The level of donor chimerism in her bone marrow was 47.9%. induction chemotherapy and subsequently achieved complete remission with the D-CLAG regimen. No severe hematological or extramedullary toxicity was observed. Subsequently, the patient received a second D-CLAG regimen as a Kenpaullone bridge therapy and directly underwent haploidentical related HSCT. Following HSCT, the marrow showed complete hematologic and cytogenetic remission. Currently, 1 year after transplantation, the patients general condition remains good. Conclusions This case suggests that the D-CLAG regimen can be an option for reinduction in relapsed refractory AML patients as a bridge to transplantation. Nevertheless, further research will be required in the future as this report explains only a single case. strong class=”kwd-title” Keywords: D-CLAG, Relapse, Acute myeloid leukemia, Bridge chemotherapy, Second transplantation Background Based on previous studies, 30C37% of patients with acute Kenpaullone myeloid leukemia (AML) relapse after transplantation within 5?years [1, 2]. Of the AML patients who relapse after transplantation, only 10C32% achieve new remission [2, 3]. Therefore, these patients face a very poor prognosis with a 2-12 months survival rate of 14% [2, 4]. The optimal treatment for relapse of acute leukemia after hematopoietic stem cell transplantation (HSCT) remains unclear. Usually, the treatment options for these patients are limited. The cladribine, cytarabine, and granulocyte-stimulating factor (CLAG) regimen has been used for the treatment of relapsed/refractory AML either alone or followed by HSCT, resulting in a complete remission (CR) rate of 49C62% [5, 6]. The key chemotherapy drug in the CLAG regimen is usually cladribine, which is an adenosine deaminase-resistant analog of adenosine that induces apoptosis in myeloid cells primarily by interfering with DNA synthesis . In addition, cladribine may modulate the bioactivation of cytarabine. Interestingly, mononuclear leukemia cells appear to be more sensitive than other leukemia cells to deoxyadenosine analogs because these analogs induce the differentiation of myelomonocytic leukemia cells . However, the CR rate declines in patients who relapse after HSCT . Therefore, adjusting the CLAG regimen is urgent for obtaining a higher CR rate and improving efficacy. Here, we combined another chemotherapy with CLAG to strengthen its antileukemia activity in an AML patient who relapsed after the first HSCT. Increasing evidence emphasizes the importance of epigenetic modifications in the pathogenesis of acute leukemia. In contrast to DNA mutations, epigenetic changes, such as methylation or acetylation, can be reversed pharmacologically . The purine analog decitabine acts primarily by inhibiting DNA methyltransferase and improving epigenetic deterioration. Furthermore, decitabine can sensitize AML cells to conventional chemotherapeutics, such as cytarabine and daunorubicin . Several studies have found that decitabine is especially beneficial Rabbit polyclonal to Hsp90 in AML patients with complex karyotypes . Therefore, some researchers have indicated that decitabine is usually a well-tolerated treatment for patients with relapsed/refractory AML, even in cases with increased age and merged burden. Although consensus regarding the optimal donor for a second transplantation is lacking, a previous study performed at our center indicated that this graft-versus-leukemia effect in high-risk leukemia patients is superior when haploidentical related donors are used compared with that when matched sibling donors Kenpaullone or unrelated matched donors are used . Based on the above information, we designed a salvage regimen for an AML-M5 patient who relapsed after her first transplantation. Decitabine followed by CLAG was used as the bridge chemotherapy. After CR, the same chemotherapy was used again prior to haploidentical HSCT. We attempted to perform the transplantation Kenpaullone under a low tumor load and achieved success. Case presentation A 38-year-old Chinese female was first admitted to our hospital in December 2011 due to a complaint of constipation for 1 month. Her diet and lifestyle were normal. She had no history of serious illness or family genetic diseases. During the physical examination, no abnormalities were identified. The peripheral blood counts revealed a white cell count of 1 1.3??109/L, a hemoglobin level of 93?g/L, and a platelet count of 94??109/L. The blood chemistry findings showed normal lactate dehydrogenase, C-reactive protein, and albumin levels. Her bone marrow was hypercellular, exhibited infiltration and included 91.5% blast cells comprising primitive monocytes and naive monocytes. The immunophenotype analysis showed that 54% of the cells were abnormal, and positive labeling for CD34, CD10, and CD71 and unfavorable labeling for CD19 were observed. The overall findings were consistent with acute monocytic leukemia. G-banding revealed 45, XX, ??2, der(11)(p15) /46,XX/92,XXXX . The genetic tests, including screens for FLT3, IDH1/2 and tp53 mutants, were all negative. The patient was diagnosed with high-risk acute monocytic leukemia. The patient did not respond to idarubicin and cytarabine (IA) or subsequent aclacinomycin, cytarabine, and etoposide (AAE). Then, the patient achieved CR following one additional AAE regimen as previously described. Furthermore, she received aclacinomycin and cytarabine (AA) twice, mitoxantrone and cytarabine (MA) once, and intermediate-dose cytarabine.