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A novel t(5;7)(q31;q21/CDK6::IL3 in immature T-cell acute lymphoblastic leukemia with IL3 overexpression and reactive eosinophilia [WTE]

ABSTRACT: IL3 expression and reactive eosinophils

ORGANISM(S): Homo sapiens

PROVIDER: GSE211476 | GEO | 2025/08/11

REPOSITORIES: GEO

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A novel t(5;7)(q31;q21/CDK6::IL3 in immature T-cell acute lymphoblastic leukemia with IL3 overexpression and reactive eosinophilia [SNP]

Project description:IL3 expression and reactive eosinophils

2025-08-11 | GSE211170 | GEO

A novel t(5 7)(q31 q21/CDK6::IL3 in immature T-cell acute lymphoblastic leukemia with IL3 overexpression and reactive eosinophilia

Project description:A novel t(5 7)(q31 q21/CDK6::IL3 in immature T-cell acute lymphoblastic leukemia with IL3 overexpression and reactive eosinophilia

| PRJNA870479 | ENA

A novel t(5 7)(q31 q21/CDK6::IL3 in immature T-cell acute lymphoblastic leukemia with IL3 overexpression and reactive eosinophilia [SNP]

Project description:A novel t(5 7)(q31 q21/CDK6::IL3 in immature T-cell acute lymphoblastic leukemia with IL3 overexpression and reactive eosinophilia [SNP]

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A novel t(5 7)(q31 q21/CDK6::IL3 in immature T-cell acute lymphoblastic leukemia with IL3 overexpression and reactive eosinophilia [WTE]

Project description:A novel t(5 7)(q31 q21/CDK6::IL3 in immature T-cell acute lymphoblastic leukemia with IL3 overexpression and reactive eosinophilia [WTE]

| PRJNA870485 | ENA

A novel t(5;7)(q31;q21/CDK6::IL3 in immature T-cell acute lymphoblastic leukemia with IL3 overexpression and reactive eosinophilia

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-08-11 | GSE211484 | GEO

A Novel t(5;7)(q31;q21)/CDK6::IL3 in Immature T-cell Acute Lymphoblastic Leukemia With IL3 Expression and Eosinophilia.

Project description: Not available

| S-EPMC9584195 | biostudies-literature

Targeting the CDK6 Dependence of Ph+ Acute Lymphoblastic Leukemia.

Project description:Ph+ ALL is a poor-prognosis leukemia subtype driven by the BCR-ABL1 oncogene, either the p190- or the p210-BCR/ABL isoform in a 70:30 ratio. Tyrosine Kinase inhibitors (TKIs) are the drugs of choice in the therapy of Ph+ ALL. In combination with standard chemotherapy, TKIs have markedly improved the outcome of Ph+ ALL, in particular if this treatment is followed by bone marrow transplantation. However, resistance to TKIs develops with high frequency, causing leukemia relapse that results in <5-year overall survival. Thus, new therapies are needed to address relapsed/TKI-resistant Ph+ ALL. We have shown that expression of cell cycle regulatory kinase CDK6, but not of the highly related CDK4 kinase, is required for the proliferation and survival of Ph+ ALL cells. Comparison of leukemia suppression induced by treatment with the clinically-approved dual CDK4/6 inhibitor palbociclib versus CDK6 silencing revealed that the latter treatment was markedly more effective, probably reflecting inhibition of CDK6 kinase-independent effects. Thus, we developed CDK4/6-targeted proteolysis-targeting chimeras (PROTACs) that preferentially degrade CDK6 over CDK4. One compound termed PROTAC YX-2-107, which degrades CDK6 by recruiting the Cereblon ubiquitin ligase, markedly suppressed leukemia burden in mice injected with de novo or TKI-resistant Ph+ ALL. The effect of PROTAC YX-2-107 was comparable or superior to that of palbociclib. The development of CDK6-selective PROTACs represents an effective strategy to exploit the "CDK6 dependence" of Ph+ ALL cells while sparing a high proportion of normal hematopoietic progenitors that depend on both CDK6 and CDK6 for their survival. In combination with other agents, CDK6-selective PROTACs may be valuable components of chemotherapy-free protocols for the therapy of Ph+ ALL and other CDK6-dependent hematological malignancies.

| S-EPMC8467343 | biostudies-literature

Targeting CDK6 and BCL2 Exploits the "MYB Addiction" of Ph+ Acute Lymphoblastic Leukemia.

Project description:Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL) is currently treated with BCR-ABL1 tyrosine kinase inhibitors (TKI) in combination with chemotherapy. However, most patients develop resistance to TKI through BCR-ABL1-dependent and -independent mechanisms. Newly developed TKI can target Ph+ ALL cells with BCR-ABL1-dependent resistance; however, overcoming BCR-ABL1-independent mechanisms of resistance remains challenging because transcription factors, which are difficult to inhibit, are often involved. We show here that (i) the growth of Ph+ ALL cell lines and primary cells is highly dependent on MYB-mediated transcriptional upregulation of CDK6, cyclin D3, and BCL2, and (ii) restoring their expression in MYB-silenced Ph+ ALL cells rescues their impaired proliferation and survival. Levels of MYB and CDK6 were highly correlated in adult Ph+ ALL (P = 0.00008). Moreover, Ph+ ALL cells exhibited a specific requirement for CDK6 but not CDK4 expression, most likely because, in these cells, CDK6 was predominantly localized in the nucleus, whereas CDK4 was almost exclusively cytoplasmic. Consistent with their essential role in Ph+ ALL, pharmacologic inhibition of CDK6 and BCL2 markedly suppressed proliferation, colony formation, and survival of Ph+ ALL cells ex vivo and in mice. In summary, these findings provide a proof-of-principle, rational strategy to target the MYB "addiction" of Ph+ ALL.Significance: MYB blockade can suppress Philadelphia chromosome-positive leukemia in mice, suggesting that this therapeutic strategy may be useful in patients who develop resistance to imatinib and other TKIs used to treat this disease. Cancer Res; 78(4); 1097-109. ©2017 AACR.

| S-EPMC5815914 | biostudies-literature

CCL11/CCR3-dependent eosinophilia alleviates malignant pleural effusions and improves prognosis

Project description:The role of eosinophils in the development and progression of malignant pleural effusion (MPE) remains unclear. However, MPE is a frequently occurring manifestation of advanced cancer and is often associated with a poor prognosis. While current treatment options for MPE can provide palliative care, alternative therapies are urgently needed. To investigate this role, eosinophil counts were determined using flow cytometry and immunofluorescence. Eosinophil-deficient mice (Eos-null) and Cd3δ -promoter Il5 transgenic (Il5 Tg) mice were subjected to a mouse model of MPE. Eosinophils were isolated by magnetic-activated cell sorting (MACS) and fluorescence-activated cell sorting (FACS), and their transcriptional profile was obtained by RNA sequencing. Finally, we evaluated the effects of the C-C motif chemokine ligand 11 (CCL11) and a C-C motif chemokine receptor 3 (CCR3) axis on MPE pathology using recombinant mouse CCL11 and a CCR3 inhibitor. In humans, eosinophil counts were increased in MPE and negatively correlated with the LENT score. In animal models, eosinophils were rapidly recruited to the pleural cavity when challenged with tumor cells. Interestingly, eosinophil deficiency worsened MPE, while an increase in eosinophils through various methods improved MPE. Furthermore, the recruitment of eosinophils may be influenced by the CCL11-CCR3 axis. Taken together, the study highlights the protective role of eosinophils against MPE formation, indicating their potential as a therapeutic strategy. Moreover, the CCL11-CCR3 axis may be a viable target for MPE treatment.

2024-08-01 | GSE245575 | GEO

A neoplasm with FIP1L1-PDGFRA fusion presenting as pediatric T-cell lymphoblastic leukemia/lymphoma without eosinophilia.

Project description:The 2016 World Health Organization (2016 WHO) classification of hematopoietic malignancies classifies neoplasms with a fusion between the FIP1L1 and PDGFRA genes in 4q12 into a group called "myeloid and lymphoid neoplasms with eosinophilia and abnormalities of PDGFRA, PDGFRB or FGFR1 or with PCM1-JAK2". Neoplasms characterized by this fusion are pluripotent stem cell disorders that can show both myeloid and lymphoid differentiation. They typically occur in adult patients and most are characterized by eosinophilia. We describe identification of a FIP1L1-PDGFRA fusion in a 13-year-old boy who presented with T-lymphoblastic leukemia/lymphoma without eosinophilia. Detection of FIP1L1-PDGFRA driven neoplasms at diagnosis is usually critical for proper treatment, since almost all reported cases responded to tyrosine kinase inhibitors. However, our patient's leukemia was refractory to standard chemotherapy, and did not show a meaningful response to tyrosine kinase inhibitor therapy. Testing for a FIP1L1-PDGFRA rearrangement is at present limited to patients with idiopathic hypereosinophilia, and we hypothesize that this abnormality may be under-diagnosed in children with acute leukemias.

| S-EPMC7469920 | biostudies-literature

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