Oncoscience最新文献

{"title":"Checkpoint blockade therapy for functioning pituitary adenomas.","authors":"Selena J Lorrey, Hanna R Kemeny, Peter E Fecci","doi":"10.18632/oncoscience.509","DOIUrl":"https://doi.org/10.18632/oncoscience.509","url":null,"abstract":"","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7343575/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38163243","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The advent of precision epigenetics for medulloblastoma.","authors":"Chaoxi Li, Erwin G Van Meir","doi":"10.18632/oncoscience.507","DOIUrl":"https://doi.org/10.18632/oncoscience.507","url":null,"abstract":"Medulloblastoma (MB) is the most common and fatal malignant pediatric brain tumor, is located in the cerebellum and is associated with significant therapyrelated morbidity [1]. MB can be subdivided into four clinically and molecularly distinct groups: wingless (WNT), sonic hedgehog (SHH), and groups 3 and 4 [2]. The standard of care for MB patients irrespective of group consists of surgical resection, cranio-spinal radiation and combination chemotherapy. This intensive regimen improves survival, especially in WNT-MB patients. SHH and group 4 patients have intermediate benefit, while most group 3 patients relapse and die from the disease. Moreover, therapy-induced damage to the developing brain remains a significant problem: young survivors suffer from life-long cognitive, neurological and neuroendocrine side effects. Less toxic novel therapies are urgently needed to improve quality of life of these children and young adults. Genomic studies have identified frequent alterations in epigenetic regulators in MBs, suggesting that incorporating epigenetic reprogramming therapy into the standard of care for MB patients may be beneficial and potentially less toxic. Polycomb group proteins are transcriptional repressors essential for normal gene regulation during development and are perturbed in a wide range of human cancers. They usually belong to either of two protein complexes: Polycomb Repressive Complex 1 (PRC1) that adds a ubiquityl moiety to histone H2A at lysine 119 (H2AK119ubl) and PRC2 that catalyzes the addition of one to three methyl groups to histone H3 at lysine 27, leading to H3K27me1, H3K27me2 and H3K27me3 [3]. EZH2, the catalytic component of PRC2, writes the suppressive chromatin marker H3K27me3 and is Research Perspective","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7458335/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38472140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Future directions of neoadjuvant therapy in pancreatic cancer.","authors":"Carmen Mota Reyes,&nbsp;Ümmügülsüm Yurteri,&nbsp;Helmut Friess,&nbsp;Ihsan Ekin Demir","doi":"10.18632/oncoscience.506","DOIUrl":"https://doi.org/10.18632/oncoscience.506","url":null,"abstract":"<p><p>Neoadjuvant therapy with conventional chemotherapies have visibly improved the prognosis of locally advanced pancreatic cancer (PCa). However, molecular targeted therapies that have provided durable responses in other tumor entities, have not yet found access into neoadjuvant therapy of PCa. In fact, due to the presence of the tumor burden serving as an antigen source for T cell priming, neoadjuvant chemotherapy may unleash a more potent antitumoral immune response than adjuvant or palliative chemotherapy.</p>","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7458337/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38472139","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"4-1BB Agonism as a strategy to license immune checkpoint blockade in glioblastoma.","authors":"Karolina Woroniecka,&nbsp;Peter E Fecci","doi":"10.18632/oncoscience.505","DOIUrl":"https://doi.org/10.18632/oncoscience.505","url":null,"abstract":"","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7343573/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38163241","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identifying new targets for rectal cancer treatment.","authors":"Sylvain Ferrandon,&nbsp;Matthew F Kalady","doi":"10.18632/oncoscience.508","DOIUrl":"https://doi.org/10.18632/oncoscience.508","url":null,"abstract":"","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7343572/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38163242","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HUNK Signaling in Metastatic Breast Cancer.","authors":"Tinslee Dilday,&nbsp;Nicole Ramos,&nbsp;Elizabeth Yeh","doi":"10.18632/oncoscience.504","DOIUrl":"https://doi.org/10.18632/oncoscience.504","url":null,"abstract":"<p><p>Once metastatic disease has occurred, there is no cure for breast cancer. Consequently, identifying factors that promote and support breast cancer metastasis is critical for understanding how to pharmacologically target this process. Hormonally up-regulated neu-associated kinase (HUNK) is a serine/threonine protein kinase related to the sucrose non-fermenting-1 (Snf-1)/5' adenosine monophosphate-activated protein kinase (AMPK) family of kinases. HUNK has been found to play a role in breast cancer metastasis. However, conflicting reports indicate HUNK is a metastasis promoting factor as well as an inhibiting factor. Our group recently provided evidence that supports the conclusion that HUNK is a metastasis promoting factor by showing that HUNK regulates breast cancer metastasis through phosphorylation of EGFR. Here, we summarize our findings and discuss their implications toward pharmacological targeting of HUNK in breast cancer.</p>","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7343571/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38163240","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deciphering high risk molecular alterations in gastrointestinal malignancy utilizing an extreme outlier strategy.","authors":"Austin R Dosch,&nbsp;Siddharth Mehra,&nbsp;Nipun B Merchant,&nbsp;Jashodeep Datta","doi":"10.18632/oncoscience.503","DOIUrl":"https://doi.org/10.18632/oncoscience.503","url":null,"abstract":"","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7343576/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38163238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Computational disease progression modeling can provide insights into cancer evolution.","authors":"Steve Goodison,&nbsp;Mark E Sherman,&nbsp;Yijun Sun","doi":"10.18632/oncoscience.501","DOIUrl":"https://doi.org/10.18632/oncoscience.501","url":null,"abstract":"Steve Goodison1, Mark E. Sherman1, Yijun Sun2,3,4 1 Department of Health Sciences Research, Mayo Clinic, Jacksonville, FL, USA 2 Department of Microbiology and Immunology, The State University of New York, Buffalo, NY, USA 3 Department of Computer Science and Engineering, The State University of New York, Buffalo, NY, USA 4 Department of Biostatistics, The State University of New York, Buffalo, NY, USA","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7217135/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37952840","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Heavenly HELLS? A potential new therapeutic target for retinoblastoma.","authors":"Loredana Zocchi,&nbsp;Stephanie C Wu,&nbsp;Claudia A Benavente","doi":"10.18632/oncoscience.502","DOIUrl":"https://doi.org/10.18632/oncoscience.502","url":null,"abstract":"Although the role of the retinoblastoma protein (pRB) in cell cycle control has been extensively studied, druggable targets downstream of pRB remain to be identified. Retinoblastoma is the most common childhood intraocular malignancy caused by bi-allelic inactivation of the retinoblastoma gene (RB1). Despite recent progress in clinical outcomes of retinoblastoma, enucleation (eye removal) remains a frequent treatment for retinoblastoma and the survival rate for metastatic retinoblastoma is just over 10%. Thus, there is a pressing clinical need to determine the factors responsible for tumor progression following RB1 inactivation in order to facilitate the development of new therapeutic strategies. Furthermore, the loss of pRB function contributes to a wide array of human cancers. A few years ago, we elucidated how tumors progress quickly following RB1 inactivation, showing that while the retinoblastoma genome is stable – with RB1 being the only known tumor suppressor gene mutated – multiple cancer pathways can be deregulated epigenetically [1]. HELLS (helicase, lymphoid specific; also known as LSH, ICF4, PASG, and SMARCA6) belongs to the SNF2 family of chromatin-remodeling ATPases. It remodels chromatin to allow accessibility of DNMT3A or DNMT3B to DNA in order to support de novo DNA methylation and stable gene silencing during cellular differentiation [2]. We have previously identified that upregulation of HELLS following RB1 inactivation could cause the epigenetic gene expression deregulation that results in tumorigenesis [3]. HELLS has an interesting connection to the RB/E2F pathway: the HELLS gene is a direct target of E2F1 [4] and HELLS protein interacts with E2F3 at several E2F target genes that control cell cycle entry [5,6]. Similar to what we observed in retinoblastoma, depletion of HELLS in glioblastoma and several carcinomas impairs tumor growth, suggesting that HELLS may contribute to the malignant progression of various tumors. We have also reported that HELLS is overexpressed in osteosarcoma; however, we found no evidence of HELLS serving as a driver of malignancy in these tumors [7]. The osteosarcoma study offered a precautionary perspective indicating that while HELLS level may reflect RB/E2F pathway inactivation, its upregulation may not always be synonymous with a critical role in tumor formation or tumor maintenance across all malignancies, and therefore should not be a Research Perspective","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7217136/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37952841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cancer research - can the entity be bigger than the sum of its parts?","authors":"Georg F Weber","doi":"10.18632/oncoscience.499","DOIUrl":"https://doi.org/10.18632/oncoscience.499","url":null,"abstract":"<p><p>Cancer Research has benefitted from substantial expenditures by federal and nonprofit organizations. The resulting success in patient care has been uneven. Two lessons from the 20^th century history of science suggest infrastructural changes that can boost success. We need to better organize big science, explicitly aiming for expedient clinical translation. In parallel, resource allocation should enable investigator-initiated exploration on the basis of productivity per research dollars spent.</p>","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7217137/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37952428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}