Philippe Rousselot
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View article: Evaluating a predictive model of tyrosine kinase inhibitor therapy failure in a European-type cohort: a step towards population-specific tools
Evaluating a predictive model of tyrosine kinase inhibitor therapy failure in a European-type cohort: a step towards population-specific tools Open
Predicting therapeutic failure in patients with chronic phase-chronic myeloid leukemia (CP-CML) treated with tyrosine kinase inhibitors (TKI) remains a major challenge for personalized care management. The Sokal and EUTOS long-term surviva…
View article: 2025 European LeukemiaNet recommendations for the management of chronic myeloid leukemia
2025 European LeukemiaNet recommendations for the management of chronic myeloid leukemia Open
View article: Asciminib for relapsed or refractory Philadelphia chromosome–positive acute lymphoblastic leukemia
Asciminib for relapsed or refractory Philadelphia chromosome–positive acute lymphoblastic leukemia Open
View article: <scp>BCR</scp>::<scp>ABL1</scp> Tyrosine Kinase Inhibitors During Pregnancy, a Disproportionality Analysis of Vigibase
<span>BCR</span>::<span>ABL1</span> Tyrosine Kinase Inhibitors During Pregnancy, a Disproportionality Analysis of Vigibase Open
Tyrosine kinase inhibitors (TKIs) targeting BCR::ABL1 have greatly improved the survival of patients with chronic myeloid leukemia (CML), and their teratogenicity appears as an important factor for individuals of childbearing potential. Th…
View article: Harnessing ALDH1A2 vulnerability in T-cell acute lymphoblastic leukemia
Harnessing ALDH1A2 vulnerability in T-cell acute lymphoblastic leukemia Open
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematologic malignancy with limited therapeutic options, particularly in the relapsed/refractory (R/R) setting. Unlike other hematological malignancies, which benefit from target…
View article: A metabolic synthetic lethality of phosphoinositide 3-kinase-driven cancer
A metabolic synthetic lethality of phosphoinositide 3-kinase-driven cancer Open
The deregulated activation of the phosphoinositide 3-kinase (PI3K) pathway is a hallmark of aggressive tumors with metabolic plasticity, eliciting their adaptation to the microenvironment and resistance to chemotherapy. A significant gap l…
View article: Clinical outcomes in patients in any phase of <scp>CML</scp> treated with ponatinib in France—Data from the <scp>TOPASE</scp> observational study
Clinical outcomes in patients in any phase of <span>CML</span> treated with ponatinib in France—Data from the <span>TOPASE</span> observational study Open
Summary The TOPASE study was set up to evaluate the outcomes of chronic myeloid leukaemia [CML] patients treated with ponatinib (PON) in a real‐world setting in France. One hundred and twenty CML patients, 105 in chronic phase (CP), 8 in a…
View article: Correction: Dose modification dynamics of ponatinib in patients with chronic-phase chronic myeloid leukemia (CP-CML) from the PACE and OPTIC trials
Correction: Dose modification dynamics of ponatinib in patients with chronic-phase chronic myeloid leukemia (CP-CML) from the PACE and OPTIC trials Open
View article: Constitutional DNA Polymorphisms Associated with the Plasma Imatinib Concentration in Chronic Myeloid Leukemia Patients
Constitutional DNA Polymorphisms Associated with the Plasma Imatinib Concentration in Chronic Myeloid Leukemia Patients Open
The tyrosine kinase Inhibitor (TKI) imatinib is approved for the treatment of the chronic phase of chronic myeloid leukemia (CP-CML). Pharmacokinetic studies have highlighted the importance of inter-patient variability on imatinib plasma t…
View article: Ponatinib vs Imatinib in Frontline Philadelphia Chromosome–Positive Acute Lymphoblastic Leukemia
Ponatinib vs Imatinib in Frontline Philadelphia Chromosome–Positive Acute Lymphoblastic Leukemia Open
Importance In newly diagnosed Philadelphia chromosome–positive (Ph+) acute lymphoblastic leukemia (ALL), disease progression due to acquired resistance to first- or second-generation BCR::ABL1 tyrosine kinase inhibitors is common. Ponatini…
View article: The initial molecular response predicts the deep molecular response but not treatment-free remission maintenance in a real-world chronic myeloid leukemia cohort
The initial molecular response predicts the deep molecular response but not treatment-free remission maintenance in a real-world chronic myeloid leukemia cohort Open
In chronic myeloid leukemia, the identification of early molecular predictors of stable treatment-free remission (TFR) after tyrosine kinase inhibitor (TKI) discontinuation is challenging. The predictive values of residual disease (BCR::AB…
View article: European Stop Tyrosine Kinase Inhibitor Trial (EURO-SKI) in Chronic Myeloid Leukemia: Final Analysis and Novel Prognostic Factors for Treatment-Free Remission
European Stop Tyrosine Kinase Inhibitor Trial (EURO-SKI) in Chronic Myeloid Leukemia: Final Analysis and Novel Prognostic Factors for Treatment-Free Remission Open
Clinical trials frequently include multiple end points that mature at different times. The initial report, typically based on the primary end point, may be published when key planned co-primary or secondary analyses are not yet available. …
View article: Nilotinib with or without cytarabine for Philadelphia-positive acute lymphoblastic leukemia
Nilotinib with or without cytarabine for Philadelphia-positive acute lymphoblastic leukemia Open
We previously demonstrated that a reduced-intensity chemotherapy schedule can safely replace hyper-CVAD (cyclophosphamide-vincristine-doxorubicin [Adriamycin]-dexamethasone) cycle 1 when combined with imatinib in adults with Philadelphia-p…
View article: A metabolic synthetic lethality of PI3K-driven cancer
A metabolic synthetic lethality of PI3K-driven cancer Open
The deregulated activation of the PI3 kinase (PI3K) pathway is a hallmark of aggressive tumors with metabolic plasticity, eliciting their adaptation to the microenvironment and resistance to chemotherapy. A significant gap lies between the…
View article: Management of ALL in adults: 2024 ELN recommendations from a European expert panel
Management of ALL in adults: 2024 ELN recommendations from a European expert panel Open
Experts from the European Leukemia Net (ELN) working group for adult acute lymphoblastic leukemia have identified an unmet need for guidance regarding management of adult acute lymphoblastic leukemia (ALL) from diagnosis to aftercare. The …
View article: Diagnosis, prognostic factors, and assessment of ALL in adults: 2024 ELN recommendations from a European expert panel
Diagnosis, prognostic factors, and assessment of ALL in adults: 2024 ELN recommendations from a European expert panel Open
Working groups of the European LeukemiaNet have published several important consensus guidelines. Acute lymphoblastic leukemia (ALL) has many different clinical and biological subgroups and the knowledge on disease biology and therapeutic …
View article: Dose modification dynamics of ponatinib in patients with chronic-phase chronic myeloid leukemia (CP-CML) from the PACE and OPTIC trials
Dose modification dynamics of ponatinib in patients with chronic-phase chronic myeloid leukemia (CP-CML) from the PACE and OPTIC trials Open
Ponatinib, the only approved all known-BCR::ABL1 inhibitor, is a third-generation tyrosine-kinase inhibitor (TKI) designed to inhibit BCR::ABL1 with or without any single resistance mutation, including T315I, and induced robust and durable…
View article: Data from <i>PHF6</i>-altered T-ALL Harbor Epigenetic Repressive Switch at Bivalent Promoters and Respond to 5-Azacitidine and Venetoclax
Data from <i>PHF6</i>-altered T-ALL Harbor Epigenetic Repressive Switch at Bivalent Promoters and Respond to 5-Azacitidine and Venetoclax Open
Purpose:To assess the impact of PHF6 alterations on clinical outcome and therapeutical actionability in T-cell acute lymphoblastic leukemia (T-ALL).Experimental Design:We described PHF6 alterations in an adult cohort of T-ALL from the Fren…
View article: Supplementary Table S2 from <i>PHF6</i>-altered T-ALL Harbor Epigenetic Repressive Switch at Bivalent Promoters and Respond to 5-Azacitidine and Venetoclax
Supplementary Table S2 from <i>PHF6</i>-altered T-ALL Harbor Epigenetic Repressive Switch at Bivalent Promoters and Respond to 5-Azacitidine and Venetoclax Open
Bivalent genes hypermethylated in PHF6 altered T-ALL and targeted by PHF6
View article: Supplementary Table S2 from <i>PHF6</i>-altered T-ALL Harbor Epigenetic Repressive Switch at Bivalent Promoters and Respond to 5-Azacitidine and Venetoclax
Supplementary Table S2 from <i>PHF6</i>-altered T-ALL Harbor Epigenetic Repressive Switch at Bivalent Promoters and Respond to 5-Azacitidine and Venetoclax Open
Bivalent genes hypermethylated in PHF6 altered T-ALL and targeted by PHF6
View article: Supplementary Table S2 from <i>PHF6</i>-altered T-ALL Harbor Epigenetic Repressive Switch at Bivalent Promoters and Respond to 5-Azacitidine and Venetoclax
Supplementary Table S2 from <i>PHF6</i>-altered T-ALL Harbor Epigenetic Repressive Switch at Bivalent Promoters and Respond to 5-Azacitidine and Venetoclax Open
Bivalent genes hypermethylated in PHF6 altered T-ALL and targeted by PHF6
View article: Supplementary Table S3 from <i>PHF6</i>-altered T-ALL Harbor Epigenetic Repressive Switch at Bivalent Promoters and Respond to 5-Azacitidine and Venetoclax
Supplementary Table S3 from <i>PHF6</i>-altered T-ALL Harbor Epigenetic Repressive Switch at Bivalent Promoters and Respond to 5-Azacitidine and Venetoclax Open
Patient cohort used for in vitro drug sensitivity assay.
View article: Supplementary Table S1 from <i>PHF6</i>-altered T-ALL Harbor Epigenetic Repressive Switch at Bivalent Promoters and Respond to 5-Azacitidine and Venetoclax
Supplementary Table S1 from <i>PHF6</i>-altered T-ALL Harbor Epigenetic Repressive Switch at Bivalent Promoters and Respond to 5-Azacitidine and Venetoclax Open
PHF6 variant allelic frequencies of the additional 37 non protocolar paired diagnosis/relapsed PHF6ALT patients.
View article: Supplementary Table S3 from <i>PHF6</i>-altered T-ALL Harbor Epigenetic Repressive Switch at Bivalent Promoters and Respond to 5-Azacitidine and Venetoclax
Supplementary Table S3 from <i>PHF6</i>-altered T-ALL Harbor Epigenetic Repressive Switch at Bivalent Promoters and Respond to 5-Azacitidine and Venetoclax Open
Patient cohort used for in vitro drug sensitivity assay.
View article: Supplementary Table S3 from <i>PHF6</i>-altered T-ALL Harbor Epigenetic Repressive Switch at Bivalent Promoters and Respond to 5-Azacitidine and Venetoclax
Supplementary Table S3 from <i>PHF6</i>-altered T-ALL Harbor Epigenetic Repressive Switch at Bivalent Promoters and Respond to 5-Azacitidine and Venetoclax Open
Patient cohort used for in vitro drug sensitivity assay.
View article: Supplementary Figure S1 from <i>PHF6</i>-altered T-ALL Harbor Epigenetic Repressive Switch at Bivalent Promoters and Respond to 5-Azacitidine and Venetoclax
Supplementary Figure S1 from <i>PHF6</i>-altered T-ALL Harbor Epigenetic Repressive Switch at Bivalent Promoters and Respond to 5-Azacitidine and Venetoclax Open
Supplementary Figure 1 (A) Circos plot representing mutations co-occurrences in PHF6WT (left) and PHF6ALT T-ALL (right). (B) Variant allele frequencies (VAF) of mutations at diagnosis and relapse. Genes are ordered by decreasing VAF at dia…
View article: Supplementary Figure S2 from <i>PHF6</i>-altered T-ALL Harbor Epigenetic Repressive Switch at Bivalent Promoters and Respond to 5-Azacitidine and Venetoclax
Supplementary Figure S2 from <i>PHF6</i>-altered T-ALL Harbor Epigenetic Repressive Switch at Bivalent Promoters and Respond to 5-Azacitidine and Venetoclax Open
Supplementary Figure 2 (A) Bar graphs showing the significant association between PHF6 status and methylation clusters previously described by our team (1). (B) Kaplan-Meier curve of overall survival between PHF6ALT and PHF6WT patients wit…
View article: Supplementary Table S1 from <i>PHF6</i>-altered T-ALL Harbor Epigenetic Repressive Switch at Bivalent Promoters and Respond to 5-Azacitidine and Venetoclax
Supplementary Table S1 from <i>PHF6</i>-altered T-ALL Harbor Epigenetic Repressive Switch at Bivalent Promoters and Respond to 5-Azacitidine and Venetoclax Open
PHF6 variant allelic frequencies of the additional 37 non protocolar paired diagnosis/relapsed PHF6ALT patients.
View article: Supplementary Table S2 from <i>PHF6</i>-altered T-ALL Harbor Epigenetic Repressive Switch at Bivalent Promoters and Respond to 5-Azacitidine and Venetoclax
Supplementary Table S2 from <i>PHF6</i>-altered T-ALL Harbor Epigenetic Repressive Switch at Bivalent Promoters and Respond to 5-Azacitidine and Venetoclax Open
Bivalent genes hypermethylated in PHF6 altered T-ALL and targeted by PHF6
View article: Supplementary Table S3 from <i>PHF6</i>-altered T-ALL Harbor Epigenetic Repressive Switch at Bivalent Promoters and Respond to 5-Azacitidine and Venetoclax
Supplementary Table S3 from <i>PHF6</i>-altered T-ALL Harbor Epigenetic Repressive Switch at Bivalent Promoters and Respond to 5-Azacitidine and Venetoclax Open
Patient cohort used for in vitro drug sensitivity assay.