IF 6.3 2区医学 Q1 ONCOLOGY

Neoplasia

Pub Date : 2024-11-18 DOI: 10.1016/j.neo.2024.101077

Qiao-Xin Lin, Wen-Wen Song, Wen-Xia Xie, Yi-Ting Deng, Yan-Na Gong, Yi-Ru Liu, Yi Tian, Wen-Ya Zhao, Ling Tian, Dian-Na Gu

Objective: Anti-angiogenic therapy and immune checkpoint blockade therapy are currently important treatments for non-small cell lung cancer. However, the combined use of the two therapies is controversial, and few studies have investigated the effects of different time sequences of the two therapies on treatment outcomes.

Methods: The tumor-bearing mouse model was established and the mice were divided into four groups, including AA-ICB sequence group, ICB-AA sequence group, synchronization group and the control group. Immunohistochemistry was used to assess tumor microvessels and PD-L1 expression. Selected immune cell populations were evaluated using flow cytometry. Meta-analysis and clinical information were used to elucidate the clinical effects of administration sequence.

Results: We found that anti-PD-L1 treatment followed by anti-VEGFR2 therapy exerts the best inhibitory effect on tumor growth. Different sequences of anti-angiogenic therapy and immune checkpoint blockade therapy resulted in different proportions of tumor microvessels and immune cell populations in the tumor microenvironment. We further revealed that the administration of anti-PD-L1 before anti-VEGFR brought more normalized tumor blood vessels and CD8⁺T cell infiltration and reduced immunosuppressive cells in the tumor microenvironment. Subsequent re-transplantation experiments confirmed the long-term benefits of this treatment strategy. The meta-analysis reinforced that immunotherapy prior to anti-angiogenic therapy or combination therapy have better therapeutic effects in advanced non-small cell lung cancer.

Conclusion: Our study demonstrated that the therapeutic effect of anti-angiogenic treatment after immune checkpoint therapy was superior to that of concurrent therapy, whereas anti-angiogenic therapy followed by immunotherapy did not bring more significant clinical benefits than independent monotherapy.

目的：抗血管生成疗法和免疫检查点阻断疗法是目前治疗非小细胞肺癌的重要方法：抗血管生成疗法和免疫检查点阻断疗法是目前治疗非小细胞肺癌的重要方法。然而，这两种疗法的联合使用存在争议，很少有研究调查两种疗法的不同时间顺序对治疗效果的影响：方法：建立肿瘤小鼠模型，将小鼠分为四组，包括 AA-ICB 序列组、ICB-AA 序列组、同步组和对照组。采用免疫组化方法评估肿瘤微血管和 PD-L1 的表达。使用流式细胞术评估选定的免疫细胞群。元分析和临床信息用于阐明给药序列的临床效果：结果：我们发现抗PD-L1治疗后再进行抗血管内皮生长因子受体2治疗对肿瘤生长的抑制效果最好。抗血管生成治疗和免疫检查点阻断治疗的不同顺序导致肿瘤微环境中肿瘤微血管和免疫细胞群的比例不同。我们进一步发现，在抗血管内皮生长因子受体（anti-VEGFR）治疗前给予抗PD-L1可使肿瘤血管和CD8+T细胞浸润趋于正常，并减少肿瘤微环境中的免疫抑制细胞。随后的再移植实验证实了这一治疗策略的长期疗效。荟萃分析证实，晚期非小细胞肺癌患者在接受抗血管生成治疗或联合治疗前接受免疫治疗，疗效更佳：我们的研究表明，免疫检查点治疗后抗血管生成治疗的疗效优于同期治疗，而抗血管生成治疗后再进行免疫治疗并不比独立的单药治疗带来更显著的临床获益。

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引用次数: 0

DCZ0014, a novel compound in the therapy of diffuse large B-cell lymphoma via the B cell receptor signaling pathway. DCZ0014，一种通过B细胞受体信号通路治疗弥漫性大B细胞淋巴瘤的新化合物。

IF 4.8 2区医学 Q1 ONCOLOGY

Neoplasia

Pub Date : 2020-08-01 DOI: 10.21203/rs.3.rs-48447/v1

Shuaikang Chang, Bo Li, Yongsheng Xie, Yingcong Wang, Zhijian Xu, Shuhan Jin, D. Yu, Huaping Wang, Yumeng Lu, Yong Zhang, Ruye Ma, Cheng Huang, Weiming Lai, Xiaosong Wu, Weiliang Zhu, Jumei Shi

Diffuse large B cell lymphoma (DLBCL) is a clinical and genetically heterogeneous lymphoid malignancy. Although R-CHOP (rituximab plus cyclophosphamide, vincristine, doxorubicin, and prednisone) treatment can improve the survival rate of patients with DLBCL, more than 30% of patients exhibit treatment failure, relapse, or refractory disease. Therefore, novel drugs or targeted therapies are needed to improve the survival of patients with DLBCL. The compound DCZ0014 is a novel chemical similar to berberine. In this study, we found that DCZ0014 significantly inhibited the proliferation and activity of DLBCL cells, and induced cell apoptosis. Following treatment with DCZ0014, DLBCL cells accumulated in G0/G1-phase of the cell cycle and showed decreased mitochondrial membrane potential. Additionally, DCZ0014 inhibited DNA synthesis, enhanced DNA damage in DLBCL cells, as well as inhibited Lyn/Syk in B cell receptor signaling pathway. Further experiments demonstrated that DCZ0014 did not significantly affect peripheral blood mononuclear cells. Tumor xenograft model showed that DCZ0014 not only inhibited tumor growth but also extended the survival time of mice. Thus, DCZ0014 showed potential for clinical application in the treatment of patients with DLBCL.

弥漫性大B细胞淋巴瘤(DLBCL)是一种临床和遗传异质性的淋巴细胞恶性肿瘤。虽然R-CHOP(利妥昔单抗联合环磷酰胺、新碱、多柔比星和强尼松)治疗可以提高DLBCL患者的生存率，但超过30%的患者出现治疗失败、复发或难治性疾病。因此，需要新的药物或靶向治疗来提高DLBCL患者的生存率。化合物DCZ0014是一种类似小檗碱的新型化学物质。在本研究中，我们发现DCZ0014明显抑制DLBCL细胞的增殖和活性，并诱导细胞凋亡。DCZ0014处理后，DLBCL细胞在细胞周期的G0/ g1期聚集，线粒体膜电位下降。DCZ0014抑制DNA合成，增强DLBCL细胞DNA损伤，抑制B细胞受体信号通路Lyn/Syk。进一步实验表明，DCZ0014对外周血单核细胞无明显影响。肿瘤移植模型显示，DCZ0014不仅能抑制肿瘤生长，还能延长小鼠的生存时间。因此，DCZ0014在DLBCL患者的治疗中具有临床应用潜力。

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引用次数: 0

Corrigendum to "Hodgkin Lymphoma Cell Lines Are Characterized by a Specific miRNA Expression Profile." Neoplasia 2009, Feb;11(2):167-176. “霍奇金淋巴瘤细胞系以特定的miRNA表达谱为特征”的更正。肿瘤学报，2009;11(2):167-176。

IF 4.8 2区医学 Q1 ONCOLOGY

Neoplasia

Pub Date : 2018-01-28 DOI: 10.1016/J.NEO.2017.11.008

J. Gibcus, L. Tan, G. Harms, R. Schakel, D. de Jong, T. Blokzijl, P. Möller, S. Poppema, B. Kroesen, A. van den Berg

引用次数: 0

The dual PI3K/mTOR inhibitor NVP-BEZ235 is a potent inhibitor of ATM- and DNA-PKCs-mediated DNA damage responses. 双PI3K/mTOR抑制剂NVP-BEZ235是ATM和DNA- pkcs介导的DNA损伤反应的有效抑制剂。

IF 4.8 2区医学 Q1 ONCOLOGY

Neoplasia

Pub Date : 2012-04-15 DOI: 10.1158/1538-7445.AM2012-3745

B. Mukherjee, N. Tomimatsu, K. Amancherla, Cristel V. Camacho, N. Pichamoorthy, S. Burma

Inhibitors of PI3K/Akt signaling are being actively developed for tumor therapy owing to the frequent mutational activation of the PI3K-Akt-mTORC1 pathway in many cancers, including glioblastomas (GBMs). NVP-BEZ235 is a novel and potent dual PI3K/mTOR inhibitor that is currently in phase 1/2 clinical trials for advanced solid tumors. Here, we show that NVP-BEZ235 also potently inhibits ATM and DNA-PKcs, the two major kinases responding to ionizing radiation (IR)-induced DNA double-strand breaks (DSBs). Consequently, NVP-BEZ235 blocks both nonhomologous end joining and homologous recombination DNA repair pathways resulting in significant attenuation of DSB repair. In addition, phosphorylation of ATMtargets and implementation of the G(2)/M cell cycle checkpoint are also attenuated by this drug. As a result, NVP-BEZ235 confers an extreme degree of radiosensitization and impairs DSB repair in a panel of GBM cell lines irrespective of their Akt activation status. NVP-BEZ235 also significantly impairs DSB repair in a mouse tumor model thereby validating the efficacy of this drug as a DNA repair inhibitor in vivo. Our results, showing that NVP-BEZ235 is a potent and novel inhibitor of ATM and DNA-PKcs, have important implications for the informed and rational design of clinical trials involving this drug and also reveal the potential utility of NVP-BEZ235 as an effective radiosensitizer for GBMs in the clinic.

由于PI3K-Akt- mtorc1信号通路在包括胶质母细胞瘤(GBMs)在内的许多癌症中经常发生突变激活，PI3K/Akt信号通路抑制剂正被积极开发用于肿瘤治疗。NVP-BEZ235是一种新型有效的PI3K/mTOR双抑制剂，目前处于晚期实体瘤的1/2期临床试验中。在这里，我们发现NVP-BEZ235也能有效抑制ATM和DNA- pkcs，这两种主要的激酶对电离辐射(IR)诱导的DNA双链断裂(DSBs)有反应。因此，NVP-BEZ235阻断了非同源末端连接和同源重组DNA修复途径，导致DSB修复的显著衰减。此外，atm靶点的磷酸化和G(2)/M细胞周期检查点的实施也被这种药物减弱。结果表明，无论Akt激活状态如何，nlp - bez235在一组GBM细胞系中具有极端程度的放射致敏性，并损害DSB修复。在小鼠肿瘤模型中，NVP-BEZ235也显著损害DSB修复，从而验证了该药物作为DNA修复抑制剂在体内的功效。我们的研究结果表明，NVP-BEZ235是一种有效的新型ATM和DNA-PKcs抑制剂，这对涉及该药物的临床试验的知情和合理设计具有重要意义，同时也揭示了NVP-BEZ235在临床中作为GBMs有效放射增敏剂的潜在用途。

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引用次数: 169

Sensitization of pancreatic cancer stem cells to gemcitabine by Chk1 inhibition. 通过Chk1抑制胰腺癌干细胞对吉西他滨的增敏。

IF 4.8 2区医学 Q1 ONCOLOGY

Neoplasia

Pub Date : 2011-04-15 DOI: 10.1158/1538-7445.AM2011-3919

V. A. Venkatesha, L. A. Parsels, J. Parsels, Lili Zhao, S. Zabludoff, D. Simeone, J. Maybaum, T. Lawrence, M. Morgan

Checkpoint kinase 1 (Chk1) inhibition sensitizes pancreatic cancer cells and tumors to gemcitabine. We hypothesized that Chk1 inhibition would sensitize pancreatic cancer stem cells to gemcitabine. We tested this hypothesis by using two patient-derived xenograft models (designated J and F) and the pancreatic cancer stem cell markers CD24, CD44, and ESA. We determined the percentage of marker-positive cells and their tumor-initiating capacity (by limiting dilution assays) after treatment with gemcitabine and the Chk1 inhibitor, AZD7762. We found that marker-positive cells were significantly reduced by the combination of gemcitabine and AZD7762. In addition, secondary tumor initiation was significantly delayed in response to primary tumor treatment with gemcitabine + AZD7762 compared with control, gemcitabine, or AZD7762 alone. Furthermore, for the same number of stem cells implanted from gemcitabine- versus gemcitabine + AZD7762-treated primary tumors, secondary tumor initiation at 10 weeks was 83% versus 43%, respectively. We also found that pS345 Chk1, which is a measure of DNA damage, was induced in marker-positive cells but not in the marker-negative cells. These data demonstrate that Chk1 inhibition in combination with gemcitabine reduces both the percentage and the tumor-initiating capacity of pancreatic cancer stem cells. Furthermore, the finding that the Chk1-mediated DNA damage response was greater in stem cells than in non-stem cells suggests that Chk1 inhibition may selectively sensitize pancreatic cancer stem cells to gemcitabine, thus making Chk1 a potential therapeutic target for improving pancreatic cancer therapy.

检查点激酶1 (Chk1)抑制使胰腺癌细胞和肿瘤对吉西他滨敏感。我们假设Chk1抑制会使胰腺癌干细胞对吉西他滨敏感。我们通过使用两种患者来源的异种移植模型(指定为J和F)和胰腺癌干细胞标记物CD24、CD44和ESA来验证这一假设。在用吉西他滨和Chk1抑制剂AZD7762治疗后，我们测定了标记阳性细胞的百分比及其肿瘤启动能力(通过限制稀释试验)。我们发现吉西他滨和AZD7762联合使用显著减少了标记阳性细胞。此外，与对照组、吉西他滨或AZD7762单独治疗相比，吉西他滨+ AZD7762治疗原发性肿瘤的继发性肿瘤发生明显延迟。此外，从吉西他滨-与吉西他滨+ azd7762治疗的原发肿瘤中植入相同数量的干细胞，10周时继发肿瘤起始率分别为83%和43%。我们还发现pS345 Chk1(一种DNA损伤的测量方法)在标记阳性细胞中被诱导，而在标记阴性细胞中则没有。这些数据表明，Chk1抑制联合吉西他滨可降低胰腺癌干细胞的百分比和肿瘤启动能力。此外，研究发现Chk1介导的DNA损伤反应在干细胞中比在非干细胞中更大，这表明Chk1抑制可能选择性地使胰腺癌干细胞对吉西他滨敏感，从而使Chk1成为改善胰腺癌治疗的潜在治疗靶点。

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引用次数: 88

Astrocytes upregulate survival genes in tumor cells and induce protection from chemotherapy. 星形胶质细胞上调肿瘤细胞中的生存基因并诱导对化疗的保护。

IF 4.8 2区医学 Q1 ONCOLOGY

Neoplasia

Pub Date : 2010-04-15 DOI: 10.1158/1538-7445.AM10-3428

Sun-jin Kim, Jang‐Seong Kim, E. Park, Ju-Seog Lee, Qingtang Lin, R. Langley, Marva Maya, Junqin He, S. Kim, Weihua Zhang, K. Balasubramanian, D. Fan, G. Mills, M. Hung, I. Fidler

In the United States, more than 40% of cancer patients develop brain metastasis. The median survival for untreated patients is 1 to 2 months, which may be extended to 6 months with conventional radiotherapy and chemotherapy. The growth and survival of metastasis depend on the interaction of tumor cells with host factors in the organ microenvironment. Brain metastases are surrounded and infiltrated by activated astrocytes and are highly resistant to chemotherapy. We report here that coculture of human breast cancer cells or lung cancer cells with murine astrocytes (but not murine fibroblasts) led to the up-regulation of survival genes, including GSTA5, BCL2L1, and TWIST1, in the tumor cells. The degree of up-regulation directly correlated with increased resistance to all tested chemotherapeutic agents. We further show that the up-regulation of the survival genes and consequent resistance are dependent on the direct contact between the astrocytes and tumor cells through gap junctions and are therefore transient. Knocking down these genes with specific small interfering RNA rendered the tumor cells sensitive to chemotherapeutic agents. These data clearly demonstrate that host cells in the microenvironment influence the biologic behavior of tumor cells and reinforce the contention that the organ microenvironment must be taken into consideration during the design of therapy.

在美国，超过40%的癌症患者会发生脑转移。未治疗患者的中位生存期为1 ~ 2个月，常规放化疗可延长至6个月。肿瘤细胞在器官微环境中与宿主因子的相互作用决定了肿瘤细胞的生长和转移存活。脑转移瘤被活化的星形胶质细胞包围和浸润，对化疗具有高度耐药性。我们在这里报道了人乳腺癌细胞或肺癌细胞与小鼠星形胶质细胞(而不是小鼠成纤维细胞)共培养导致肿瘤细胞中生存基因(包括GSTA5, BCL2L1和TWIST1)的上调。上调的程度与对所有化疗药物的耐药性增加直接相关。我们进一步表明，生存基因的上调和随之而来的抗性依赖于星形胶质细胞和肿瘤细胞之间通过间隙连接的直接接触，因此是短暂的。用特定的小干扰RNA敲除这些基因使肿瘤细胞对化疗药物敏感。这些数据清楚地表明，微环境中的宿主细胞影响肿瘤细胞的生物学行为，并加强了在设计治疗时必须考虑器官微环境的论点。

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引用次数: 239

Enhanced resistance to tamoxifen by the c-ABL proto-oncogene in breast cancer. 乳腺癌中c-ABL原癌基因增强对他莫昔芬的耐药性。

IF 4.8 2区医学 Q1 ONCOLOGY

Neoplasia

Pub Date : 2010-04-15 DOI: 10.1158/1538-7445.AM10-LB-179

Huajun Zhao, F. Ou-Yang, I. Chen, M. Hou, S. Yuan, Hsueh-Ling Chang, Yi-Chen Lee, R. Plattner, S. Waltz, S. Ho, J. Sims, Shao-Chun Wang

Targeting the estrogen receptor is an important strategy in breast cancer therapy. However, although inhibiting estrogen receptor function with specific estrogen receptor modulators can achieve a primary response in cancer patients, intrinsic or subsequently acquired resistance to the therapy remains a major obstacle in the clinic. Thus, it is critical to gain a more thorough understanding of how estrogen receptor functions are regulated in breast cancer.Here, we demonstrate that the non-receptor tyrosine kinase c-ABL is a functional partner of the estrogen receptor, as expression of c-ABL sustained transcriptional activity of the estrogen receptor. More importantly, inhibition of c-ABL resulted in sensitization to treatment by tamoxifen (TAM) in estrogen receptor-positive breast cancer cells, as manifested by inhibition of cell survival and suppression of anchorage-independent growth. We found that c-ABL interacts with estrogen receptor in breast cancer cells and that expression of c-ABL is a frequent event in primary breast cancer tumor tissues. In estrogen receptor-positive tumors, the expression of c-ABL significantly correlated with disease progression and metastasis. This study shows that c-ABL regulates the cellular response to TAM through functional interaction with the estrogen receptor, which suggests c-ABL as a therapeutic target and a prognostic tumor marker for breast cancer.

靶向雌激素受体是乳腺癌治疗的重要策略。然而，尽管用特异性雌激素受体调节剂抑制雌激素受体功能可以在癌症患者中获得原发性应答，但对治疗的内在或随后获得性耐药仍然是临床的主要障碍。因此，更深入地了解雌激素受体的功能在乳腺癌中是如何调节的是至关重要的。在这里，我们证明了非受体酪氨酸激酶c-ABL是雌激素受体的功能伙伴，因为c-ABL的表达维持了雌激素受体的转录活性。更重要的是，抑制c-ABL导致雌激素受体阳性乳腺癌细胞对他莫昔芬(TAM)治疗增敏，表现为抑制细胞存活和抑制锚定非依赖性生长。我们发现c-ABL在乳腺癌细胞中与雌激素受体相互作用，并且c-ABL的表达在原发性乳腺癌肿瘤组织中是一个常见的事件。在雌激素受体阳性肿瘤中，c-ABL的表达与疾病进展和转移有显著相关性。本研究表明，c-ABL通过与雌激素受体的功能相互作用调节细胞对TAM的反应，提示c-ABL可作为乳腺癌的治疗靶点和预后肿瘤标志物。

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引用次数: 28

Prognostic relevance of hTERT mRNA expression in ductal adenocarcinoma of the pancreas. 胰腺导管腺癌中hTERT mRNA表达与预后的相关性。

IF 4.8 2区医学 Q1 ONCOLOGY

Neoplasia

Pub Date : 2008-09-17 DOI: 10.1055/S-0028-1089530

L. Grochola, T. Greither, H. Taubert, P. Möller, U. Knippschild, A. Udelnow, D. Henne-Bruns, P. Würl

Telomerase is thought to play an essential role in tumorigenesis and progression. Its activity is directly correlated with the expression of its catalytic subunit, human telomerase reverse transcriptase (hTERT). A correlation of transcript expression with a poor prognosis has been detected in different human malignancies. However, data on hTERT in pancreatic ductal adenocarcinoma (PDAC) are purely descriptive so far. Therefore, we evaluated the impact of hTERT expression on patients' prognosis. Human telomerase reverse transcriptase mRNA isolates from 56 human microdissected PDAC tissues were analyzed by quantitative reverse transcription-polymerase chain reaction and multivariate Cox regression hazard test. Elevated hTERT transcript levels were measured in 23 of 56 PDAC tissues, 33 patients showed no detectable transcripts. Unexpectedly, a low expression of hTERT mRNA levels was associated with a worse prognosis for overall survival (relative risk = 5.33; P = .013) when compared to high levels, whereas undetectable expression showed an intermediate risk of tumor-related death. These data challenge previous findings outlining hTERT's negative impact on overall survival. The risk pattern obtained in PDAC suggests a more complex regulation of hTERT.

端粒酶被认为在肿瘤发生和发展中起重要作用。其活性与其催化亚基——人端粒酶逆转录酶(hTERT)的表达直接相关。在不同的人类恶性肿瘤中发现了转录表达与预后不良的相关性。然而，到目前为止，hTERT在胰腺导管腺癌(PDAC)中的数据纯粹是描述性的。因此，我们评估了hTERT表达对患者预后的影响。采用定量逆转录-聚合酶链反应和多因素Cox回归危害检验对56例人PDAC微解剖组织中分离的人端粒酶逆转录酶mRNA进行分析。56例PDAC组织中有23例检测到hTERT转录物水平升高，33例患者未检测到转录物。出乎意料的是，hTERT mRNA水平的低表达与总生存预后较差相关(相对风险= 5.33;P = 0.013)，而无法检测到的表达显示肿瘤相关死亡的中等风险。这些数据挑战了先前关于hTERT对总体生存的负面影响的发现。在PDAC中获得的风险模式表明hTERT的监管更为复杂。

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引用次数: 9

Utility of a herpes oncolytic virus for the detection of neural invasion by cancer. 一种疱疹溶瘤病毒用于检测癌症的神经侵犯。

IF 4.8 2区医学 Q1 ONCOLOGY

Neoplasia

Pub Date : 2008-04-01 DOI: 10.1055/s-2008-1093272

Z. Gil, K. Kelly, P. Brader, J. Shah, Y. Fong, R. Wong

Prostate, pancreatic, and head and neck carcinomas have a high propensity to invade nerves. Surgical resection is a treatment modality for these patients, but it may incur significant deficits. The development of an imaging method able to detect neural invasion (NI) by cancer cells may guide surgical resection and facilitate preservation of normal nerves. We describe an imaging method for the detection of NI using a herpes simplex virus, NV1066, carrying tyrosine kinase and enhanced green fluorescent protein (eGFP). Infection of pancreatic (MiaPaCa2), prostate (PC3 and DU145), and adenoid cystic carcinoma (ACC3) cell lines with NV1066 induced a high expression of eGFP in vitro. An in vivo murine model of NI was established by implanting tumors into the sciatic nerves of nude mice. Nerves were then injected with NV1066, and infection was confirmed by polymerase chain reaction. Positron emission tomography with [(18)F]-2'-fluoro-2'-deoxyarabinofuranosyl-5-ethyluracil performed showed significantly higher uptake in NI than in control animals. Intraoperative fluorescent stereoscopic imaging revealed eGFP signal in NI treated with NV1066. These findings show that NV1066 may be an imaging method to enhance the detection of nerves infiltrated by cancer cells. This method may improve the diagnosis and treatment of patients with neurotrophic cancers by reducing injury to normal nerves and facilitating identification of infiltrated nerves requiring resection.

前列腺癌、胰腺癌和头颈癌有侵犯神经的高倾向。手术切除是治疗这些患者的一种方式，但它可能会产生显著的缺陷。一种能够检测癌细胞神经侵犯(NI)的成像方法的发展可能指导手术切除并促进正常神经的保存。我们描述了一种利用携带酪氨酸激酶和增强绿色荧光蛋白(eGFP)的单纯疱疹病毒NV1066检测NI的成像方法。用NV1066体外感染胰腺(MiaPaCa2)、前列腺(PC3和DU145)和腺样囊性癌(ACC3)细胞系可诱导eGFP高表达。采用裸鼠坐骨神经植入肿瘤的方法建立小鼠体内NI模型。神经注射NV1066，经聚合酶链反应证实感染。用[(18)F]-2′-氟-2′-脱氧阿拉伯糖呋喃基-5-乙基尿嘧啶进行的正电子发射断层扫描显示，NI的摄取明显高于对照动物。术中荧光立体成像显示NV1066处理的NI有eGFP信号。这些结果表明，NV1066可能是一种增强检测癌细胞浸润神经的成像方法。该方法可减少对正常神经的损伤，方便识别需要切除的浸润神经，从而提高神经营养性癌患者的诊断和治疗水平。

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引用次数: 24

Antagonistic effects of sodium butyrate and N-(4-hydroxyphenyl)-retinamide on prostate cancer. 丁酸钠和N-(4-羟基苯基)-维甲酸对前列腺癌的拮抗作用。

IF 4.8 2区医学 Q1 ONCOLOGY

Neoplasia

Pub Date : 2007-03-01 DOI: 10.1016/S1569-9056(08)60821-0

R. Kuefer, F. Genze, Waltraud Zugmaier, R. Hautmann, L. Rinnab, J. Gschwend, Marina Angelmeier, A. Estrada, B. Buechele

引用次数: 19

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