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Editors' Selections from Relevant Scientific Publications 编辑对相关科学出版物的选择
3区 医学 Q2 ONCOLOGY Pub Date : 2023-10-02 DOI: 10.1158/1940-6207.capr-16-10-hfl
Highlights from the Literature| October 02 2023 Editors' Selections from Relevant Scientific Publications Author & Article Information Online ISSN: 1940-6215 Print ISSN: 1940-6207 ©2023 American Association for Cancer Research2023American Association for Cancer Research Cancer Prev Res (Phila) (2023) 16 (10): 539. https://doi.org/10.1158/1940-6207.CAPR-16-10-HFL Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Article Versions Icon Versions Version of Record October 2 2023 Citation Editors' Selections from Relevant Scientific Publications. Cancer Prev Res (Phila) 1 October 2023; 16 (10): 539. https://doi.org/10.1158/1940-6207.CAPR-16-10-HFL Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest Search Advanced Search Breast cancer cells (by Annie Cavanagh via Flickr) Using phylogenetic of microdissected samples of cancer and non-cancer proliferative lesions, Nishimura et al. explored the genetic evolution of breast cancer, revealing a unique evolutionary pattern harboring der(1;16), a common driver alteration in 20% of all breast cancers and one-third of Luminal A breast cancers. In der(1;16)(+) cancers, the derivative chromosome was acquired from early puberty to late adolescence, followed by the emergence of a common ancestor by the patient's early 30s, leading to both cancerous and non-cancerous clones. These clones expanded significantly within the premenopausal breast before cancer diagnosis. Interestingly, multiple cancer clones originated from noncancer ancestors and there was no correlation between histology and the number of driver events, suggesting the involvement of epigenetic or microenvironmental factors in cancer development. These findings contribute to a better understanding of breast carcinogenesis and may improve early detection and prevention strategies. Nishimura... You do not currently have access to this content.
文献要义| 2023年10月2日编辑精选相关科学出版物作者与文章信息在线ISSN: 1940-6215印刷ISSN: 1940-6207©2023美国癌症研究协会2023美国癌症研究协会癌症预防研究(费城)(2023)16(10):539。https://doi.org/10.1158/1940-6207.CAPR-16-10-HFL查看图标查看文章内容图表和表格视频音频补充数据同行评审共享图标共享Facebook Twitter LinkedIn电子邮件工具图标工具获得权限引用图标引用搜索网站文章版本图标版本记录版本2023年10月2日引文编辑从相关科学出版物的选择。癌症预防中心(费城)2023年10月1日;16(10): 539。https://doi.org/10.1158/1940-6207.CAPR-16-10-HFL下载引文文件:Ris (Zotero)参考管理器EasyBib Bookends Mendeley论文EndNote RefWorks BibTex工具栏搜索搜索下拉菜单工具栏搜索搜索输入搜索输入自动建议搜索高级搜索乳腺癌细胞(by Annie Cavanagh via Flickr)利用癌症和非癌症增生病变的微解剖样本的系统发育,Nishimura等人探索了乳腺癌的遗传进化,揭示了一种独特的进化模式(1;16)。在20%的乳腺癌和三分之一的Luminal a型乳腺癌中,这是一种常见的驱动因素改变。在der(1;16)(+)癌症中,从青春期早期到青春期晚期获得衍生染色体,随后在患者30岁出头时出现共同祖先,导致癌性和非癌性克隆。这些克隆在癌症诊断前的绝经前乳腺癌中显著扩大。有趣的是,多个癌症克隆起源于非癌症祖先,组织学和驱动事件的数量之间没有相关性,这表明表观遗传或微环境因素参与了癌症的发展。这些发现有助于更好地了解乳腺癌的发生,并可能改善早期发现和预防策略。Nishimura……您目前没有访问此内容的权限。
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引用次数: 0
Editors' Selections from Relevant Scientific Publications 编辑对相关科学出版物的选择
3区 医学 Q2 ONCOLOGY Pub Date : 2023-08-01 DOI: 10.1158/1940-6207.capr-16-8-hfl
Highlights from the Literature| August 01 2023 Editors' Selections from Relevant Scientific Publications Author & Article Information Online ISSN: 1940-6215 Print ISSN: 1940-6207 ©2023 American Association for Cancer Research2023American Association for Cancer Research Cancer Prev Res (Phila) (2023) 16 (8): 419. https://doi.org/10.1158/1940-6207.CAPR-16-8-HFL Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Article Versions Icon Versions Version of Record August 1 2023 Citation Editors' Selections from Relevant Scientific Publications. Cancer Prev Res (Phila) 1 August 2023; 16 (8): 419. https://doi.org/10.1158/1940-6207.CAPR-16-8-HFL Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest Search Advanced Search Polygenic risk scores for screening (from Centers for Disease Control and Prevention) Using UK metrics, Huntley et al. conducted a modeling analysis on the performance of polygenic risk score (PRS) tools and PRS-stratified cancer screening. They estimated the potential annual numbers of cancer cases detected and deaths averted for eight different cancers. The results suggested that, under favorable assumptions, hypothetical PRS-stratified screening programs could modestly improve efficiency for three cancer types. Specifically, they could reduce maximum number of annual deaths from 102 to 80 for breast cancer, 188 to 155 for prostate cancer, and 158 to 95 for colorectal cancer. However, UK-specific cluster-randomized trials are required to evaluate the real-world clinical impact, costs, and potential harm of PRS stratification. Huntley C, … Turnbull C. Lancet Oncol. 2023 Jun;24(6): 658-668. Illustration of deep learning (by OpenClipart via FreeSVG) Pancreatic cancer is often diagnosed too late to achieve good clinical outcomes,... You do not currently have access to this content.
文献亮点| 2023年8月1日编辑精选相关科学出版物作者与文章信息在线ISSN: 1940-6215印刷ISSN: 1940-6207©2023美国癌症研究协会2023美国癌症研究协会癌症预防研究(费城)(2023)16(8):419。https://doi.org/10.1158/1940-6207.CAPR-16-8-HFL查看图标查看文章内容图表和表格视频音频补充数据同行评审共享图标共享Facebook Twitter LinkedIn电子邮件工具图标工具获得权限引用图标引用搜索网站文章版本图标版本记录版本2023年8月1日引文编辑从相关科学出版物的选择。癌症预防中心(费城)2023年8月1日;16(8): 419。https://doi.org/10.1158/1940-6207.CAPR-16-8-HFL下载引文文件:Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex工具栏搜索搜索下拉菜单工具栏搜索搜索输入搜索输入自动建议搜索高级搜索筛选多基因风险评分(来自疾病控制和预防中心)使用英国指标,Huntley等人对多基因风险评分(PRS)工具和PRS分层癌症筛查的性能进行了建模分析。他们估计了八种不同癌症每年可能发现的癌症病例和避免的死亡人数。结果表明,在有利的假设下,假设的prs分层筛查方案可以适度提高三种癌症类型的效率。具体来说,他们可以将每年乳腺癌死亡人数从102人减少到80人,前列腺癌死亡人数从188人减少到155人,结肠直肠癌死亡人数从158人减少到95人。然而,需要英国特定的集群随机试验来评估PRS分层的实际临床影响、成本和潜在危害。张建军,张建军,张建军,等。中华医学杂志,2013,31(6):658-668。胰腺癌通常诊断得太晚,无法获得良好的临床结果。您目前没有访问此内容的权限。
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引用次数: 0
Editors' Selections from Relevant Scientific Publications 编辑对相关科学出版物的选择
3区 医学 Q2 ONCOLOGY Pub Date : 2023-06-01 DOI: 10.1158/1940-6207.capr-16-6-hfl
Highlights from the Literature| June 01 2023 Editors' Selections from Relevant Scientific Publications Author & Article Information Online ISSN: 1940-6215 Print ISSN: 1940-6207 ©2023 American Association for Cancer Research2023American Association for Cancer Research Cancer Prev Res (Phila) (2023) 16 (6): 303. https://doi.org/10.1158/1940-6207.CAPR-16-6-HFL Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Article Versions Icon Versions Version of Record June 1 2023 Citation Editors' Selections from Relevant Scientific Publications. Cancer Prev Res (Phila) 1 June 2023; 16 (6): 303. https://doi.org/10.1158/1940-6207.CAPR-16-6-HFL Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest Search Advanced Search Obese adipose tissue in the mammary gland (by Arendt et al. via Cancer Research Bhardwaj et al. investigated whether high body mass index (BMI) increases breast cancer risks for women carrying BRCA 1 or BRCA2 mutations. They examined noncancerous breast tissue from 69 such women and found that BMI and biomarkers of metabolic dysfunction were positively correlated with DNA damage in epithelia. RNA sequencing data revealed that obesity altered breast adipose microenvironment and activated estrogen biosynthesis. Blocking signaling pathways mediated by either estrogen or obesity-associated factors leptin or insulin, reduced DNA damage. Additionally, a high-fat diet increased DNA damage and mammary tumors in Brca1+/−mice. These results provide mechanistic insight linking obesity and breast cancer in BRCA mutation carriers, and suggest that reducing risk may involve maintaining a lower body weight, addressing metabolic problems and targeting estrogen. Bhardwaj P, … Brown KA. Sci Transl Med. 2023 Feb 22;15(684):eade1857.... You do not currently have access to this content.
文献摘录2023年6月1日编辑精选相关科学出版物作者和文章信息在线ISSN: 1940-6215印刷ISSN: 1940-6207©2023美国癌症研究协会2023美国癌症研究协会癌症预防研究(费城)(2023)16(6):303。https://doi.org/10.1158/1940-6207.CAPR-16-6-HFL查看图标查看文章内容图表和表格视频音频补充数据同行评审共享图标共享Facebook Twitter LinkedIn电子邮件工具图标工具获得权限引用图标引用搜索网站文章版本图标版本记录版本2023年6月1日引文编辑从相关科学出版物的选择。癌症预防中心(费城)2023年6月1日;16(6): 303。https://doi.org/10.1158/1940-6207.CAPR-16-6-HFL下载引文文件:Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex工具栏搜索搜索下拉菜单工具栏搜索搜索输入搜索输入自动建议搜索高级搜索乳腺中的肥胖脂肪组织(由Arendt等人通过Cancer Research) Bhardwaj等人研究了高体重指数(BMI)是否会增加携带BRCA 1或BRCA2突变的女性患乳腺癌的风险。他们检查了69名女性的非癌性乳腺组织,发现BMI和代谢功能障碍的生物标志物与上皮细胞的DNA损伤呈正相关。RNA测序数据显示,肥胖改变了乳房脂肪微环境,激活了雌激素的生物合成。阻断由雌激素或肥胖相关因子瘦素或胰岛素介导的信号通路,减少DNA损伤。此外,高脂肪饮食增加了Brca1+/−小鼠的DNA损伤和乳腺肿瘤。这些结果为BRCA突变携带者的肥胖和乳腺癌之间的联系提供了机制见解,并表明降低风险可能涉及保持较低的体重,解决代谢问题和靶向雌激素。Bhardwaj P, Brown KA。科学转化医学。2023 Feb 22;15(684):eade1857....您目前没有访问此内容的权限。
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引用次数: 0
Acknowledgment to Reviewers 对审稿人的感谢
3区 医学 Q2 ONCOLOGY Pub Date : 2023-01-04 DOI: 10.1158/1940-6207.capr-16-1-ar
The Cancer Prevention Research editors wish to acknowledge with sincere appreciation the assistance of the following reviewers who have generously contributed their time and effort during the past year1 in the appraisal of manuscripts. These reviewers have been enormously helpful in assessing the merit of original articles: their careful analysis and critique and their constructive recommendations have greatly enhanced the value of manuscripts they have handled. The quality of the journal can be attributed in large measure to the quality of their effort. We are sincerely grateful.Abdelwadoud, M.Agarwal, R.Alexeeff, S.Allanson, E.Alshalalfa, M.Amos, C.Anderson, K.Arayici, M.Arendt, L.Arthur, R.Aslam, M.Ballester, V.Bansal, A.Barry, K.Beane, J.Behrens, G.Benedetti, I.Benjaminsen Borch, K.Beretta, L.Bergan, R.Boland, R.Bosland, M.Bossuyt, P.Bouras, E.Bowers, L.Bresalier, R.Brooks, J.Brown, K.Brown, R.Burris, J.Butsch Kovacic, M.Butt, J.Carchman, E.Carlo, M.Chan, A.Chan, C.Chang, G.Charvat, H.Chen, H.Chen, J.Chen, M.Chen, W.Cho, H.Choi, J.Clapper, M.Colditz, G.Coronado, G.Cronin-Fenton, D.Croy, R.Cummings, K.D'Angelo, H.Daly, M.DeCensi, A.DeStephano, C.Djuric, Z.Dmitrovsky, E.Dooley, W.Dossus, L.Dubinett, S.Dwivedi, C.El-Bayoumy, K.Ellaithi, M.Eltoum, I.Eshak, E.Esserman, L.Evans, D.Falk, D.Fang, C.Figueroa, J.Ford, M.Fournier, A.Fowke, J.Franco, E.Freedland, S.Freisling, H.Friedenreich, C.Gail, M.Genkinger, J.George, S.Gershenwald, J.Giorgi-Rossi, P.Giovannucci, E.Gleber-Netto, F.Goetz, L.Goodwin, P.Gowans, E.Grant, E.Groopman, J.Grossman, D.Gu, J.Guerrero-Preston, R.Gümüş, Z.Han, Y.Hanash, S.Harper, D.Hecht, S.Heckman-Stoddard, B.Henry, K.Hilakivi-Clarke, L.Hodge, A.Hong, C.Hong, Y.Huang, Y.Hung, M.Huo, D.Hur, J.Imperiale, T.Inadomi, J.Iwasaki, M.Janakiram, N.Kadara, H.Kassie, F.Kensler, K.Khairan, P.Khan, S.Kim, J.Kim, R.Kingham, T.Kinney, A.Kong, A.Kratz, C.Kühn, T.Kypriotakis, G.La Vecchia, C.Lam, S.Land, S.Lazcano-Ponce, E.Lebwohl, B.Lee, H.Lee, J.Liby, K.Lipkin, S.Longatto-Filho, A.Lopez, D.Lu, J.Lu, Q.Lundberg, A.Luu, H.Lynch, P.MacInnis, R.Mandle, H.Manne, S.Mao, J.Mariosa, D.Marshall, J.Matthews, C.Mayrand, M.Mehta, A.Melkonian, S.Michail, G.Miller, M.Milne, R.Mitzner, W.Mix, J.Mohammed, A.Molokwu, J.Montuenga, L.Mousavi Seresht, L.Muller, D.Müller, M.Mulshine, J.Murphy, G.Murphy, N.Narayanapillai, S.Nash, S.Nasrollahzadeh, D.Neale, R.Nelson, K.Noh, H.Nounu, A.O'Dwyer, P.O'Mara, T.Ogunsina, K.Oh, H.Ondrey, F.Ortiz, A.Ose, J.Park, H.Parker, B.Paskett, E.Pass, H.Passarelli, M.Pepper, J.Perkins, R.Permuth, J.Petrick, J.Phillips, K.Piazza, G.Playdon, M.Porter, W.Qiao, Y.Quaife, S.Rachocki, C.Ramsey, A.Rao, C.Rauh-Hain, J.Robbins, H.Robson, M.Rosenberg, D.Sawada, N.Sboner, A.Scalbert, A.Schmeler, K.Schnoll, R.Seno, H.Sethi, S.Shahid, A.Shaukat, A.Shen, Q.Shen, Z.Sherman, M.Shibata, D.Shu, X.Shureiqi, I.Singh, S.Smith, S.Sporn, M.Srivastava, S.Stanton, S.Stevens, V.Stewart, S.Stoffel, E.Stoner, G.Sturgeon, S.Sukumar, S.Sun, C.Sun, Y.Surh, Y.Tabun
《癌症预防研究》的编辑们衷心感谢以下审稿人,他们在过去一年中慷慨地贡献了他们的时间和精力1来审稿。这些审稿人在评估原创文章的价值方面提供了极大的帮助:他们的仔细分析和批评以及建设性的建议大大提高了他们所处理的手稿的价值。期刊的质量在很大程度上要归功于他们的努力。我们衷心感激。Abdelwadoud, M.Agarwal, R.Alexeeff, S.Allanson, E.Alshalalfa, M.Amos, C.Anderson, K.Arayici, m . arthur, R.Aslam, M.Ballester, V.Bansal, A.Barry, K.Beane, J.Behrens, G.Benedetti, m . benjaminsen Borch, K.Beretta, L.Bergan, R.Boland, R.Bosland, M.Bossuyt, P.Bouras, E.Bowers, L.Bresalier, R.Brooks, J.Brown, K.Brown, R.Burris, J.Butsch Kovacic, M.Butt, J.Carchman, G.Charvat, H.Chen, H.Chen, J.Chen, J.Clapper, M.Colditz, G.Coronado,g .克罗宁-芬顿,d .克罗伊,r .卡明斯,k .迪安吉洛,h .戴利,m .德森西,a .德斯蒂法诺,c .德尤里奇,z .德米特罗夫斯基,e .杜利,w .杜苏斯,l .杜宾内特,s .德维维迪,c .艾尔-巴约米,k .埃尔图姆,i .埃沙克,e .埃瑟曼,l .埃文斯,d .福尔尼克,d .方,c .菲格罗亚,j .福特,m .富尼耶,a .福克,j .弗朗哥,e .弗里德兰,s .弗莱斯林,h .弗里登赖希,c .盖尔,m .根金格,j .乔治,s .格申瓦尔德,j .乔吉-罗西,e .乔万努奇,e .格莱伯-内托,f .戈茨,l .古德温,p .戈文斯,e .格兰特,e .格鲁普曼,j .格罗斯曼,d .古j . guerrro - preston, r . g m, Z.Han, Y.Hanash, S.Harper, D.Hecht, S.Heckman-Stoddard, B.Henry, K.Hilakivi-Clarke, L.Hodge, A.Hong, C.Hong, Y.Huang, Y.Hung, M.Huo, D.Hur, J.Imperiale, T.Inadomi, J.Iwasaki, M.Janakiram, N.Kadara, H.Kassie, F.Kensler, K.Khairan, P.Khan, S.Kim, J.Kim, R.Kingham, T.Kinney, A.Kong, A.Kratz, c . k hn, T.Kypriotakis, G.La Vecchia, C.Lam, S.Land, S.Lazcano-Ponce, E.Lebwohl, B.Lee, H.Lee, J.Liby, k . longatto - filho, A.Lopez, D.Lu, J.Lu, Q.Lundberg, A.Luu, H.Lynch,p .麦金尼斯,r .曼德尔,h .曼恩,s .毛,j .马里奥萨,d .马歇尔,j .马修斯,c .梅兰德,m .梅塔,a .梅尔科尼安,s .米勒,m .米尔恩,r .米茨纳,w .米克斯,j .穆罕默德,a .莫洛克乌,j .蒙图恩加,l .穆萨维·塞列希特,l .穆勒,d .米斯勒,m .穆尔辛,j .墨菲,g .墨菲,n .纳拉亚纳皮莱,s .纳什,s .纳斯罗拉扎德,d .尼尔,r .尼尔森,k .诺亚,h .努努,a .欧德威尔,p .奥马拉,t .奥古斯纳,k .欧,h .奥德雷,f .奥尔蒂斯,a .奥斯,j .帕克,h .帕克,b .帕斯特,e .帕斯,h .帕萨雷利,m .佩珀,j .珀金斯,r .珀姆斯,j .佩特里,J.Phillips, K.Piazza, G.Playdon, M.Porter, W.Qiao, Y.Quaife, S.Rachocki, C.Ramsey, A.Rao, C.Rauh-Hain, J.Robbins, H.Robson, M.Rosenberg, D.Sawada, N.Sboner, H.Sethi, S.Shahid, A.Shaukat, A.Shen, Q.Shen, Z.Sherman, M.Shibata, D.Shu, X.Shureiqi, I.Singh, S.Smith, S.Sporn, M.Srivastava, S.Stanton, S.Stevens, V.Stewart, S.Stoffel, E.Stoner, g . sukumar, S.Sun, k . sun, Y.Surh, Y.Tabung, f .田口,K.Tanaka, T.Thompson, H.Toll, B.Toriola,A.Toumazis, I.Trachootham, D.Umar, A.Uttam, S.Vadaparampil, S.van Duijnhoven, F.Van Guelpen, B.Vaughan-Shaw, P.Viallon, V.Vidman, L.Vilar, E.Vinson, C.Vogel, V.Volk, R.Wallace, K.Walsh, M.Wang, t.y.w weiss, N.Wender, R.Wernli, K.Wesolowski, R.Willis, J.Wong, L.Wood, M.Wuertz, B.Xiao, H.Yang, P.Yanik, E.Yarmolinsky, J.Yu, H.Yu, M.Zhang,郑少森,周军,朱强,X。
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Cancer Prevention Research
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