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Neoplasia: An International Journal for Oncology Research

Emil Chteinberg, Christopher Martin Sauer, Dorit Rennspiess, Lukas Beumers, Lisa Schiffelers, Jonathan Eben, Anke Haugg, Véronique Winnepenninckx, Anna Kordelia Kurz, Ernst-Jan Speel, Martin Zenke, Axel Zur Hausen
Merkel cell carcinoma (MCC) is a highly aggressive non-melanoma skin cancer of the elderly which is associated with the Merkel cell polyomavirus (MCPyV). MCC reveals a trilinear differentiation characterized by neuroendocrine, epithelial and pre/pro B-cell lymphocytic gene expression disguising the cellular origin of MCC. Here we investigated the expression of the neuroendocrine key regulators RE1 silencing transcription factor (REST), neurogenic differentiation 1 (NeuroD1) and the Achaete-scute homolog 1 (ASCL1) in MCC...
November 7, 2018: Neoplasia: An International Journal for Oncology Research
Hiroya Taniguchi, Wataru Okamoto, Kei Muro, Kiwamu Akagi, Hiroki Hara, Tomohiro Nishina, Takeshi Kajiwara, Tadamichi Denda, Shuichi Hironaka, Toshihiro Kudo, Taroh Satoh, Takeharu Yamanaka, Yukiko Abe, Yoshiyuki Fukushima, Takayuki Yoshino
Detection of RAS and BRAF mutations is essential to determine the optimal treatment strategy for metastatic colorectal cancer (CRC). We prospectively evaluated the MEBGEN RASKET-B KIT (RASKET-B), a novel multiplex kit, simultaneously detecting 48 types of RAS mutations and the BRAF V600E mutation using Luminex xMAP technology. The aim was to obtain market approval for RASKET-B as an in vitro diagnostic (IVD) option in Japan. Genomic DNA was extracted from 302 formalin-fixed paraffin-embedded tissues obtained from CRC patients...
November 6, 2018: Neoplasia: An International Journal for Oncology Research
Kari E Hacker, Danielle E Bolland, Lijun Tan, Anjan K Saha, Yashar S Niknafs, David M Markovitz, Karen McLean
DNA damage repair alterations play a critical role in ovarian cancer tumorigenesis. Mechanistic drivers of the DNA damage response consequently present opportunities for therapeutic targeting. The chromatin-binding DEK oncoprotein functions in DNA double-strand break repair. We therefore sought to determine the role of DEK in epithelial ovarian cancer. DEK is overexpressed in both primary epithelial ovarian cancers and ovarian cancer cell lines. To assess the impact of DEK expression levels on cell growth, small interfering RNA and short hairpin RNA approaches were utilized...
November 6, 2018: Neoplasia: An International Journal for Oncology Research
Katharina M Schmidt, Peter Dietrich, Christina Hackl, Jessica Guenzle, Peter Bronsert, Christine Wagner, Stefan Fichtner-Feigl, Hans J Schlitt, Edward K Geissler, Claus Hellerbrand, Sven A Lang
Mammalian target of rapamycin complex 2 (mTORC2) with its pivotal component rapamycin-insensitive companion of mTOR (RICTOR) is the major regulator of AKT phosphorylation and is increasingly implicated in tumor growth and progression. In cutaneous melanoma, an extremely aggressive and highly metastatic disease, RICTOR overexpression is involved in tumor development and invasiveness. Therefore, we investigated the impact of RICTOR inhibition in melanoma cells in vitro and in vivo with special emphasis on hepatic metastasis...
November 4, 2018: Neoplasia: An International Journal for Oncology Research
Jeng-Wei Lu, Divya Raghuram, Pei-Shi Angelina Fong, Zhiyuan Gong
KRAS mutations are a major risk factor in colorectal cancers. In particular, a point mutation of KRAS of amino acid 12, such as KRASV12 , renders it stable activity in oncogenesis. We found that krasV12 promotes intestinal carcinogenesis by generating a transgenic zebrafish line with inducible krasV12 expression in the intestine, Tg(ifabp:EGFP-krasV12 ). The transgenic fish generated exhibited significant increases in the rates of intestinal epithelial outgrowth, proliferation, and cross talk in the active Ras signaling pathway involving in epithelial-mesenchymal transition (EMT)...
October 31, 2018: Neoplasia: An International Journal for Oncology Research
Annette K Brenner, Øystein Bruserud
The S100 protein family contains 20 functionally expressed members, which are commonly dysregulated in cancer. Their wide range of functions includes cell proliferation, cell differentiation, regulation of transcription factors, inflammation, chemotaxis, and angiogenesis. S100 proteins have in several types of cancer proven to be biomarkers for disease progression and prognosis. Acute myeloid leukemia (AML) is a highly heterogeneous and aggressive disease in which immature myeloblasts replace normal hematopoietic cells in the bone marrow...
October 23, 2018: Neoplasia: An International Journal for Oncology Research
Kathrin Rothfelder, Ilona Hagelstein, Malte Roerden, Gunnar Blumenstock, Martin Hofmann, Tina Nuebling, Gundram Jung, Helmut Rainer Salih, Daniela Dörfel
OX40 and its ligand are members of the TNF/TNF receptor superfamily, which includes various molecules influencing cellular signaling and function of both tumor and immune cells. The ability of OX40 to promote proliferation and differentiation of activated T cells fueled present attempts to modulate this immune checkpoint to reinforce antitumor immunity. While we recently found evidence for the involvement of OX40 in pathophysiology of acute myeloid leukemia including natural killer (NK) cell immunosurveillance, less is known on its role in acute lymphoblastic leukemia (ALL)...
October 6, 2018: Neoplasia: An International Journal for Oncology Research
Oorvashi Roy Puli, Brian P Danysh, Elena McBeath, Deepankar K Sinha, Nguyet M Hoang, Reid T Powell, Heather E Danysh, Maria E Cabanillas, Gilbert J Cote, Marie-Claude Hofmann
The ETS family of transcription factors is involved in several normal remodeling events and pathological processes including tumor progression. ETS transcription factors are divided into subfamilies based on the sequence and location of the ETS domain. ETV5 (Ets variant gene 5; also known as ERM) is a member of the PEA3 subfamily. Our meta-analysis of normal, benign, and malignant thyroid samples demonstrated that ETV5 expression is upregulated in papillary thyroid cancer and was predominantly associated with BRAF V600E or RAS mutations...
September 25, 2018: Neoplasia: An International Journal for Oncology Research
Albert Job, Lisa-Maria Schmitt, Lisa von Wenserski, Brigitte Lankat-Buttgereit, Thomas M Gress, Malte Buchholz, Eike Gallmeier
The phosphoinositide 3-kinase-related kinase ATR is a central regulator of the DNA damage response. Its chemical inhibition eliminates subsets of cancer cells in various tumor types. This effect is caused at least partly by the synthetically lethal relationship between ATR and certain DNA repair genes. In a previous screen using an siRNA library against DNA repair genes, we identified PRIM1, a part of the polymerase α-primase complex, as acting synthetically lethal with ATR. Applying a genetic ATR knock-in model of colorectal cancer cells, we confirmed that PRIM1 depletion inhibited proliferation of ATR-deficient cells and excluded artifacts due to clonal variation using an ATR reexpressing cell clone...
September 23, 2018: Neoplasia: An International Journal for Oncology Research
Rabindranath Bera, Ming-Chun Chiu, Ying-Jung Huang, Der-Cherng Liang, Yun-Shien Lee, Lee-Yung Shih
DNA methyltransferase 3A (DNMT3A) is mutated in various myeloid neoplasms including acute myeloid leukemia (AML), especially at the Arg882 and associated with inferior outcomes. Here, we report that the DNMT3A-Arg882His/Cys (R882H/C) mutations led to inactivation of apoptosis through DNA damage signaling following the impairment of differentiation of myeloid leukemia cells. Gene expression profiling analysis revealed aberrant expression of several cell-cycle and apoptosis-related genes, and the DNA methylation assay identified both hypo- and hypermethylation features in different regions throughout the whole genome of DNMT3A mutants-transduced myeloid cells...
September 20, 2018: Neoplasia: An International Journal for Oncology Research
Riyue Feng, Xuefei Wang, Jianning Li, Ke Chen, Guijie Guo, Yuan Liao, Liping Sun, Shile Huang, Ji-Long Chen
Suppressor of cytokine signaling 3 (SOCS3) is involved in Bcr-Abl-induced tumorigenesis. However, how SOCS3 interacts with Bcr-Abl and is regulated by Abl kinases remains largely unknown. Since c-Abl plays a critical role in tumorigenesis, we asked whether SOCS3 is regulated by c-Abl-dependent phosphorylation. Here, we found that SOCS3 interacted with all three Abl kinases (Bcr-Abl, v-Abl, and c-Abl), and SH1 domain of the Abl kinases was critically required for such interaction. Furthermore, the SH2 domain of SOCS3 was sufficient to pull down the SH1 domain but not the full length of Bcr-Abl...
September 17, 2018: Neoplasia: An International Journal for Oncology Research
Lauren E Hillers, Joseph V D'Amato, Tamara Chamberlin, Gretchen Paderta, Lisa M Arendt
Obese women diagnosed with breast cancer have an increased risk for metastasis, and the underlying mechanisms are not well established. Within the mammary gland, adipose-derived stromal cells (ASCs) are heterogeneous cells with the capacity to differentiate into multiple mesenchymal lineages. To study the effects of obesity on ASCs, mice were fed a control diet (CD) or high-fat diet (HFD) to induce obesity, and ASCs were isolated from the mammary glands of lean and obese mice. We observed that obesity increased ASCs proliferation, decreased differentiation potential, and upregulated expression of α-smooth muscle actin, a marker of activated fibroblasts, compared to ASCs from lean mice...
November 2018: Neoplasia: An International Journal for Oncology Research
Yashar S Niknafs, Balaji Pandian, Tilak Gajjar, Zach Gaudette, Kevin Wheelock, Mitra P Maz, Rohan K Achar, Melinda Song, Cory Massaro, Xuhong Cao, Arul M Chinnaiyan
The Michigan Portal for the Analysis of NGS data portal ( is an open-access online resource that provides the scientific community with access to the results of a large-scale computational analysis of thousands of high-throughput RNA sequencing (RNA-seq) samples. The portal provides access to gene expression profiles, enabling users to interrogate expression of genes across myriad normal and cancer tissues and cell lines. From these data, tissue- and cancer-specific expression patterns can be identified...
November 2018: Neoplasia: An International Journal for Oncology Research
Kartik Angara, Thaiz F Borin, Mohammad H Rashid, Iryna Lebedyeva, Roxan Ara, Ping-Chang Lin, Asm Iskander, Roni J Bollag, Bhagelu R Achyut, Ali S Arbab
BACKGROUND: Glioblastoma (GBM) was shown to relapse faster and displayed therapeutic resistance to antiangiogenic therapies (AATs) through an alternative tumor cell-driven mechanism of neovascularization called vascular mimicry (VM). We identified highly upregulated interleukin 8 (IL-8)-CXCR2 axis in tumor cells in high-grade human glioma and AAT-treated orthotopic GBM tumors. METHODS: Human GBM tissue sections and tissue array were used to ascertain the clinical relevance of CXCR2-positive tumor cells in the formation of VM...
October 2018: Neoplasia: An International Journal for Oncology Research
Taishi Akimoto, Akira Takasawa, Kumi Takasawa, Tomoyuki Aoyama, Masaki Murata, Makoto Osanai, Tsuyoshi Saito, Norimasa Sawada
Cervical adenocarcinomas are believed to lose estrogen response on the basis of no expression of a nuclear estrogen receptor such as ERα in clinical pathology. Here, we demonstrated that cervical adenocarcinoma cells respond to a physiological concentration of estrogen to upregulate claudin-1, a cell surface molecule highly expressed in cervical adenocarcinomas. Knockout of claudin-1 induced apoptosis and significantly inhibited proliferation, migration, and invasion of cervical adenocarcinoma cells and tumorigenicity in vivo...
October 2018: Neoplasia: An International Journal for Oncology Research
Yangying Zhou, Wei Liu, Zhijie Xu, Hong Zhu, Desheng Xiao, Weiping Su, Ruolan Zeng, Yuhua Feng, Yumei Duan, Jianhua Zhou, Meizuo Zhong
Primary central nervous system lymphoma (PCNSL) is a rare and special type of non-Hodgkin lymphoma. The treatment of PCNSL is comprehensive, combining surgery, radiotherapy, and chemotherapy. However, the outcome is poor because of its high invasiveness and rate of recurrence. We analyzed 22 cases of PCNSL using next-generation sequencing (NGS) to detect 64 candidate genes. We used immunohistochemical methods to analyze gene expression in 57 PCNSL samples. NGS showed that recurrent mutations in KMT2D and CD79B, components of the NF-κB pathway, accounted for 65% of total mutations in PCNSL samples...
October 2018: Neoplasia: An International Journal for Oncology Research
Zonghui Ding, Harshil Dhruv, Aneta Kwiatkowska-Piwowarczyk, Rosamaria Ruggieri, Jean Kloss, Marc Symons, Patrick Pirrotte, Jennifer M Eschbacher, Nhan L Tran, Joseph C Loftus
Glioblastoma multiforme (GBM) is the most common type of malignant brain tumors in adults and has a dismal prognosis. The highly aggressive invasion of malignant cells into the normal brain parenchyma renders complete surgical resection of GBM tumors impossible, increases resistance to therapeutic treatment, and leads to near-universal tumor recurrence. We have previously demonstrated that TROY (TNFRSF19) plays an important role in glioblastoma cell invasion and therapeutic resistance. However, the potential downstream effectors of TROY signaling have not been fully characterized...
October 2018: Neoplasia: An International Journal for Oncology Research
Boya Deng, Yunus Emre Tarhan, Koji Ueda, Lili Ren, Toyomasa Katagiri, Jae-Hyun Park, Yusuke Nakamura
Alteration of protein O-glycosylation in various human cancers including breast cancer is well known, but molecular roles of their aberrant glycosylations on cancer have not been fully understood. We previously reported critical roles of polypeptide N-acetylgalactosaminyltransferase 6 (GALNT6 or GalNAc-T6) that was upregulated in a great majority of breast cancer tissues. Here we further report O-glycosylation of estrogen receptor alpha (ER-α) by GALNT6 and the significant role of its nuclear localization in breast cancer cells...
October 2018: Neoplasia: An International Journal for Oncology Research
Miranda Brun, Saket Jain, Elizabeth A Monckton, Roseline Godbout
Glioblastomas (GBMs) are highly aggressive brain tumors with a dismal prognosis. Nuclear factor I (NFI) is a family of transcription factors that controls glial cell differentiation in the developing central nervous system. NFIs have previously been shown to regulate the expression of astrocyte markers such as glial fibrillary acidic protein (GFAP) in both normal brain and GBM cells. We used chromatin immunoprecipitation (ChIP)-on-chip to identify additional NFI targets in GBM cells. Analysis of our ChIP data revealed ~400 putative NFI target genes including an effector of the Notch signaling pathway, HEY1, implicated in the maintenance of neural stem cells...
October 2018: Neoplasia: An International Journal for Oncology Research
Shuyang Wang, Shanshan Yan, Shaowei Zhu, Yali Zhao, Junyu Yan, Zhiyuan Xiao, Jiaxin Bi, Junfeng Qiu, Dan Zhang, Zexuan Hong, Lingjie Zhang, Chengmei Huang, Tingting Li, Li Liang, Wenting Liao, Hongli Jiao, Yanqing Ding, Yaping Ye
Forkhead Box F1 (FOXF1) has been recently implicated in cancer progression and metastasis of lung cancer and breast cancer. However, the biological functions and underlying mechanisms of FOXF1 in the regulation of the progression of colorectal cancer (CRC) are largely unknown. We showed that FOXF1 was up-regulated in 93 paraffin-embedded archived human CRC tissue, and both high expression and nuclear location of FOXF1 were significantly associated with the aggressive characteristics and poorer survival of CRC patients...
October 2018: Neoplasia: An International Journal for Oncology Research
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