IF 7.7 2区医学

Neoplasia Pub Date : 2025-10-01 Epub Date: 2025-08-09 DOI: 10.1016/j.neo.2025.101218

Shih-Chi Su, Chiao-Wen Lin, Mu-Kuan Chen, Yi-Chan Lee, Chun-Wen Su, Shi Bai, Hansraj Jangir, Chun-Yi Chuang, Wen-Hung Chung, Lun-Ching Chang, Shun-Fa Yang

{"title":"Multimodal profiling of oral squamous cell carcinoma identifies genomic alterations and expression programs associated with betel quid chewing.","authors":"Shih-Chi Su, Chiao-Wen Lin, Mu-Kuan Chen, Yi-Chan Lee, Chun-Wen Su, Shi Bai, Hansraj Jangir, Chun-Yi Chuang, Wen-Hung Chung, Lun-Ching Chang, Shun-Fa Yang","doi":"10.1016/j.neo.2025.101218","DOIUrl":"10.1016/j.neo.2025.101218","url":null,"abstract":"Betel quid (BQ) chewing is a profound risk for oral squamous cell carcinoma (OSCC) in Southeast Asia. Yet, the detailed mechanisms by which BQ chewing damages the genome and creates a unique tumor niche that ultimately cause OSCC are still not fully understood. To address this, we conducted a multi-omics survey, including exome sequencing of tumor-normal pairs from 261 male patients with OSCC (129 habitual BQ chewers and 132 non-BQ users), alone with integrated single-cell and spatial transcriptomics of a set of tumors. Comparative analyses of the mutational catalog identified enrichment of significantly altered genes (e.g. mutations of TP53 and CHUK, copy gains of MAP3K13 and FADD, copy losses of CDKN2A) associated with BQ chewing. Assessment of oncogenic and co-occurring actionable alterations demonstrated frequently altered oncogenic pathways (Hippo and p53 signaling) and potential combination therapy opportunities linked to BQ use. In addition, evaluation of epithelial, immune, stromal expression programs in the corresponding tissue compartments revealed a shift of tumor microenvironment in BQ-related OSCC, characterized by induced hypoxia of tumor epithelium, altered immunosuppression of dendritic cells, and raised sprouting angiogenesis of tumor endothelium. Quantitative predictions of intercellular communications inferred a more heterogeneous cell-cell crosstalk among BQ-related OSCC, highlighted by extensive interactions of fibroblasts and dendritic cells with other non-epithelial cell types via mostly extracellular matrix-receptor signaling pathways. Collectively, these differences in genomic landscape and tumor niche suggest that OSCC caused by BQ chewing could be an etiological subtype different from their BQ-negative counterparts.","PeriodicalId":48716,"journal":{"name":"Neoplasia","volume":"68 ","pages":"101218"},"PeriodicalIF":7.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12357113/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144817959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

High-dose DFMO alters protein translation in neuroblastoma. 大剂量DFMO改变神经母细胞瘤中的蛋白质翻译。

IF 7.7 2区医学

Neoplasia Pub Date : 2025-10-01 Epub Date: 2025-08-06 DOI: 10.1016/j.neo.2025.101215

Andrea T Franson, Kangning Liu, Rohan Vemu, Elizabeth Scadden, Yimei Li, Annette Vu, Michael D Hogarty

{"title":"High-dose DFMO alters protein translation in neuroblastoma.","authors":"Andrea T Franson, Kangning Liu, Rohan Vemu, Elizabeth Scadden, Yimei Li, Annette Vu, Michael D Hogarty","doi":"10.1016/j.neo.2025.101215","DOIUrl":"10.1016/j.neo.2025.101215","url":null,"abstract":"DFMO has been studied as a cancer therapeutic at doses ranging from 500 to 9,000 mg/m2/day. Lower doses are favored for cancer prevention studies while higher doses, often with chemotherapy, are studied in refractory cancers. DFMO inhibits the rate-limiting enzyme in polyamine synthesis, ornithine decarboxylase (ODC), an oncogene transcriptionally regulated by MYC. MYC genes are the principal oncogenic drivers of neuroblastoma, and ODC1 is co-amplified in a subset with dismal outcome, so DFMO is a rational therapeutic candidate. Low-dose DFMO has now been FDA-approved for high-risk patients though the mechanisms for its anti-tumor activity, and the exposures required to elicit them, remain obscure. We sought to define biomarkers of activity across exposures achieved in the clinic with low through high-dose DFMO. Polyamines support protein translation by providing spermidine, which is essential to hypusinate (and activate) the elongation factor, eIF5A. Selective binding of polyamines with tRNA and rRNA provide eIF5A-independent mechanisms of translation support. We show that low-dose DFMO does not extend survival in mouse models in vivo nor alter translation biomarkers in vitro. High-dose DFMO consistently extends survival in neuroblastoma models, and, in a subset of neuroblastoma cell lines, inhibits eIF5A hypusination and global translation at achievable concentrations. However, the concentration required to engage these changes across many cell lines exceeded that achievable even with high-dose DFMO. No correlation was seen among MYCN and/or ODC1 copy number and sensitivity to DFMO. Combining high-dose DFMO with additional agents to further deplete tumor polyamines may be necessary to fully engage polyamine-depletion effects on tumors, and more granular measures of translation, including codon-resolution ribosome profiling, may be required to define these effects.","PeriodicalId":48716,"journal":{"name":"Neoplasia","volume":"68 ","pages":"101215"},"PeriodicalIF":7.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12355086/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144800599","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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

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

{"title":"DCZ0014, a novel compound in the therapy of diffuse large B-cell lymphoma via the B cell receptor signaling pathway.","authors":"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","doi":"10.21203/rs.3.rs-48447/v1","DOIUrl":"https://doi.org/10.21203/rs.3.rs-48447/v1","url":null,"abstract":"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.","PeriodicalId":48716,"journal":{"name":"Neoplasia","volume":"212 7","pages":"50-61"},"PeriodicalIF":4.8,"publicationDate":"2020-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72436607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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

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

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

{"title":"The dual PI3K/mTOR inhibitor NVP-BEZ235 is a potent inhibitor of ATM- and DNA-PKCs-mediated DNA damage responses.","authors":"B. Mukherjee, N. Tomimatsu, K. Amancherla, Cristel V. Camacho, N. Pichamoorthy, S. Burma","doi":"10.1158/1538-7445.AM2012-3745","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2012-3745","url":null,"abstract":"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.","PeriodicalId":48716,"journal":{"name":"Neoplasia","volume":"14 1","pages":"34-43"},"PeriodicalIF":4.8,"publicationDate":"2012-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88970982","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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

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

{"title":"Sensitization of pancreatic cancer stem cells to gemcitabine by Chk1 inhibition.","authors":"V. A. Venkatesha, L. A. Parsels, J. Parsels, Lili Zhao, S. Zabludoff, D. Simeone, J. Maybaum, T. Lawrence, M. Morgan","doi":"10.1158/1538-7445.AM2011-3919","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2011-3919","url":null,"abstract":"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.","PeriodicalId":48716,"journal":{"name":"Neoplasia","volume":"43 1","pages":"519-25"},"PeriodicalIF":4.8,"publicationDate":"2011-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91335129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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

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

{"title":"Astrocytes upregulate survival genes in tumor cells and induce protection from chemotherapy.","authors":"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","doi":"10.1158/1538-7445.AM10-3428","DOIUrl":"https://doi.org/10.1158/1538-7445.AM10-3428","url":null,"abstract":"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.","PeriodicalId":48716,"journal":{"name":"Neoplasia","volume":"34 1","pages":"286-98"},"PeriodicalIF":4.8,"publicationDate":"2010-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74009150","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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

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

{"title":"Enhanced resistance to tamoxifen by the c-ABL proto-oncogene in breast cancer.","authors":"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","doi":"10.1158/1538-7445.AM10-LB-179","DOIUrl":"https://doi.org/10.1158/1538-7445.AM10-LB-179","url":null,"abstract":"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.","PeriodicalId":48716,"journal":{"name":"Neoplasia","volume":"1 1","pages":"214-23"},"PeriodicalIF":4.8,"publicationDate":"2010-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80715255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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

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

{"title":"Prognostic relevance of hTERT mRNA expression in ductal adenocarcinoma of the pancreas.","authors":"L. Grochola, T. Greither, H. Taubert, P. Möller, U. Knippschild, A. Udelnow, D. Henne-Bruns, P. Würl","doi":"10.1055/S-0028-1089530","DOIUrl":"https://doi.org/10.1055/S-0028-1089530","url":null,"abstract":"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.","PeriodicalId":48716,"journal":{"name":"Neoplasia","volume":"27 1","pages":"973-6"},"PeriodicalIF":4.8,"publicationDate":"2008-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87333941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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

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

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

{"title":"Utility of a herpes oncolytic virus for the detection of neural invasion by cancer.","authors":"Z. Gil, K. Kelly, P. Brader, J. Shah, Y. Fong, R. Wong","doi":"10.1055/s-2008-1093272","DOIUrl":"https://doi.org/10.1055/s-2008-1093272","url":null,"abstract":"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.","PeriodicalId":48716,"journal":{"name":"Neoplasia","volume":"1 1","pages":"347-53"},"PeriodicalIF":4.8,"publicationDate":"2008-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88833322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 24

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