NIK may be sufficient to mediate processing of p100NFKB2 which can then support basal-like mammary tumor formation. Lastly, in contrast to the pregnancy specific role of IKKα in lobuloalveogenesis, NIK is obligatory for normal mammary gland development.","PeriodicalId":23364,"journal":{"name":"Tumor Biology","volume":" ","pages":"187-203"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33462098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0