Biomodulatory therapy induces complete molecular remission in chemorefractory acute myeloid leukemia

Thomas, Simone; Schelker, Roland Christian; Klobuch, Sebastian; Zaiss, Sascha; Troppmann, M; Rehli, Michael; Haferlach, Torsten; Herr, Wolfgang; Reichle, Albrecht

doi:10.3324/haematol.2014.115055

Cited by 32 publications

(63 citation statements)

References 15 publications

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“…Therefore, genetically different acute myelocytic leukemias constitute a unique phenotype, rapidly displaced normal hematopoiesis in the bone marrow. Accordingly, unique pro-anakoinotic therapy approaches may differentiate blasts from genetically different acute myelocytic leukemias into granulocyte-like cells (32, 34,[38][39][40][41][42].…”

Section: Communication Unifies All Systems Levelsmentioning

confidence: 99%

“…At the same time available biological and clinical response data indicate the administered drugs' activity profile can define them as master modifiers of tumor tissue (9). In addition to this clinical data, there is increasing biological data indicating master modifiers' mechanisms of action (22,32,41,42,(54)(55)(56).…”

Section: Anakoinosis Induces Changes In the Flux Of Informationmentioning

confidence: 99%

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Anakoinosis: Correcting Aberrant Homeostasis of Cancer Tissue—Going Beyond Apoptosis Induction

et al. 2019

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The current approach to systemic therapy for metastatic cancer is aimed predominantly at inducing apoptosis of cancer cells by blocking tumor-promoting signaling pathways or by eradicating cell compartments within the tumor. In contrast, a systems view of therapy primarily considers the communication protocols that exist at multiple levels within the tumor complex, and the role of key regulators of such systems. Such regulators may have far-reaching influence on tumor response to therapy and therefore patient survival. This implies that neoplasia may be considered as a cell non-autonomous disease. The multi-scale activity ranges from intra-tumor cell compartments, to the tumor, to the tumor-harboring organ to the organism. In contrast to molecularly targeted therapies, a systems approach that identifies the complex communications networks driving tumor growth offers the prospect of disrupting or "normalizing" such aberrant communicative behaviors and therefore attenuating tumor growth. Communicative reprogramming, a treatment strategy referred to as anakoinosis, requires novel therapeutic instruments, so-called master modifiers to deliver concerted tumor growth-attenuating action. The diversity of biological outcomes following pro-anakoinotic tumor therapy, such as differentiation, trans-differentiation, control of tumor-associated inflammation, etc. demonstrates that long-term tumor control may occur in multiple forms, inducing even continuous complete remission. Accordingly, pro-anakoinotic therapies dramatically extend the repertoire for achieving tumor control and may activate apoptosis pathways for controlling resistant metastatic tumor disease and hematologic neoplasia.

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Section: Communication Unifies All Systems Levelsmentioning

confidence: 99%

Section: Anakoinosis Induces Changes In the Flux Of Informationmentioning

confidence: 99%

Anakoinosis: Correcting Aberrant Homeostasis of Cancer Tissue—Going Beyond Apoptosis Induction

et al. 2019

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“…Interestingly, methylation of DNMT1 by LSD1 stabilizes DNMT1, and combination of HMA with LSD1 inhibitors could synergize in inducing global hypomethylation 102 . Combination of HMA with myeloid differentiating agents such as vitamin D or vitamin A derivatives including RAR and RXR agonists has also been investigated [104][105][106] , again without clinical evidence for strong synergism.…”

Section: Accepted Manuscriptmentioning

confidence: 98%

New therapeutic approaches in myelodysplastic syndromes: Hypomethylating agents and lenalidomide

Loiseau¹,

Ali²,

Itzykson³

2015

Experimental Hematology

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“…Obatoclax (a novel inhibitor of anti-apoptotic Bcl-2 family proteins and a pan-Bcl-2 inhibitor) enhances cytarabineinduced apoptosis by enhancing DNA damage or double strand breaks and improves outcome in AML patients harboring Bcl-2 proteins [228]. In a small cohort of elderly AML patients with primary chemorefractory disease, a combination of low-dose azacytidine, ATRA and pioglitazone (peroxisome proliferator-activated receptor γ ligand) has induced CRs, thus bimodulatory therapy may bypass genetically based chemotherapy resistance in AML [229].…”

Section: Obatoclaxmentioning

confidence: 99%

Update on Non-M3 Acute Myeloid Leukemia — Etiology, Classification, Risk Stratification, Emergencies, Complications, Disease in Special Circumstances and Current and Future Therapeutics

Al-Anazi¹

2015

Leukemias - Updates and New Insights

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Acute myeloid leukemia (AML) is a heterogeneous condition characterized by clonal proliferation of myeloid precursors and accumulation of leukemic blasts in the bone marrow (BM), ultimately resulting in failure of the BM. It accounts for approximately 80% of cases of acute leukemia in adults. AML has several life-threatening complications. After establishing the diagnosis of AML, classifying the disease into the appropriate subtype, stratifying the risk group and determining fitness of the patient for chemotherapy, induction treatment is usually commenced. For elderly individuals and those unfit for chemotherapy, several alternative therapeutic options are available. After achieving complete remission of the disease, the patient will either receive consolidation therapy or will be subjected to hematopoietic stem cell transplantation (HSCT). Autologous and allogeneic forms of HSCT have their own indications, inclusion as well as exclusion criteria. The recent advancements in the diagnostics and therapeutics have facilitated the introduction of personalized therapy in patients with AML. There are several targeted therapies for AML and their clinical use is increasing with time. Evaluation of minimal residual disease and determination of drug resistance are vital tools to improve the outcome of AML therapy.

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Biomodulatory therapy induces complete molecular remission in chemorefractory acute myeloid leukemia

Cited by 32 publications

References 15 publications

Anakoinosis: Correcting Aberrant Homeostasis of Cancer Tissue—Going Beyond Apoptosis Induction

Anakoinosis: Correcting Aberrant Homeostasis of Cancer Tissue—Going Beyond Apoptosis Induction

New therapeutic approaches in myelodysplastic syndromes: Hypomethylating agents and lenalidomide

Update on Non-M3 Acute Myeloid Leukemia — Etiology, Classification, Risk Stratification, Emergencies, Complications, Disease in Special Circumstances and Current and Future Therapeutics

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