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  1. Article: Advances in the treatment of BRAF-mutant low-grade glioma with MAPK inhibitors.

    Houghton, Peter J

    Translational pediatrics

    2024  Volume 13, Issue 3, Page(s) 513–517

    Language English
    Publishing date 2024-03-18
    Publishing country China
    Document type Editorial ; Comment
    ZDB-ID 2901309-4
    ISSN 2224-4344 ; 2224-4344 ; 2224-4336
    ISSN (online) 2224-4344
    ISSN 2224-4344 ; 2224-4336
    DOI 10.21037/tp-23-541
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Book: mTOR pathway and mTOR inhibitors in cancer therapy

    Polunovsky, Vitaly A. / Houghton, Peter J.

    (Cancer drug discovery and development)

    2010  

    Author's details Vitaly A. Polunovsky ; Peter J. Houghton, ed
    Series title Cancer drug discovery and development
    Language English
    Size XII, 301 S. : Ill., graph. Darst.
    Publisher Humana Press
    Publishing place New York u.a.
    Publishing country United States
    Document type Book
    HBZ-ID HT016509132
    ISBN 978-1-60327-270-4 ; 9781603272711 ; 1-60327-270-4 ; 1603272712
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2010 A 4623 order for loan Magazin

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  3. Article ; Online: Genomic disparities between cancers in adolescent and young adults and in older adults.

    Wang, Xiaojing / Langevin, Anne-Marie / Houghton, Peter J / Zheng, Siyuan

    Nature communications

    2022  Volume 13, Issue 1, Page(s) 7223

    Abstract: Cancers cause significant mortality and morbidity in adolescents and young adults (AYAs), but their biological underpinnings are incompletely understood. Here, we analyze clinical and genomic disparities between AYAs and older adults (OAs) in more than ... ...

    Abstract Cancers cause significant mortality and morbidity in adolescents and young adults (AYAs), but their biological underpinnings are incompletely understood. Here, we analyze clinical and genomic disparities between AYAs and older adults (OAs) in more than 100,000 cancer patients. We find significant differences in clinical presentation between AYAs and OAs, including sex, metastasis rates, race and ethnicity, and cancer histology. In most cancer types, AYA tumors show lower mutation burden and less genome instability. Accordingly, most cancer genes show less mutations and copy number changes in AYAs, including the noncoding TERT promoter mutations. However, CTNNB1 and BRAF mutations are consistently overrepresented in AYAs across multiple cancer types. AYA tumors also exhibit more driver gene fusions that are frequently observed in pediatric cancers. We find that histology is an important contributor to genetic disparities between AYAs and OAs. Mutational signature analysis of hypermutators shows stronger endogenous mutational processes such as MMR-deficiency but weaker exogenous processes such as tobacco exposure in AYAs. Finally, we demonstrate a panoramic view of clinically actionable genetic events in AYA tumors.
    MeSH term(s) Child ; Humans ; Young Adult ; Adolescent ; Aged ; Neoplasms/genetics ; Genomics ; Mutation ; Oncogenes
    Language English
    Publishing date 2022-11-24
    Publishing country England
    Document type Journal Article
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-022-34959-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: EWSR1 maintains centromere identity.

    Kitagawa, Risa / Niikura, Yohei / Becker, Argentina / Houghton, Peter J / Kitagawa, Katsumi

    Cell reports

    2023  Volume 42, Issue 6, Page(s) 112568

    Abstract: The centromere is essential for ensuring high-fidelity transmission of chromosomes. CENP-A, the centromeric histone H3 variant, is thought to be the epigenetic mark of centromere identity. CENP-A deposition at the centromere is crucial for proper ... ...

    Abstract The centromere is essential for ensuring high-fidelity transmission of chromosomes. CENP-A, the centromeric histone H3 variant, is thought to be the epigenetic mark of centromere identity. CENP-A deposition at the centromere is crucial for proper centromere function and inheritance. Despite its importance, the precise mechanism responsible for maintenance of centromere position remains obscure. Here, we report a mechanism to maintain centromere identity. We demonstrate that CENP-A interacts with EWSR1 (Ewing sarcoma breakpoint region 1) and EWSR1-FLI1 (the oncogenic fusion protein in Ewing sarcoma). EWSR1 is required for maintaining CENP-A at the centromere in interphase cells. EWSR1 and EWSR1-FLI1 bind CENP-A through the SYGQ2 region within the prion-like domain, important for phase separation. EWSR1 binds to R-loops through its RNA-recognition motif in vitro. Both the domain and motif are required for maintaining CENP-A at the centromere. Therefore, we conclude that EWSR1 guards CENP-A in centromeric chromatins by binding to centromeric RNA.
    MeSH term(s) Humans ; Autoantigens/metabolism ; Centromere/metabolism ; Centromere Protein A/genetics ; Chromosomal Proteins, Non-Histone/metabolism ; RNA ; RNA-Binding Protein EWS/genetics ; RNA-Binding Protein EWS/metabolism ; Sarcoma, Ewing
    Chemical Substances Autoantigens ; Centromere Protein A ; Chromosomal Proteins, Non-Histone ; EWSR1 protein, human ; RNA (63231-63-0) ; RNA-Binding Protein EWS
    Language English
    Publishing date 2023-05-25
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2023.112568
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Developing New Agents for Treatment of Childhood Cancer: Challenges and Opportunities for Preclinical Testing.

    Ghilu, Samson / Kurmasheva, Raushan T / Houghton, Peter J

    Journal of clinical medicine

    2021  Volume 10, Issue 7

    Abstract: Developing new therapeutics for the treatment of childhood cancer has challenges not usually associated with adult malignancies. Firstly, childhood cancer is rare, with approximately 12,500 new diagnoses annually in the U.S. in children 18 years or ... ...

    Abstract Developing new therapeutics for the treatment of childhood cancer has challenges not usually associated with adult malignancies. Firstly, childhood cancer is rare, with approximately 12,500 new diagnoses annually in the U.S. in children 18 years or younger. With current multimodality treatments, the 5-year event-free survival exceeds 80%, and 70% of patients achieve long-term "cure", hence the overall number of patients eligible for experimental drugs is small. Childhood cancer comprises many disease entities, the most frequent being acute lymphoblastic leukemias (25% of cancers) and brain tumors (21%), and each of these comprises multiple molecular subtypes. Hence, the numbers of diagnoses even for the more frequently occurring cancers of childhood are small, and undertaking clinical trials remains a significant challenge. Consequently, development of preclinical models that accurately represent each molecular entity can be valuable in identifying those agents or combinations that warrant clinical evaluation. Further, new regulations under the Research to Accelerate Cures and Equity for Children Act (RACE For Children Act) will change the way in which drugs are developed. Here, we will consider some of the limitations of preclinical models and consider approaches that may improve their ability to translate therapy to clinical trial more accurately.
    Language English
    Publishing date 2021-04-04
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2662592-1
    ISSN 2077-0383
    ISSN 2077-0383
    DOI 10.3390/jcm10071504
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Challenges and Opportunities for Childhood Cancer Drug Development.

    Houghton, Peter J / Kurmasheva, Raushan T

    Pharmacological reviews

    2019  Volume 71, Issue 4, Page(s) 671–697

    Abstract: Cancer in children is rare with approximately 15,700 new cases diagnosed in the United States annually. Through use of multimodality therapy (surgery, radiation therapy, and aggressive chemotherapy), 70% of patients will be "cured" of their disease, and ... ...

    Abstract Cancer in children is rare with approximately 15,700 new cases diagnosed in the United States annually. Through use of multimodality therapy (surgery, radiation therapy, and aggressive chemotherapy), 70% of patients will be "cured" of their disease, and 5-year event-free survival exceeds 80%. However, for patients surviving their malignancy, therapy-related long-term adverse effects are severe, with an estimated 50% having chronic life-threatening toxicities related to therapy in their fourth or fifth decade of life. While overall intensive therapy with cytotoxic agents continues to reduce cancer-related mortality, new understanding of the molecular etiology of many childhood cancers offers an opportunity to redirect efforts to develop effective, less genotoxic therapeutic options, including agents that target oncogenic drivers directly, and the potential for use of agents that target the tumor microenvironment and immune-directed therapies. However, for many high-risk cancers, significant challenges remain.
    MeSH term(s) Animals ; Antineoplastic Agents/adverse effects ; Antineoplastic Agents/chemistry ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Child ; Drug Development/methods ; Humans ; Neoplasms/drug therapy ; Tumor Microenvironment/drug effects
    Chemical Substances Antineoplastic Agents
    Language English
    Publishing date 2019-06-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 209898-2
    ISSN 1521-0081 ; 0031-6997
    ISSN (online) 1521-0081
    ISSN 0031-6997
    DOI 10.1124/pr.118.016972
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uf I Zs.148: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  7. Article ; Online: New insights into drug development for pediatric solid tumors: what preclinical data justify clinical trials in pediatric cancer?

    Houghton, Peter J

    Expert review of anticancer therapy

    2013  Volume 13, Issue 10, Page(s) 1135–1138

    MeSH term(s) Animals ; Antineoplastic Agents/pharmacology ; Child ; Clinical Trials as Topic/methods ; Disease Models, Animal ; Drug Design ; Drug Evaluation, Preclinical/methods ; Drug Evaluation, Preclinical/standards ; Humans ; Neoplasms/drug therapy ; Neoplasms/pathology
    Chemical Substances Antineoplastic Agents
    Language English
    Publishing date 2013-10
    Publishing country England
    Document type Editorial
    ZDB-ID 2112544-2
    ISSN 1744-8328 ; 1473-7140
    ISSN (online) 1744-8328
    ISSN 1473-7140
    DOI 10.1586/14737140.2013.845094
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5907: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  8. Article ; Online: Regulation of DNA duplication by the mTOR signaling pathway.

    He, Zhengfu / Houghton, Peter J / Williams, Terence M / Shen, Changxian

    Cell cycle (Georgetown, Tex.)

    2021  Volume 20, Issue 8, Page(s) 742–751

    Abstract: Accurate and complete DNA replication and separation are essential for genetic information inheritance and organism maintenance. Errors in DNA duplication are the main source of genetic instability. Understanding DNA duplication regulation is the key to ... ...

    Abstract Accurate and complete DNA replication and separation are essential for genetic information inheritance and organism maintenance. Errors in DNA duplication are the main source of genetic instability. Understanding DNA duplication regulation is the key to elucidate the mechanisms and find treatment strategies for human genetic disorders, especially cancer. The mechanistic target of rapamycin (mTOR) is a central regulator of cell growth and proliferation by integrating and processing extracellular and intracellular signals to monitor the well-being of cell physiology. mTOR signaling dysregulation is associated with many human diseases including cancer and diabetes. Emerging evidence has demonstrated that mTOR signaling plays a key role in DNA duplication. We herein review the current knowledge of mTOR signaling in the regulation of DNA replication origin licensing, replication fork progression, and stabilization.
    MeSH term(s) Animals ; Cell Proliferation/physiology ; DNA Replication/physiology ; Humans ; Signal Transduction/physiology ; TOR Serine-Threonine Kinases/genetics ; TOR Serine-Threonine Kinases/metabolism
    Chemical Substances MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2021-03-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.1080/15384101.2021.1897271
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5881: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  9. Article ; Online: Approaches to identifying drug resistance mechanisms to clinically relevant treatments in childhood rhabdomyosarcoma.

    Ghilu, Samson / Morton, Christopher L / Vaseva, Angelina V / Zheng, Siyuan / Kurmasheva, Raushan T / Houghton, Peter J

    Cancer drug resistance (Alhambra, Calif.)

    2022  Volume 5, Page(s) 80–89

    Abstract: Aim: Despite aggressive multiagent protocols, patients with metastatic rhabdomyosarcoma (RMS) have poor prognosis. In a recent high-risk trial (ARST0431), 25% of patients failed within the first year, while on therapy and 80% had tumor progression ... ...

    Abstract Aim: Despite aggressive multiagent protocols, patients with metastatic rhabdomyosarcoma (RMS) have poor prognosis. In a recent high-risk trial (ARST0431), 25% of patients failed within the first year, while on therapy and 80% had tumor progression within 24 months. However, the mechanisms for tumor resistance are essentially unknown. Here we explore the use of preclinical models to develop resistance to complex chemotherapy regimens used in ARST0431.
    Methods: A Single Mouse Testing (SMT) protocol was used to evaluate the sensitivity of 34 RMS xenograft models to one cycle of vincristine, actinomycin D, cyclophosphamide (VAC) treatment. Tumor response was determined by caliper measurement, and tumor regression and event-free survival (EFS) were used as endpoints for evaluation. Treated tumors at regrowth were transplanted into recipient mice, and the treatment was repeated until tumors progressed during the treatment period (i.e., became resistant). At transplant, tumor tissue was stored for biochemical and omics analysis.
    Results: The sensitivity to VAC of 34 RMS models was determined. EFS varied from 3 weeks to > 20 weeks. Tumor models were classified as having intrinsic resistance, intermediate sensitivity, or high sensitivity to VAC therapy. Resistance to VAC was developed in multiple models after 2-5 cycles of therapy; however, there were examples where sensitivity remained unchanged after 3 cycles of treatment.
    Conclusion: The SMT approach allows for
    Language English
    Publishing date 2022-01-04
    Publishing country United States
    Document type Journal Article
    ISSN 2578-532X
    ISSN (online) 2578-532X
    DOI 10.20517/cdr.2021.112
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Identifying novel therapeutic agents using xenograft models of pediatric cancer.

    Kurmasheva, Raushan T / Houghton, Peter J

    Cancer chemotherapy and pharmacology

    2016  Volume 78, Issue 2, Page(s) 221–232

    Abstract: In the USA, the overall cure rate for all childhood cancers is seventy percent, and in many patients that ultimately fail curative therapy, initial responses to current multimodality treatments (surgery, radiation therapy and chemotherapy) is good, with ... ...

    Abstract In the USA, the overall cure rate for all childhood cancers is seventy percent, and in many patients that ultimately fail curative therapy, initial responses to current multimodality treatments (surgery, radiation therapy and chemotherapy) is good, with overall 5-year event-free survival approaching 80 %. However, current approaches to curative therapy result in significant morbidity and long-term sequelae, including cardiac dysfunction and cognitive impairment. Furthermore, dose-intensive chemotherapy with conventional agents has not significantly improved outcomes for patients that present with advanced or metastatic disease. Classical cytotoxic agents remain the backbone for curative therapy of both hematologic and solid tumors of childhood. While 'molecularly' targeted agents have shown some clinical activity, responses are often modest and of short duration; hence, there is a need to identify new classes of cytotoxic agent that are effective in patients at relapse and that have reduced or different toxicity profiles to normal tissues. Here we review the pediatric preclinical testing program experience of testing novel agents, and the value and limitations of preclinical xenograft models and genetically engineered mouse models for developing novel agents for treatment of childhood cancer.
    MeSH term(s) Animals ; Antineoplastic Agents/administration & dosage ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Child ; Dose-Response Relationship, Drug ; Drug Design ; Humans ; Mice ; Mice, Transgenic ; Molecular Targeted Therapy ; Neoplasms/drug therapy ; Neoplasms/pathology ; Survival Rate ; Treatment Outcome ; Xenograft Model Antitumor Assays/methods
    Chemical Substances Antineoplastic Agents
    Language English
    Publishing date 2016-05-18
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 6820-2
    ISSN 1432-0843 ; 0344-5704 ; 0943-9404
    ISSN (online) 1432-0843
    ISSN 0344-5704 ; 0943-9404
    DOI 10.1007/s00280-016-3042-6
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    Zs.A 1420: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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