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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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE211484 | 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 [WTE]

Project description:IL3 expression and reactive eosinophils

2025-08-11 | GSE211476 | GEO

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 Expression and Eosinophilia.

Project description: Not available

| S-EPMC9584195 | biostudies-literature

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

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

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]

| PRJNA869310 | ENA

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

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

Acute lymphoblastic leukemia

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

2010-09-10 | GSE24001 | GEO

Immature B-cell progenitors survive oncogenic stress and efficiently initiate Ph+ B-acute lymphoblastic leukemia.

Project description:Philadelphia chromosome-positive (Ph(+)) B-acute lymphoblastic leukemia (B-ALL) can initiate in committed B-cell progenitors. However, the stages of B-cell differentiation in which disease can initiate and the efficiency with which this occurs are unclear. We now demonstrate that B-cell progenitors, up to and including the pro-B cell, efficiently initiate Ph(+) B-ALL. However, cells at the pre-B-cell stage of development did not initiate disease. We show that this difference in leukemia initiating potential is due to the level at which the Arf tumor suppressor gene is induced in specific stages of B lymphopoiesis. Whereas immature B-cell progenitors survive the relatively low levels of Arf that are induced after oncogene expression, pre-B cells express the tumor suppressor gene at high levels and undergo massive apoptosis. These data demonstrate that the molecular events that control Ph(+) B-ALL initiation and tumor suppression in the B-cell lineage are developmentally regulated.

| S-EPMC2953887 | biostudies-other

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