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CTCF puts a new twist on UV damage and repair in skin cancer CTCF为紫外线损伤和皮肤癌修复提供了新的思路
IF 2.1 Q3 ONCOLOGY
Molecular and Cellular Oncology
Pub Date : 2021-11-02 DOI: 10.1080/23723556.2021.2009424
Bastian Stark, G. Poon, John J. Wyrick
ABSTRACT Somatic mutations in skin cancers are highly enriched at binding sites for CCCTC-binding factor (CTCF). We have discovered that CTCF binding alters the DNA structure to render it more susceptible to UV damage. Elevated UV damage formation at CTCF binding sites, in conjunction with subsequent repair inhibition, promotes UV mutagenesis.
摘要皮肤癌中的体细胞突变在CCCTC结合因子（CTCF）的结合位点高度富集。我们发现CTCF结合会改变DNA结构，使其更容易受到紫外线损伤。CTCF结合位点的紫外线损伤形成增加，再加上随后的修复抑制，促进了紫外线诱变。
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引用次数: 5
Biomimetic human bone marrow tissues: models to study hematopoiesis and platforms for drug testing 仿生人骨髓组织：研究造血的模型和药物测试平台
IF 2.1 Q3 ONCOLOGY
Molecular and Cellular Oncology
Pub Date : 2021-11-02 DOI: 10.1080/23723556.2021.2007030
A. García-García, I. Martin
ABSTRACT We propose an in vitro 3D culture system combining perfusion bioreactors, scaffolds and human primary cells to engineer fully-humanized, biomimetic and customizable bone marrow tissues. This system could serve as a model to investigate human hematopoietic stem cell niches, but also as a drug testing platform for pharmaceutical research and patient-personalized medicine.
摘要：我们提出了一种结合灌注生物反应器、支架和人类原代细胞的体外3D培养系统，以设计完全人源化、仿生和可定制的骨髓组织。该系统可以作为研究人类造血干细胞生态位的模型，也可以作为药物研究和患者个性化用药的药物测试平台。
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引用次数: 1
Turning end-joining upside down in mitosis 有丝分裂中的翻转末端连接
IF 2.1 Q3 ONCOLOGY
Molecular and Cellular Oncology
Pub Date : 2021-11-02 DOI: 10.1080/23723556.2021.2007029
M. Llorens-Agost, M. Ensminger, H. Le, W. Heyer, M. Löbrich
ABSTRACT How cells deal with DNA breaks during mitosis is not well understood. While canonical non-homologous end-joining predominates in interphase, it is inhibited in mitosis to avoid telomere fusions. DNA polymerase θ mediated end-joining appears to be repressed in interphase, but promotes break repair in mitosis. The nature and induction time of breaks might determine their fate during mitosis.
细胞在有丝分裂过程中如何处理DNA断裂尚不清楚。虽然典型的非同源末端连接在间期占主导地位，但在有丝分裂中被抑制以避免端粒融合。DNA聚合酶θ介导的末端连接似乎在间期受到抑制，但在有丝分裂中促进断裂修复。断裂的性质和诱导时间可能决定它们在有丝分裂中的命运。
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引用次数: 0
Mitotic WNT: aligning chromosomes through KIF2A 有丝分裂WNT：通过KIF2A排列染色体
IF 2.1 Q3 ONCOLOGY
Molecular and Cellular Oncology
Pub Date : 2021-11-02 DOI: 10.1080/23723556.2021.2011564
A. Bufe, S. Acebrón
ABSTRACT WNT signaling regulates cell cycle progression and fate determination through β-catenin dependent transcription, and its misregulation is often associated with tumorigenesis. Our recent work demonstrated that basal WNT activity is also required to ensure proper chromosome alignment during mitosis through the regulation of kinesin family member 2A (KIF2A).
摘要WNT信号通过β-连环蛋白依赖性转录调节细胞周期进展和命运决定，其失调通常与肿瘤发生有关。我们最近的工作表明，在有丝分裂过程中，通过调节驱动蛋白家族成员2A（KIF2A），还需要基础的WNT活性来确保染色体的正确排列。
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引用次数: 1
KMT2D deficiency confers a therapeutic vulnerability to glycolytic and IGFR inhibitors in melanoma. KMT2D缺陷赋予黑色素瘤对糖酵解和IGFR抑制剂的治疗脆弱性。
IF 2.1 Q3 ONCOLOGY
Molecular and Cellular Oncology
Pub Date : 2021-11-01 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1984827
Navya Murugesan, Mayinuer Maitituoheti

We reported that histone H3 lysine (K) 4 methyltransferase, KMT2D, serves as a potent tumor-suppressor in melanoma, which was identified via in vivo epigenome-focused RNA interference (RNAi) screen. KMT2D-deficient tumors show substantial reprogramming of key metabolic pathways including glycolysis via reduction of H3K4me1 (Histone H3K4 mono-methylation)-marked active enhancers, conferring sensitivity to inhibitors of glycolysis and IGFR (Insulin Growth Factor Receptor) pathway.

我们报道了组蛋白H3赖氨酸(K) 4甲基转移酶，KMT2D，在黑色素瘤中作为一种有效的肿瘤抑制因子，通过体内表观基因组聚焦RNA干扰(RNAi)筛选鉴定。kmt2d缺陷肿瘤显示出关键代谢途径的大量重编程，包括通过减少H3K4me1(组蛋白H3K4单甲基化)标记的活性增强子进行糖酵解，赋予糖酵解抑制剂和IGFR(胰岛素生长因子受体)途径的敏感性。
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引用次数: 1
ERBB3 as a therapeutic target in glioblastoma: overexpression can make the difference. ERBB3作为胶质母细胞瘤的治疗靶点:过表达会产生差异。
IF 2.1 Q3 ONCOLOGY
Molecular and Cellular Oncology
Pub Date : 2021-10-27 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1990677
Francesca De Bacco, Carla Boccaccio
ABSTRACT By exploiting an integrated experimental platform based on patient-derived cancer stem cells, we identified a glioblastoma subset characterized by inheritable Erb-B2 Receptor Tyrosine Kinase 3 (ERBB3) overexpression, metabolic dependency on ERBB3 signaling, and liability to ERBB3 targeting. We provide insights on why some glioblastomas may rely on ERBB3 and how to recognize them.
通过利用基于患者来源的癌症干细胞的综合实验平台，我们确定了一个胶质母细胞瘤亚群，其特征是可遗传的Erb-B2受体酪氨酸激酶3 (ERBB3)过表达，对ERBB3信号的代谢依赖以及对ERBB3靶向的依赖性。我们提供了一些胶质母细胞瘤可能依赖ERBB3的原因以及如何识别它们的见解。
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引用次数: 2
Targeting cancer’s sweet spot: UGP2 as a therapeutic vulnerability 靶向癌症的最佳点:作为治疗弱点的UGP2
IF 2.1 Q3 ONCOLOGY
Molecular and Cellular Oncology
Pub Date : 2021-10-27 DOI: 10.1080/23723556.2021.1990676
Sunghoon Kim, A. Wolfe, S. Kim
ABSTRACT Understanding the mechanisms governing metabolic reprogramming that underlie potential vulnerabilities in cancer cells is key to developing novel therapeutic strategies. The catalytic enzyme UDP-glucose pyrophosphorylase 2 (UGP2) drives the production of UDP-glucose. Our recent work demonstrated the crucial role of UGP2 in cancer growth and its regulation of cellular metabolic processes.
了解癌症细胞中潜在脆弱性的代谢重编程控制机制是开发新的治疗策略的关键。催化酶udp -葡萄糖焦磷酸化酶2 (UGP2)驱动udp -葡萄糖的产生。我们最近的工作证明了UGP2在癌症生长及其对细胞代谢过程的调节中的关键作用。
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引用次数: 0
Targeting the immune microenvironment during immunotherapy for solid tumors. 实体肿瘤免疫治疗中的免疫微环境靶向。
IF 2.1 Q3 ONCOLOGY
Molecular and Cellular Oncology
Pub Date : 2021-10-27 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1994327
Aiman Sabaawy, Saman Zeeshan

JAK/STAT signaling is a central hub in cancer development, progression, immunosurveillance and response to immunotherapy. We discuss recent advances in the role of the JAK/STAT pathway in immunotherapies. We stress the importance of fully understanding how JAK/STAT modifies the immune response before implementing clinical trials combining JAK/STAT inhibitors with immunotherapy.

JAK/STAT信号是癌症发生、进展、免疫监测和免疫治疗反应的中心枢纽。我们讨论了JAK/STAT通路在免疫治疗中的作用的最新进展。我们强调在实施JAK/STAT抑制剂联合免疫治疗的临床试验之前，充分了解JAK/STAT如何改变免疫反应的重要性。
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引用次数: 3
Chromatin state profiling reveals PRC2 inhibition as a therapeutic target in NRAS-mutant melanoma. 染色质状态分析揭示PRC2抑制是nras突变黑色素瘤的治疗靶点。
IF 2.1 Q3 ONCOLOGY
Molecular and Cellular Oncology
Pub Date : 2021-10-27 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1986350
Christopher J Terranova

Recently, we have generated 284 epigenomic maps in melanoma. Using chromatin state profiling we identify an association of NRAS-mutants with bivalent Histone H3 lysine 27 trimethylation (H3K27me3) and broad H3K4me3 domains. Reprogramming of bivalent H3K27me3 occurs on critical invasive-regulators and its resolution using Enhancer of Zeste Homolog 2 (EZH2) inhibition reduces invasive capacity and tumor burden in NRAS-mutant patient samples.

最近，我们已经生成了284个黑色素瘤的表观基因组图谱。通过染色质状态分析，我们确定了nras突变体与二价组蛋白H3赖氨酸27三甲基化(H3K27me3)和广泛的H3K4me3结构域的关联。在nras突变患者样本中，双价H3K27me3重编程发生在关键的侵入性调节因子上，使用Zeste同源物增强子2 (Enhancer of Zeste Homolog 2, EZH2)抑制可以降低侵入能力和肿瘤负荷。
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引用次数: 0
Dedifferentiation of esophageal progenitors in metaplasia and cancer 化生和癌中食管祖细胞的去分化
IF 2.1 Q3 ONCOLOGY
Molecular and Cellular Oncology
Pub Date : 2021-10-21 DOI: 10.1080/23723556.2021.1991758
Alizée Vercauteren Drubbel, Benjamin Beck
ABSTRACT Barrett syndrome is a squamo-columnar metaplasia increasing the risk of developing esophageal adenocarcinoma. Recently, we showed that esophageal cells can transdifferentiate into undifferentiated columnar cells in vivo. Here, we discuss about the potential of these cells to be a reservoir for intestinal metaplasia and/or esophageal adenocarcinoma.
摘要Barrett综合征是一种鳞状柱状化生，增加了患食道腺癌的风险。最近，我们发现食管细胞可以在体内转分化为未分化的柱状细胞。在这里，我们讨论了这些细胞作为肠化生和/或食管腺癌宿主的潜力。
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引用次数: 0
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