Response to Tyrosine Kinase Inhibitors in Myeloproliferative Neoplasia with 8p11 Translocation and <i>CEP110</i>-<i>FGFR1</i> Rearrangement

Wehrli, Marc; Leibundgut, Elisabeth Oppliger; Gattiker, Heinrich H.; Manz, Markus G.; Müller, Antonia; Goede, Jeroen S.

doi:10.1634/theoncologist.2016-0354

Cited by 9 publications

(6 citation statements)

References 14 publications

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“…Our data show a consistent relationship between the capacity of each TKI to specifically target FGFR1 and their effectiveness in killing CNTRL‐FGFR1‐expressing Ba/F3 cells. However, this is at odds with reports of apparent clinical responses to combination treatment regimens that included imatinib or dasatinib with vincristine, including in Patient 1 . Ba/F3 cells expressing flCNTRL‐FGFR1 were treated with ponatinib or imatinib, together with vincristine and dexamethasone, and imatinib induced no additional decrease in cell viability (Figure S6).…”

Section: Methods and Resultsmentioning

confidence: 89%

“…Previous case reports (including Patient 1 here) described treatment of FGFR1 fusion‐driven leukaemias with a range of tyrosine kinase inhibitors (TKIs), including imatinib . We measured the viability of Ba/F3 cells expressing tCNTRL‐FGFR1 (Figure S5) or flCNTRL‐FGFR1 (Figure ) after TKI treatment, and measured FGFR1 phosphorylation and fusion expression (using a CNTRL antibody) by Western blot.…”

Section: Methods and Resultsmentioning

confidence: 99%

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Targeted therapy and disease monitoring in CNTRL‐FGFR1‐driven leukaemia

Brown

Bartolo

Davidson

et al. 2019

Pediatric Blood & Cancer

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We report two patients with leukaemia driven by the rare CNTRL-FGFR1 fusion oncogene. This fusion arises from a t(8;9)(p12;q33) translocation, and is a rare driver of biphenotypic leukaemia in children. We used RNA sequencing to report novel features of expressed CNTRL-FGFR1, including CNTRL-FGFR1 fusion alternative splicing. From this knowledge, we designed and tested a Droplet Digital PCR assay that detects CNTRL-FGFR1 expression to approximately one cell in 100 000 using fusion breakpoint-specific primers and probes. We also utilised cell-line models to show that effective tyrosine kinase inhibitors, which may be included in treatment regimens for this disease, are only those that block FGFR1 phosphorylation.

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Section: Methods and Resultsmentioning

confidence: 89%

Section: Methods and Resultsmentioning

confidence: 99%

Targeted therapy and disease monitoring in CNTRL‐FGFR1‐driven leukaemia

Brown

Bartolo

Davidson

et al. 2019

Pediatric Blood & Cancer

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“…Dasatinib is an oral small molecule inhibitor that inhibits nonmutated BCR-ABL and most known BCR-ABL mutants; its targeting includes PDGFR, cKIT, SFK (SRC family kinase), FGFR1, and EGFR ( 114 ). Several clinical examples suggest that dasatinib is more suitable for EMS patients with cardiovascular disease than ponatinib, and the patients benefited for more than 9 months and significantly improved the patient’s quality of life ( 118 , 119 ). Perhaps dasatinib might be more suitable for the treatment of elderly and frail EMS patients with cardiovascular disease, and it improves the PB, prolongs the survival time of patients, and provides another treatment option in addition to hematopoietic stem cell transplantation.…”

Section: Targeted Therapy With Tyrosine Kinase Inhibitorsmentioning

confidence: 99%

The 8p11 myeloproliferative syndrome: Genotypic and phenotypic classification and targeted therapy

Zhang

Lin

et al. 2022

Front. Oncol.

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EMS(8p11 myeloproliferative syndrome, EMS) is an aggressive hematological neoplasm with/without eosinophilia caused by a rearrangement of the FGFR1 gene at 8p11-12. It was found that all cases carry chromosome abnormalities at the molecular level, not only the previously reported chromosome translocation and insertion but also a chromosome inversion. These abnormalities produced 17 FGFR1 fusion genes, of which the most common partner genes are ZNF198 on 13q11-12 and BCR of 22q11.2. The clinical manifestations can develop into AML (acute myeloid leukemia), T-LBL (T-cell lymphoblastic lymphoma), CML (chronic myeloid leukemia), CMML (chronic monomyelocytic leukemia), or mixed phenotype acute leukemia (MPAL). Most patients are resistant to traditional chemotherapy, and a minority of patients achieve long-term clinical remission after stem cell transplantation. Recently, the therapeutic effect of targeted tyrosine kinase inhibitors (such as pemigatinib and infigratinib) in 8p11 has been confirmed in vitro and clinical trials. The TKIs may become an 8p11 treatment option as an alternative to hematopoietic stem cell transplantation, which is worthy of further study.

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“…The drugs here we found are imatinib, dasatinib and nilotinib. [54] The most common toxic manifestations in this group are diarrhea, nausea, pleural effusion and hepatotoxicity.…”

Section: Inhibitors Of Tyrosine Kinase Proteinmentioning

confidence: 99%

Cannabinoids/Endocannabinoids As Possible Antineoplastic Therapy In Comparisson To Cancer Pharmacological Treatments Used Today. Narrative Review

Niño

Alvarado²

2019

EJMO

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C ancer therapy is a complex process. It can be physical (radiotherapy) or chemical (chemotherapy), as well as psychological. Chemotherapy has only been partially successful due to its highly toxic nature, although .many lives have been able to be saved using these drugs, but not without severe side effects. For several years scientists have been performing a considerable amount of studies in order to try to understand the roles of the endocannabinoid system (ECS) and its concern in physiological and pathophysiological processes. [1] On the other hand, there are many research groups in the world working on the new pharmacological tools for cancer treatment. Cannabinoids and endocannabinoids constitute one of the newest subject of interest on this topic, since ∆ 9-THC was shown to present an interesting antineoplastic action [2] and the following finding of the same activity of endocannabinoids. [3] One Cancer is a complex pathophysiological condition that produces an important number of death around the world. At present, there are different ways to treat cancer: chemotherapy, radiotherapy and surgery. Cancer chemotherapy used today in many cases is effective, but it is very toxic too. The endocannabinoid system is implicated in a variety of physiological and pathological processes, including cancer. Many studies have shown, since 1975, that both phytocannabinoids Δ9-tetrahydrocannabinol (THC) and cannabidiol (CBD) offer an antioneoplastic activity. Latter, other researchers have displayed that endocannabinoids as anandamide (ANA) and 2-arachidonoylglycerol (2-AG) also present the same potential activity. Phytocannabinoids and endocannabinoids act through CB1 and CB2 receptors to produce that effect. However, THC-the main phytocannabinoid presenting anticancer action-as well as anandamide employed in pharmacological doses, produce important phycotropic effects, but these cannabinoid compounds do not produce major adverse reactions like conventional antineoplastic drugs. On this basis, scientists have to develop analogs or derivatives of cannabinoids/endocannabinoids that cannot induce psychotropic effects. It is important to study more deeply chronopharmacological aspects of cannabinoids/endocannabinoids in cancer therapy, although some is known today.

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Response to Tyrosine Kinase Inhibitors in Myeloproliferative Neoplasia with 8p11 Translocation and CEP110-FGFR1 Rearrangement

Cited by 9 publications

References 14 publications

Targeted therapy and disease monitoring in CNTRL‐FGFR1‐driven leukaemia

Targeted therapy and disease monitoring in CNTRL‐FGFR1‐driven leukaemia

The 8p11 myeloproliferative syndrome: Genotypic and phenotypic classification and targeted therapy

Cannabinoids/Endocannabinoids As Possible Antineoplastic Therapy In Comparisson To Cancer Pharmacological Treatments Used Today. Narrative Review

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