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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
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
Selma Maacha, Jun Hong, Ariana von Lersner, Andries Zijlstra, Abbes Belkhiri
Esophageal adenocarcinoma (EAC) is a highly aggressive malignancy that is characterized by resistance to chemotherapy and a poor clinical outcome. The overexpression of the receptor tyrosine kinase AXL is frequently associated with unfavorable prognosis in EAC. Although it is well documented that AXL mediates cancer cell invasion as a downstream effector of epithelial-to-mesenchymal transition, the precise molecular mechanism underlying this process is not completely understood. Herein, we demonstrate for the first time that AXL mediates cell invasion through the regulation of lysosomes peripheral distribution and cathepsin B secretion in EAC cell lines...
October 2018: Neoplasia: An International Journal for Oncology Research
Nanda Kumar Sasi, Flavie Coquel, Yea-Lih Lin, Jeffrey P MacKeigan, Philippe Pasero, Michael Weinreich
CDC7-DBF4 kinase (DDK) initiates DNA replication in eukaryotes by activating the replicative MCM helicase. DDK has diverse and apparently conflicting roles in the replication checkpoint response in various organisms, but the underlying mechanisms are far from settled. We show that human DDK promotes limited resection of newly synthesized DNA at stalled replication forks or sites of DNA damage to initiate replication checkpoint signaling. DDK is also required for efficient fork restart and G2/M cell cycle arrest...
October 2018: Neoplasia: An International Journal for Oncology Research
Pavitra Viswanath, Shaohua Peng, Ratnakar Singh, Charles Kingsley, Peter A Balter, Faye M Johnson
Mouse models are powerful tools to study lung cancer initiation and progression in vivo and have contributed significantly to recent advances in therapy. Using micro-computed tomography to monitor and study parenchymal and extra-parenchymal metastases in existing murine models of lung cancer is challenging owing to a lack of radiographic contrast and difficulty in achieving respiratory gating. To facilitate the analysis of these in vivo imaging studies and study of tumor progression in murine models we developed a novel, rapid, semi-automated method of calculating thoracic tumor burden from computed tomography images...
October 2018: Neoplasia: An International Journal for Oncology Research
Joshua Felgenhauer, Laura Tomino, Julia Selich-Anderson, Emily Bopp, Nilay Shah
A majority of cases of high-risk neuroblastoma, an embryonal childhood cancer, are driven by MYC or MYCN-driven oncogenic signaling. While considered to be directly "undruggable" therapeutically, MYC and MYCN can be repressed transcriptionally by inhibition of Bromodomain-containing protein 4 (BRD4) or destabilized posttranslationally by inhibition of Aurora Kinase A (AURKA). Preclinical and early-phase clinical studies of BRD4 and AURKA inhibitors, however, show limited efficacy against neuroblastoma when used alone...
October 2018: Neoplasia: An International Journal for Oncology Research
Seema Shah, Ethan J Brock, Ryan M Jackson, Kyungmin Ji, Julie L Boerner, Bonnie F Sloane, Raymond R Mattingly
Diagnosis of breast ductal carcinoma in situ (DCIS) presents a challenge since we cannot yet distinguish those cases that would remain indolent and not require aggressive treatment from cases that may progress to invasive ductal cancer (IDC). The purpose of this study is to determine the role of Rap1Gap, a GTPase activating protein, in the progression from DCIS to IDC. Immunohistochemistry (IHC) analysis of samples from breast cancer patients shows an increase in Rap1Gap expression in DCIS compared to normal breast tissue and IDCs...
September 2018: Neoplasia: An International Journal for Oncology Research
Amy L Cisyk, Zoann Nugent, Robert H Wightman, Harminder Singh, Kirk J McManus
There are a substantial portion of colorectal cancers (CRCs), termed interval CRCs (I-CRCs), that are diagnosed shortly after a negative colonoscopy (i.e., no detectable polyps or CRC) and before recommended follow-up screening. The underlying cause(s) accounting for I-CRCs remain poorly understood, but may involve aberrant biology that drives genome instability. Genetic defects inducing genome instability are pathogenic events that lead to the development and progression of traditional sporadic (Sp-) CRCs...
September 2018: Neoplasia: An International Journal for Oncology Research
Nicholas E Brown, Andrew M Paluch, Madison A Nashu, Kakajan Komurov, Susan E Waltz
Current treatment strategies provide minimal results for patients with castration-resistant prostate cancer (CRPC). Attempts to target the androgen receptor have shown promise, but resistance ultimately develops, often due to androgen receptor reactivation. Understanding mechanisms of resistance, including androgen receptor reactivation, is crucial for development of more efficacious CRPC therapies. Here, we report that the RON receptor tyrosine kinase is highly expressed in the majority of human hormone-refractory prostate cancers...
September 2018: Neoplasia: An International Journal for Oncology Research
Balabhadrapatruni V S K Chakravarthi, Maria Del Carmen Rodriguez Pena, Sumit Agarwal, Darshan S Chandrashekar, Sai Akshaya Hodigere Balasubramanya, Fayez J Jabboure, Andres Matoso, Trinity J Bivalacqua, Katayoon Rezaei, Alcides Chaux, William E Grizzle, Guru Sonpavde, Jennifer Gordetsky, George J Netto, Sooryanarayana Varambally
Genomic and transcriptome sequencing of bladder cancer (BLCA) has identified multiple molecular alterations during cancer progression. Many of these identified genetic and epigenetic changes play a role in the progression of this disease. Studies have identified molecular subtypes in muscle-invasive bladder cancer (MIBC) with different sensitivities to frontline therapy suggesting the heterogeneity in these tumors and the importance of molecular characterization of MIBC to provide effective treatment. Specifically, it has become increasingly evident, as demonstrated by The Cancer Genome Atlas project, that metabolic enzymes are commonly dysregulated in BLCA...
September 2018: Neoplasia: An International Journal for Oncology Research
Salida Mirzoeva, Xin Tong, Bryan B Bridgeman, Michael P Plebanek, Olga V Volpert
We have previously demonstrated that apigenin promotes the expression of antiangiogenic protein thrombospondin-1 (TSP1) via a mechanism driven by mRNA-binding protein HuR. Here, we generated a novel mouse model with whole-body THBS-1 gene knockout on SKH-1 genetic background, which allows studies of UVB-induced acute skin damage and carcinogenesis and tests TSP1 involvement in apigenin's anticancer effects. Apigenin significantly inhibited UVB-induced carcinogenesis in the wild-type (WT) animals but not in TSP1 KO (TKO) mice, suggesting that TSP1 is a critical component of apigenin's chemopreventive function in UVB-induced skin cancer...
September 2018: Neoplasia: An International Journal for Oncology Research
Haiying Liu, Yujie Xie, Zepeng Zhang, Pingsu Mao, Jingfan Liu, Wenbin Ma, Yong Zhao
About 15% of human cancers counteract telomere loss by alternative lengthening of telomeres (ALT), which is attributed to homologous recombination (HR)-mediated events. But how telomeric HR leads to length elongation is poorly understood. Here, we explore telomere clustering and telomeric HR induced by double-stranded breaks (DSBs). We show that telomere clustering could occur at G1 and S phase of cell cycle and that three types of telomeric HR occur based on the manner of telomeric DNA exchange: equivalent telomeric sister chromatin exchange (T-SCE), inequivalent T-SCE, and No-SCE...
September 2018: Neoplasia: An International Journal for Oncology Research
Amir Farmanbar, Sanaz Firouzi, Wojciech Makałowski, Robert Kneller, Masako Iwanaga, Atae Utsunomiya, Kenta Nakai, Toshiki Watanabe
The clonal architecture of tumors plays a vital role in their pathogenesis and invasiveness; however, it is not yet clear how this clonality contributes to different malignancies. In this study we sought to address mutational intratumor heterogeneity (ITH) in adult T-cell leukemia/lymphoma (ATL). ATL is a malignancy with an incompletely understood molecular pathogenesis caused by infection with human T-cell leukemia virus type-1 (HTLV-1). To determine the clonal structure through tumor genetic diversity profiles, we investigated 142 whole-exome sequencing data of tumor and matched normal samples from 71 ATL patients...
September 2018: Neoplasia: An International Journal for Oncology Research
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