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In cancer drug resistance, germline matters too.

作者信息

Cheng Emily H, Sawyers Charles L

出版信息

Nat Med. 2012 Apr 5;18(4):494-6. doi: 10.1038/nm.2725.

DOI:10.1038/nm.2725
PMID:22481406
Abstract
摘要

相似文献

1
In cancer drug resistance, germline matters too.在癌症耐药性方面，种系因素也很重要。
Nat Med. 2012 Apr 5;18(4):494-6. doi: 10.1038/nm.2725.
2
The BIM deletion polymorphism cannot account for intrinsic TKI resistance of Chinese individuals with chronic myeloid leukemia.BIM缺失多态性不能解释中国慢性髓性白血病患者对酪氨酸激酶抑制剂的内在耐药性。
Nat Med. 2014 Oct;20(10):1090. doi: 10.1038/nm.3638.
3
Reply: the BIM deletion polymorphism cannot account for intrinsic TKI resistance of Chinese individuals with chronic myeloid leukemia.回复：BIM缺失多态性不能解释中国慢性髓性白血病患者对酪氨酸激酶抑制剂的内在耐药性。
Nat Med. 2014 Oct;20(10):1090-1. doi: 10.1038/nm.3652.
4
A common BIM deletion polymorphism mediates intrinsic resistance and inferior responses to tyrosine kinase inhibitors in cancer.一种常见的 BIM 删除多态性介导了癌症对酪氨酸激酶抑制剂的固有耐药性和较差的反应。
Nat Med. 2012 Mar 18;18(4):521-8. doi: 10.1038/nm.2713.
5
The effect of BIM deletion polymorphism on intrinsic resistance and clinical outcome of cancer patient with kinase inhibitor therapy.BIM缺失多态性对激酶抑制剂治疗的癌症患者内在耐药性及临床结局的影响。
Sci Rep. 2015 Jun 15;5:11348. doi: 10.1038/srep11348.
6
FTY720 induces apoptosis of chronic myelogenous leukemia cells via dual activation of BIM and BID and overcomes various types of resistance to tyrosine kinase inhibitors.FTY720 通过双重激活 BIM 和 BID 诱导慢性髓性白血病细胞凋亡，并克服酪氨酸激酶抑制剂的各种耐药性。
Apoptosis. 2013 Nov;18(11):1437-1446. doi: 10.1007/s10495-013-0882-y.
7
The BCL2L11 (BIM) deletion polymorphism is a possible criterion for discontinuation of imatinib in chronic myeloid leukaemia patients.BCL2L11（BIM）缺失多态性可能是慢性髓性白血病患者停用伊马替尼的一个标准。
Br J Haematol. 2013 Jan;160(2):269-71. doi: 10.1111/bjh.12111. Epub 2012 Nov 1.
8
A novel BIM deletion polymorphism: implications and lessons for cancer targeted therapies.一种新型的BIM缺失多态性：对癌症靶向治疗的启示与教训
Rinsho Ketsueki. 2013 Oct;54(10):1714-9.
9
The Bim deletion polymorphism clinical profile and its relation with tyrosine kinase inhibitor resistance in Chinese patients with non-small cell lung cancer.中国非小细胞肺癌患者中Bim缺失多态性的临床特征及其与酪氨酸激酶抑制剂耐药性的关系。
Cancer. 2014 Aug 1;120(15):2299-307. doi: 10.1002/cncr.28725. Epub 2014 Apr 15.
10
EGFR-TKI resistance due to BIM polymorphism can be circumvented in combination with HDAC inhibition.由于 BIM 多态性导致的 EGFR-TKI 耐药性可以通过与 HDAC 抑制联合来规避。
Cancer Res. 2013 Apr 15;73(8):2428-34. doi: 10.1158/0008-5472.CAN-12-3479. Epub 2013 Feb 4.

引用本文的文献

1
Understanding of Immune Escape Mechanisms and Advances in Cancer Immunotherapy.免疫逃逸机制的理解与癌症免疫治疗的进展
J Oncol. 2022 Mar 31;2022:8901326. doi: 10.1155/2022/8901326. eCollection 2022.
2
The pharmacogenomics of drug resistance to protein kinase inhibitors.蛋白激酶抑制剂耐药性的药物基因组学
Drug Resist Updat. 2016 Sep;28:28-42. doi: 10.1016/j.drup.2016.06.008. Epub 2016 Jul 5.
3
NF-κB-driven suppression of FOXO3a contributes to EGFR mutation-independent gefitinib resistance.核因子-κB驱动的FOXO3a抑制作用导致表皮生长因子受体（EGFR）突变非依赖性吉非替尼耐药。

本文引用的文献

1
A common BIM deletion polymorphism mediates intrinsic resistance and inferior responses to tyrosine kinase inhibitors in cancer.一种常见的 BIM 删除多态性介导了癌症对酪氨酸激酶抑制剂的固有耐药性和较差的反应。
Nat Med. 2012 Mar 18;18(4):521-8. doi: 10.1038/nm.2713.
2
Converting cancer therapies into cures: lessons from infectious diseases.将癌症疗法转化为治愈方法：传染病的经验教训。
Cell. 2012 Mar 16;148(6):1089-98. doi: 10.1016/j.cell.2012.02.015.
3
BID, BIM, and PUMA are essential for activation of the BAX- and BAK-dependent cell death program.
Proc Natl Acad Sci U S A. 2016 May 3;113(18):E2526-35. doi: 10.1073/pnas.1522612113. Epub 2016 Apr 18.
4
Pharmacogenomics in oncology care.肿瘤护理中的药物基因组学。
Front Genet. 2014 Apr 8;5:73. doi: 10.3389/fgene.2014.00073. eCollection 2014.
5
Epidermal growth factor receptor mutations in lung adenocarcinoma.肺腺癌中的表皮生长因子受体突变。
Lab Invest. 2014 Feb;94(2):129-37. doi: 10.1038/labinvest.2013.147. Epub 2013 Dec 30.
6
The EphB4 receptor tyrosine kinase promotes lung cancer growth: a potential novel therapeutic target.EphB4 受体酪氨酸激酶促进肺癌生长：一个潜在的新治疗靶点。
PLoS One. 2013 Jul 2;8(7):e67668. doi: 10.1371/journal.pone.0067668. Print 2013.
7
A mechanism of resistance to gefitinib mediated by cellular reprogramming and the acquisition of an FGF2-FGFR1 autocrine growth loop.细胞重编程和获得 FGF2-FGFR1 自分泌生长环介导的吉非替尼耐药机制。
Oncogenesis. 2013 Mar 25;2(3):e39. doi: 10.1038/oncsis.2013.4.
8
PUMA and BIM are required for oncogene inactivation-induced apoptosis.PUMA 和 BIM 是癌基因失活诱导凋亡所必需的。
Sci Signal. 2013 Mar 26;6(268):ra20. doi: 10.1126/scisignal.2003483.
9
Bim, a proapoptotic protein, up-regulated via transcription factor E2F1-dependent mechanism, functions as a prosurvival molecule in cancer.Bim，一种通过转录因子 E2F1 依赖性机制上调的促凋亡蛋白，在癌症中作为一种促生存分子发挥作用。
J Biol Chem. 2013 Jan 4;288(1):368-81. doi: 10.1074/jbc.M112.386102. Epub 2012 Nov 14.
10
Single nucleotide polymorphisms (SNPs) in non-small cell lung cancer (NSCLC) patients.非小细胞肺癌（NSCLC）患者中的单核苷酸多态性（SNPs）。
Oncologist. 2012;17(12):1484-5. doi: 10.1634/theoncologist.2012-0205. Epub 2012 Sep 26.
BID、BIM 和 PUMA 对于激活 Bax 和 Bak 依赖性细胞死亡程序是必不可少的。
Science. 2010 Dec 3;330(6009):1390-3. doi: 10.1126/science.1190217.
4
Chronic myeloid leukemia in Asia.亚洲的慢性髓性白血病
Int J Hematol. 2009 Jan;89(1):14-23. doi: 10.1007/s12185-008-0230-0. Epub 2008 Dec 20.
5
IAP-targeted therapies for cancer.针对癌症的IAP靶向疗法。
Oncogene. 2008 Oct 20;27(48):6252-75. doi: 10.1038/onc.2008.302.
6
The BCL-2 protein family: opposing activities that mediate cell death.BCL-2蛋白家族：介导细胞死亡的相反活性
Nat Rev Mol Cell Biol. 2008 Jan;9(1):47-59. doi: 10.1038/nrm2308.
7
Gefitinib-induced killing of NSCLC cell lines expressing mutant EGFR requires BIM and can be enhanced by BH3 mimetics.吉非替尼诱导表达突变型表皮生长因子受体（EGFR）的非小细胞肺癌细胞系死亡需要BIM，并且可被BH3模拟物增强。
PLoS Med. 2007 Oct;4(10):1681-89; discussion 1690. doi: 10.1371/journal.pmed.0040316.
8
BIM mediates EGFR tyrosine kinase inhibitor-induced apoptosis in lung cancers with oncogenic EGFR mutations.BIM介导具有致癌性EGFR突变的肺癌中表皮生长因子受体酪氨酸激酶抑制剂诱导的细胞凋亡。
PLoS Med. 2007 Oct;4(10):1669-79; discussion 1680. doi: 10.1371/journal.pmed.0040315.
9
Induction of BIM is essential for apoptosis triggered by EGFR kinase inhibitors in mutant EGFR-dependent lung adenocarcinomas.在依赖突变型表皮生长因子受体（EGFR）的肺腺癌中，BIM的诱导对于EGFR激酶抑制剂引发的细胞凋亡至关重要。
PLoS Med. 2007 Oct 9;4(10):e294. doi: 10.1371/journal.pmed.0040294.
10
Puma cooperates with Bim, the rate-limiting BH3-only protein in cell death during lymphocyte development, in apoptosis induction.在淋巴细胞发育过程中，Puma与细胞死亡中起限速作用的仅含BH3结构域的蛋白Bim协同作用，诱导细胞凋亡。
J Exp Med. 2006 Dec 25;203(13):2939-51. doi: 10.1084/jem.20061552. Epub 2006 Dec 18.