mercaptopurine delayed release (DR6MP)

Transfected cell lines or patient-derived organoids (PDO) were treated with 5-fluorouracil (5-FU) and 6-mercaptopurine (6-MP) and drug response was correlated with ADSL expression levels. Our results suggest that ADSL is a novel oncogene in CRC, modulating mitochondrial function, metabolism and oxidative stress, thus promoting cell cycle progression, proliferation and migration. Our results also suggest that ADSL is a predictive biomarker of response to 6-mercaptopurine in the pre-clinical setting.

The primary drug that causes hematotoxicity in ALL children is 6-mercaptopurine (6-MP)...We also found no association between TPMT genotypes and TPMT phenotypes. The 6-MeMP/6-TGN ratio is associated with hematotoxicity in ALL children during maintenance therapy but is not strong enough to predict hematotoxicity.

All children received 6-mercaptopurine and cis-retinoic acid, and four had azacytidine...Busulfan, cyclophosphamide, and melphalan in three children with matched sibling donors and treosulfan, thiotepa, and fludarabine in the three children with alternate donors resulted in a stable graft... The main factors determining optimal outcomes in HSCT for JMML include adequate disease control before HSCT and a myeloablative conditioning regimen. Graft rejection remains the most significant barrier to cure. Risk stratification based on molecular diagnosis helps avoid HSCT in children with CBL gene mutation

The patient failed multiple lines of treatment (dasatinib, nilotinib, hydroxyurea, cytarabine subcutaneous, 6-mercaptopurine and interferon) and progressed to the blast phase a few months later. CONCLUSIONS We report an unusual case of CML, presented with significant dysgranulopoiesis with an aggressive clinical course including SM uncovered during the disease course with subsequent transformation to the blast phase. The different biological behavior of this case underscores the need for studies on a larger number of cases to explore the significance of the aforementioned coexistent features.

With this diagnosis, chemotherapy continued with all-trans retinoic acid (ATRA ), methotrexate and mercaptopurine, going into remission three months after the start of treatment, with no need for bone marrow transplantation...The treatment is divided into 3 phases: Induction, which aims to reduce the number of leukemic cells, the most suitable drug being trans-retinoic acid (ATRA) combined with arsenic trioxide (ATO) or chemotherapy with anthracycline or anthracycline chemotherapy more ACT... Early diagnosis and treatment are essential for the successful treatment of AML subtype M3, in addition to preventing future ischemic events, which are influenced by increased blood viscosity due to the presence of blasts in peripheral blood.

No previous ALL-specific treatment, with the exception of corticosteroids and/or single dose vincristine and/or up to 3 doses of cyclophosphamide (cycloph.) plus standard prephase treatment are allowed. The 1st induction cycle consists of inotuzumab ozogamicin (InO) 0.8 mg/m2 on day1 and 0.5 mg/m2 on days 8 and 15 together with dexamethasone 10 mg/m2 (days 7-8, days 14-17) and 1 intrathecal injection of methotrexate (MTX), cytarabine (AraC) and dexamethasone (Dexa)...Patients achieving a complete remission are offered to receive 5 conventional consolidation therapies (3 x ID-MTX/asparaginase; 2 x ID-AraC) and one reinduction therapy (idarubicine/AraC/cycloph./Dexa) in combination with rituximab (for CD20+ ALL), followed by a maintenance therapy with 6-mercaptopurine/MTX... Replacement of conventional induction chemotherapy by InO is feasible, results in promising remission rates, and may reduce the risk of early morbidity and lethality, particular in older patients with acute B lymphoblastic leukemia.

The overall activity of 6MP and methotrexate in these patients was low; however, there was a small group of patients who appeared to derive longer-term clinical benefit.

Methods A drug sensitivity profiling, comprising 7 standard chemotherapeutic agents (6-mercaptopurine, cytarabine, daunorubicin, vincristine, methotrexate, prednisone, dexamethasone), was performed on 4 CD9+ (697, BV-173, RS4;11, SUP-B15) and 3 CD9- (Reh, SEM, KOPN-8) B-ALL cell lines...Conclusions Our results indicate that CD9 negativity was definitively linked to glucocorticoid resistance, which could be reversed by CD9 reactivation through a receptor-independent mechanism. Comprehensive understanding of the interaction between CD9 and glucocorticoid susceptibility could lead to improved therapeutic strategies for resistant pediatric B-ALL.

In addition to its chemosensitizing effects, CCI52 and CCI52-14 inhibited the growth of MYCN-amplified high-risk neuroblastoma cell lines and delayed tumor progression in a MYCN-driven, transgenic mouse model of neuroblastoma. These multifunctional inhibitors may be useful for the further development of anticancer agents and as tools to better understand 6-MP metabolism.

Findings of this study may provide basic knowledge for personalized medicine for thiopurine treatment in pediatric acute lymphoblastic leukemia patients.