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  1. Book: Advancing CML patient care

    Giles, Francis J.

    closing in on a cure?

    (Clinical advances in hematology & oncology ; 7,1, Suppl. 1)

    2009  

    Author's details Faculty Francis J. Giles
    Series title Clinical advances in hematology & oncology ; 7,1, Suppl. 1
    Collection
    Language English
    Size 14 S. : Ill., graph. Darst.
    Publisher Millennium Med. Publ
    Publishing place New York, NY
    Publishing country United States
    Document type Book
    HBZ-ID HT015861724
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    Zs A 6505 -7,Suppl.1- verfügbar in Königswinter Königswinter

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  2. Book: Optimizing outcomes for patients with advanced disease in chronic myelogenous leukemia

    Giles, Francis J.

    (Seminars in oncology ; 35,1, Suppl. 1)

    2008  

    Author's details [Francis J. Giles ...]
    Series title Seminars in oncology ; 35,1, Suppl. 1
    Collection
    Language English
    Size S20 S.
    Publisher Saunders
    Publishing place Philadelphia, Pa
    Publishing country United States
    Document type Book
    HBZ-ID HT015506459
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

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    Zs A 1348 -35,Suppl.1- not available for loan Zeitschriften-Lesesaal

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  3. Article: SLAM Modification as an Immune-Modulatory Therapeutic Approach in Cancer.

    Tojjari, Alireza / Giles, Francis J / Vilbert, Maysa / Saeed, Anwaar / Cavalcante, Ludimila

    Cancers

    2023  Volume 15, Issue 19

    Abstract: In the field of oncology, the Signaling Lymphocyte Activation Molecule (SLAM) family is emerging as pivotal in modulating immune responses within tumor environments. The SLAM family comprises nine receptors, mainly found on immune cell surfaces. These ... ...

    Abstract In the field of oncology, the Signaling Lymphocyte Activation Molecule (SLAM) family is emerging as pivotal in modulating immune responses within tumor environments. The SLAM family comprises nine receptors, mainly found on immune cell surfaces. These receptors play complex roles in the interaction between cancer and the host immune system. Research suggests SLAM's role in both enhancing and dampening tumor-immune responses, influencing the progression and treatment outcomes of various cancers. As immunotherapy advances, resistance remains an issue. The nuanced roles of the SLAM family might provide answers. With the rise in technologies like single-cell RNA sequencing and advanced imaging, there is potential for precise SLAM-targeted treatments. This review stresses patient safety, the importance of thorough clinical trials, and the potential of SLAM-focused therapies to transform cancer care. In summary, SLAM's role in oncology signals a new direction for more tailored and adaptable cancer treatments.
    Language English
    Publishing date 2023-09-29
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers15194808
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Elraglusib (9-ING-41), a selective small-molecule inhibitor of glycogen synthase kinase-3 beta, reduces expression of immune checkpoint molecules PD-1, TIGIT and LAG-3 and enhances CD8

    Shaw, Gary / Cavalcante, Ludimila / Giles, Francis J / Taylor, Alison

    Journal of hematology & oncology

    2022  Volume 15, Issue 1, Page(s) 134

    Abstract: Background: Glycogen synthase kinase-3 (GSK-3) is a serine/threonine kinase with multiple roles in tumour growth, cell invasion and metastasis. We have previously established GSK-3 as an upstream regulator of PD-1 gene expression in CD8 + T cells and ... ...

    Abstract Background: Glycogen synthase kinase-3 (GSK-3) is a serine/threonine kinase with multiple roles in tumour growth, cell invasion and metastasis. We have previously established GSK-3 as an upstream regulator of PD-1 gene expression in CD8 + T cells and demonstrated that GSK-3 inhibition is as effective as anti-PD-1 mAb blockade in controlling tumour growth. Elraglusib (9-ING-41) is a specific small-molecule inhibitor of GSK-3β with clinical activity in patients with advanced cancers, including a patient with refractory melanoma whose response provided the rationale for the current study.
    Methods: The B16 melanoma mouse model was used to observe the effect of elraglusib on tumour growth either as a single agent or in combination (simultaneously and sequentially) with anti-PD-1 mAb treatment. B16 tumour cells were implanted in either the flank, brain or both locations, and Kaplan-Meier plots were used to depict survival and significance determined using log rank tests. Expression of the immune checkpoint molecules, TIGIT, LAG-3 and PD-1, was evaluated using flow cytometry alongside expression of the chemokine receptor, CXCR3. Further evaluation of PD-1 expression was determined through RT-qPCR and immunohistochemistry.
    Results: We demonstrated that elraglusib has a suppressive effect against melanoma as a single agent and enhanced anti-PD-1 therapy. There was a synergistic effect when elraglusib was used in combination with anti-PD-1 mAb, and an even greater effect when used as sequential therapy. Suppression of tumour growth was associated with a reduced expression of immune checkpoint molecules, PD-1, TIGIT and LAG-3 with upregulation of CXCR3 expression.
    Conclusions: These data highlight the potential of elraglusib as an immune-modulatory agent and demonstrate the benefit of a sequential approach with immune checkpoint inhibition followed by GSK-3β inhibition in melanoma and provide a rationale for clinical investigation of elraglusib combined with immune checkpoint inhibitory molecules, including those targeting PD-1, TIGIT and LAG-3. This has several potential implications for current immunotherapy regimes, including possibly reducing the intensity of anti-PD-1 mAb treatment needed for response in patients receiving elraglusib, especially given the benign adverse event profile of elraglusib observed to date. Based on these data, a clinical study of elraglusib, an anti-PD-1 mAb and chemotherapy is ongoing (NCT NCT05239182).
    MeSH term(s) Animals ; CD8-Positive T-Lymphocytes ; Clinical Studies as Topic ; Glycogen Synthase Kinase 3 ; Glycogen Synthase Kinase 3 beta ; Immune Checkpoint Proteins ; Melanoma, Experimental/drug therapy ; Mice ; Protein Kinase Inhibitors ; Receptors, Immunologic
    Chemical Substances Immune Checkpoint Proteins ; Protein Kinase Inhibitors ; Receptors, Immunologic ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; Glycogen Synthase Kinase 3 (EC 2.7.11.26)
    Language English
    Publishing date 2022-09-14
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2429631-4
    ISSN 1756-8722 ; 1756-8722
    ISSN (online) 1756-8722
    ISSN 1756-8722
    DOI 10.1186/s13045-022-01352-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Targeting both BET and CBP/EP300 proteins with the novel dual inhibitors NEO2734 and NEO1132 leads to anti-tumor activity in multiple myeloma.

    Ryan, Katie R / Giles, Francis / Morgan, Gareth J

    European journal of haematology

    2020  Volume 106, Issue 1, Page(s) 90–99

    Abstract: Objectives: Two promising epigenetic therapeutic targets have emerged for the treatment of hematologic malignancies, BET and CBP/EP300 proteins. Several studies have shown that targeting these individual classes of proteins has anti-tumor activity in ... ...

    Abstract Objectives: Two promising epigenetic therapeutic targets have emerged for the treatment of hematologic malignancies, BET and CBP/EP300 proteins. Several studies have shown that targeting these individual classes of proteins has anti-tumor activity in multiple myeloma (MM), as well as other cancers. Here, we present the first data exploring the anti-tumor activity of two novel dual inhibitors, NEO2734 and NEO1132, of both BET and CBP/EP300 proteins in MM.
    Methods: Sixteen MM cell lines (MMCLs) were treated with the dual inhibitors NEO2734 and NEO1132, the single BET inhibitors JQ1, OTX015, IBET-762, and IBET-151, and a single CBP/EP300 inhibitor CPI-637.
    Results: The dual inhibitor NEO2734 showed strong anti-tumor activity and was consistently highly active against all MMCLs, being as potent as JQ1 and more so than other single inhibitors. NEO2734 and NEO11132 induced a significant G1 cell cycle arrest and decreased c-MYC and IRF4 protein levels in MMCLs compared to the other single inhibitors. Sensitivity to the dual inhibitors was not dependent on a specific MM molecular subgroup but correlated with c-MYC protein expression levels.
    Conclusions: The dual inhibition of BET and CBP/EP300 has potential therapeutic benefits for patients with MM.
    MeSH term(s) Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Benzimidazoles/pharmacology ; Benzimidazoles/therapeutic use ; Cell Cycle/drug effects ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Dose-Response Relationship, Drug ; Drug Resistance, Neoplasm/drug effects ; Drug Resistance, Neoplasm/genetics ; E1A-Associated p300 Protein/antagonists & inhibitors ; Humans ; Interferon Regulatory Factors/genetics ; Interferon Regulatory Factors/metabolism ; Multiple Myeloma ; Proteins/antagonists & inhibitors ; Proto-Oncogene Proteins c-myc/genetics ; Proto-Oncogene Proteins c-myc/metabolism ; Pyridones/pharmacology ; Pyridones/therapeutic use
    Chemical Substances Antineoplastic Agents ; Benzimidazoles ; Interferon Regulatory Factors ; NEO2734 ; Proteins ; Proto-Oncogene Proteins c-myc ; Pyridones ; bromodomain and extra-terminal domain protein, human ; interferon regulatory factor-4 ; E1A-Associated p300 Protein (EC 2.3.1.48) ; EP300 protein, human (EC 2.3.1.48)
    Language English
    Publishing date 2020-10-22
    Publishing country England
    Document type Journal Article
    ZDB-ID 392482-8
    ISSN 1600-0609 ; 0902-4441
    ISSN (online) 1600-0609
    ISSN 0902-4441
    DOI 10.1111/ejh.13525
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 323: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  6. Article ; Online: Efficacy and safety of bosutinib in patients treated with prior imatinib and/or dasatinib and/or nilotinib: Subgroup analyses from the phase 4 BYOND study.

    Smith, B Douglas / Brümmendorf, Tim H / Roboz, Gail J / Gambacorti-Passerini, Carlo / Charbonnier, Aude / Viqueira, Andrea / Leip, Eric / Purcell, Simon / Goldman, Erinn Hoag / Giles, Francis / Ernst, Thomas / Hochhaus, Andreas / Rosti, Gianantonio

    Leukemia research

    2024  Volume 139, Page(s) 107481

    Abstract: The BYOND study evaluated the efficacy and safety of bosutinib 500 mg once daily in patients with chronic myeloid leukemia (CML) resistant/intolerant to prior tyrosine kinase inhibitors (TKIs). These post-hoc analyses assessed the efficacy and safety of ... ...

    Abstract The BYOND study evaluated the efficacy and safety of bosutinib 500 mg once daily in patients with chronic myeloid leukemia (CML) resistant/intolerant to prior tyrosine kinase inhibitors (TKIs). These post-hoc analyses assessed the efficacy and safety of bosutinib by resistance or intolerance to prior TKIs (imatinib-resistant vs dasatinib/nilotinib-resistant vs TKI-intolerant), and cross-intolerance between bosutinib and prior TKIs (imatinib, dasatinib, nilotinib), in patients with Philadelphia chromosome-positive chronic phase CML. Data are reported after ≥3 years' follow-up. Of 156 patients with Philadelphia chromosome-positive chronic phase CML, 53 were imatinib-resistant, 29 dasatinib/nilotinib-resistant, and 74 intolerant to all prior TKIs; cumulative complete cytogenetic response rates at any time were 83.7%, 61.5%, and 86.8%, and cumulative major molecular response rates at any time were 72.9%, 40.7%, and 82.4%, respectively. Of 141, 95, and 79 patients who received prior imatinib, dasatinib, and nilotinib, 64 (45.4%), 71 (74.7%), and 60 (75.9%) discontinued the respective TKI due to intolerance; of these, 2 (3.1%), 5 (7.0%), and 0 had cross-intolerance with bosutinib. The response rates observed in TKI-resistant and TKI-intolerant patients, and low cross-intolerance between bosutinib and prior TKIs, further support bosutinib use for patients with Philadelphia chromosome-positive chronic phase CML resistant/intolerant to prior TKIs. TRIAL REGISTRATION: ClinicalTrials.gov: NCT02228382.
    MeSH term(s) Humans ; Imatinib Mesylate/adverse effects ; Dasatinib/adverse effects ; Antineoplastic Agents/adverse effects ; Philadelphia Chromosome ; Protein Kinase Inhibitors/adverse effects ; Pyrimidines ; Leukemia, Myeloid, Chronic-Phase/drug therapy ; Pathologic Complete Response ; Aniline Compounds ; Nitriles ; Quinolines
    Chemical Substances Imatinib Mesylate (8A1O1M485B) ; Dasatinib (RBZ1571X5H) ; bosutinib (5018V4AEZ0) ; Antineoplastic Agents ; Protein Kinase Inhibitors ; Pyrimidines ; Aniline Compounds ; Nitriles ; Quinolines
    Language English
    Publishing date 2024-03-11
    Publishing country England
    Document type Clinical Trial, Phase IV ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 752396-8
    ISSN 1873-5835 ; 0145-2126
    ISSN (online) 1873-5835
    ISSN 0145-2126
    DOI 10.1016/j.leukres.2024.107481
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1321: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  7. Article ; Online: Large-Cell Neuroendocrine Carcinoma of the Lung: A Focused Analysis of

    Chae, Young Kwang / Tamragouri, Keerthi B / Chung, Jon / Lin, Xiaoqi / Miller, Vincent / Ali, Siraj M / Giles, Francis J

    JCO precision oncology

    2022  Volume 2, Page(s) 1–12

    Abstract: Purpose: In advanced stages, large-cell neuroendocrine carcinoma of the lung (L-LCNEC) mimics small-cell lung cancer despite its traditional classification as a non-small-cell lung cancer. Here we present a focused analysis of : Patients and methods: ...

    Abstract Purpose: In advanced stages, large-cell neuroendocrine carcinoma of the lung (L-LCNEC) mimics small-cell lung cancer despite its traditional classification as a non-small-cell lung cancer. Here we present a focused analysis of
    Patients and methods: Comprehensive genomic profiling of tumor tissues was performed from a cohort of 300 patients with biopsy-proven L-LCNEC. Specimens were either from a primary lung lesion or metastatic site.
    Results: In 13 patients, 14 unique
    Conclusion: Although uncommon, L-LCNEC does seem to contain activating and therefore actionable alterations. We thus highlight the value of pursuing next-generation sequencing for patients with this disease.
    Language English
    Publishing date 2022-01-27
    Publishing country United States
    Document type Journal Article
    ISSN 2473-4284
    ISSN (online) 2473-4284
    DOI 10.1200/PO.17.00150
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Cancer--an increasingly target rich environment.

    Giles, Francis J

    Current drug targets

    2011  Volume 12, Issue 14, Page(s) 1998–2000

    MeSH term(s) Aurora Kinases ; Humans ; Neoplasms/drug therapy ; Protein-Serine-Threonine Kinases/antagonists & inhibitors ; Proto-Oncogene Proteins c-pim-1/antagonists & inhibitors
    Chemical Substances Aurora Kinases (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Proto-Oncogene Proteins c-pim-1 (EC 2.7.11.1) ; proto-oncogene proteins pim (EC 2.7.11.1)
    Language English
    Publishing date 2011-07-14
    Publishing country United Arab Emirates
    Document type Editorial
    ZDB-ID 2064859-5
    ISSN 1873-5592 ; 1389-4501
    ISSN (online) 1873-5592
    ISSN 1389-4501
    DOI 10.2174/138945011798829375
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    Zs.A 5578: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (2.OG)
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  9. Article ; Online: Treating imatinib resistance in the few in CML-A key step towards cure in all.

    Giles, Francis J

    Leukemia research

    2010  Volume 34, Issue 9, Page(s) 1123–1124

    MeSH term(s) Antineoplastic Agents/therapeutic use ; Benzamides ; Drug Resistance, Neoplasm ; Humans ; Imatinib Mesylate ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy ; Piperazines/therapeutic use ; Pyrimidines/therapeutic use
    Chemical Substances Antineoplastic Agents ; Benzamides ; Piperazines ; Pyrimidines ; Imatinib Mesylate (8A1O1M485B)
    Language English
    Publishing date 2010-09
    Publishing country England
    Document type Comment ; Editorial
    ZDB-ID 752396-8
    ISSN 1873-5835 ; 0145-2126
    ISSN (online) 1873-5835
    ISSN 0145-2126
    DOI 10.1016/j.leukres.2010.03.037
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1321: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
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  10. Article ; Online: Malignant glioma subset from actuate 1801: Phase I/II study of 9-ING-41, GSK-3β inhibitor, monotherapy or combined with chemotherapy for refractory malignancies.

    Odia, Yazmin / Cavalcante, Ludimila / Safran, Howard / Powell, Steven Francis / Munster, Pamela N / Ma, Wen Wee / Carneiro, Benedito A / Bastos, Bruno R / Mikrut, Stacy / Mikrut, William / Giles, Francis J / Sahebjam, Solmaz

    Neuro-oncology advances

    2022  Volume 4, Issue 1, Page(s) vdac012

    Abstract: Background: GSK3β serine/threonine kinase regulates metabolism and glycogen biosynthesis. GSK3β overexpression promotes progression and resistance through NF-κB and p53 apoptotic pathways. GSK3β inhibits immunomodulation by downregulating PD-L1 and LAG- ... ...

    Abstract Background: GSK3β serine/threonine kinase regulates metabolism and glycogen biosynthesis. GSK3β overexpression promotes progression and resistance through NF-κB and p53 apoptotic pathways. GSK3β inhibits immunomodulation by downregulating PD-L1 and LAG-3 checkpoints and increasing NK and T-cell tumor killing. 9-ING-41, a small-molecule, selective GSK3β inhibitor, showed preclinical activity in chemo-resistant PDX glioblastoma models, including enhanced lomustine antitumor effect.
    Methods: Refractory malignancies (
    Results: RP2D of 15 mg/kg IV TIW was confirmed across all 9 regimens, no accentuated chemotherapy toxicity noted. Glioma subtypes included: 13 glioblastoma, 2 anaplastic astrocytomas, 1 anaplastic oligodendroglioma, 1 astrocytoma. Median age 52 (30-69) years; 6 female, 12 male; median ECOG 1 (0-2); median recurrences 3 (1-6). All received upfront radiation/temozolomide (18/18), plus salvage nitrosoureas (15/18), bevacizumab (8/18), TTFields (6/18), or immunotherapy (4/18). IDH/mutation(3/18); 1p19q/codeletion(1/18); MGMT/methylated(1/18). Four received 9-ING-41 monotherapy, 14 concurrent with lomustine. No severe toxicities were attributed to 9-ING-41, only mild vision changes (9/18, 50%), or infusion reactions (4/18, 22%). Lomustine-related toxicities: G3/4 thrombocytopenia (3/14, 21%), G1/2 fatigue (4/14, 28%). Median days on therapy was 55 (4-305); 1 partial response (>50%) was noted. Median OS was 5.5 (95% CI: 2.8-11.4) months and PFS-6 was 16.7%.
    Conclusion: 9-ING-41 plus/minus lomustine is safe and warrants further study in glioma patients.
    Language English
    Publishing date 2022-02-07
    Publishing country England
    Document type Journal Article
    ZDB-ID 3009682-0
    ISSN 2632-2498 ; 2632-2498
    ISSN (online) 2632-2498
    ISSN 2632-2498
    DOI 10.1093/noajnl/vdac012
    Database MEDical Literature Analysis and Retrieval System OnLINE

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