BACKGROUND Acute myeloid leukemia(AML)is one of the most common types of leukemia in adults.However,AML is relatively rare in the population overall,accounting for only about 1 percent of all cancers.Treatment for AML...BACKGROUND Acute myeloid leukemia(AML)is one of the most common types of leukemia in adults.However,AML is relatively rare in the population overall,accounting for only about 1 percent of all cancers.Treatment for AML can be very effective for some patients,yet it leaves others with serious and even life-threatening side effects.Chemotherapy is still the primary treatment for most AML,but over time,leukemia cells become resistant to chemotherapy drugs.In addition,stem cell transplantation,targeted therapy,and immunotherapy are currently available.At the same time,with the progression of the disease,the patient may have corresponding complications,such as coagulation dysfunction,anemia,granulocytopenia,and repeated infection,so transfusion supportive therapy will be involved in the overall treatment regime.To date,few articles have reported on blood transfusion treatment options for patients with ABO subtypes AML-M2.Blood transfusion therapy is an important supportive treatment for AML-M2,and accurate determination of patients'blood type is one of the most important steps in the treatment process.In this study,we explored blood typing and supportive treatment strategies for a patient with A2 subtype AML-M2 to provide the basis for treatment for all patients.CASE SUMMARY In order to determine the blood type of the patient,serological and molecular biological methods were used for reference tests,and the genetic background was studied to determine the patient's final blood type and select the appropriate blood products for infusion treatment.According to the results obtained by serological and molecular biological methods,the blood type of the patient was A2 subtype;the genotype was A02/001;the irregular antibody screening was negative,and anti-A1 was found in the plasma.According to the overall treatment plan,active anti-infection,elevated cells,component blood transfusion support,and other rescue and supportive treatments were given,and the patient successfully passed the stage of myelosuppression after chemotherapy.Re-examination of bone marrow smears showed that AL was in complete remission of bone marrow signs,and minimal residual leukemia lesions suggested no cells with obvious abnormal immunophenotype(residual leukemia cells<10-4).CONCLUSION The infusion of patients with A2 subtype AML-M2 with A irradiated platelets and O washing red blood cells can meet the needs of clinical treatment.展开更多
BACKGROUND The Janus kinase 2(JAK2) V617 F mutation is common in patients with breakpoint cluster region-Abelson1(BCR-ABL1)-negative myeloproliferative neoplasms,including polycythemia vera, essential thrombocythemia ...BACKGROUND The Janus kinase 2(JAK2) V617 F mutation is common in patients with breakpoint cluster region-Abelson1(BCR-ABL1)-negative myeloproliferative neoplasms,including polycythemia vera, essential thrombocythemia and primary myelofibrosis, but is rarely detected in BCR-ABL1-positive chronic myeloid leukemia(CML) patients. Here, we report a CML patient with both a BCR-ABL1 rearrangement and JAK2 V617 F mutation.CASE SUMMARY A 45-year-old Chinese woman was admitted to our department with a history of significant thrombocytosis for 20 d. Color Doppler ultrasound examination showed mild splenomegaly. Bone marrow aspiration revealed a karyotype of 46,XX, t(9;22)(q34;q11.2) in 20/20 metaphases by cytogenetic analysis,rearrangement of BCR-ABL1(32.31%) by fluorescent polymerase chain reaction(PCR) and mutation of JAK2 V617 F(10%) by PCR and Sanger DNA sequencing.The patient was diagnosed with CML and JAK2 V617 F mutation. Following treatment with imatinib for 3 mo, the patient had an optimal response and BCRABL1(IS) was 0.143%, while the mutation rate of JAK2 V617 F rose to 15%.CONCLUSION Emphasis should be placed on the detection of JAK2 mutation when CML is diagnosed to distinguish JAK2 mutation-positive CML and formulate treatment strategies.展开更多
Myeloid-derived suppressor cells （MDSCs） play a crucial role in T cell dysfunction, which is related to poor outcome in patients with severe trauma. Cyclooxygenase-2 （Cox-2） contributes to immune disorder in traum...Myeloid-derived suppressor cells （MDSCs） play a crucial role in T cell dysfunction, which is related to poor outcome in patients with severe trauma. Cyclooxygenase-2 （Cox-2） contributes to immune disorder in trauma and infection via production of prostaglandin E2. However, the role of Cox-2 in the accumulation and function of MDSCs after traumatic stress has not been fully elucidated. In the present study, we treated murine trauma model with NS398, a selective Cox-2 inhibitor. Then the percentages of CD1 lb＋/Gr-l＋ cells, proliferation and apoptosis of CD4＋ T cells were determined. Ar- ginase activity and arginase-1 （Arg-1） protein expression of splenic CDllb＋/Gr-I＋ cells, and de- layed-type hypersensitivity （DTH） response were analyzed. The results showed that Cox-2 blockade significantly decreased the percentages of CD1 lb＋/Gr-l＋ cells in the spleen and bone marrow 48 and 72 h after traumatic stress. NS398 inhibited arginase activity and down-regulated the Arg-1 expression of splenic CD1 lb＋/Gr-l＋ ceils. Moreover, NS398 could promote proliferation and inhibit apoptosis of CD4＋ T cells. It also restored DTH response of traumatic mice. Taken together, our data revealed that Cox-2 might play a pivotal role in the accumulation and function of MDSC after traumatic stress.展开更多
Spurred by better understanding of disease biology,improvements in molecular diagnostics,and the development of targeted therapies,the treatment of acute myeloid leukemia(AML)has undergone significant evolution in rec...Spurred by better understanding of disease biology,improvements in molecular diagnostics,and the development of targeted therapies,the treatment of acute myeloid leukemia(AML)has undergone significant evolution in recent years.Arguably,the most exciting shift has come from the success of treatment with the B-cell lymphoma-2 inhibitor venetoclax.When given in combination with a hypomethylating agent or low dose cytarabine,venetoclax demonstrates high response rates,some of which are durable.In spite of this,relapses after venetoclax treatment are common,and much interest exists in elucidating the mechanisms of resistance to the drug.Alterations in leukemic stem cell metabolism have been identified as a possible escape route,and clinical trials focusing on targeting metabolism in AML are ongoing.This review article highlights current research regarding venetoclax treatment and resistance in AML with a focus on cellular metabolism.展开更多
BACKGROUND Acute myeloid leukemia(AML)harboring 11q23 translocations is classified as therapy-related AML in patients who have undergone prior treatment with cytotoxic agents.There have been only a few reports of AML ...BACKGROUND Acute myeloid leukemia(AML)harboring 11q23 translocations is classified as therapy-related AML in patients who have undergone prior treatment with cytotoxic agents.There have been only a few reports of AML that subsequently developed during imatinib mesylate(IM)treatment for gastrointestinal stromal tumors(GISTs).CASE SUMMARY A 63-year-old woman was diagnosed with a hepatic GIST recurrence in April 2012;she was administered IM 400 mg/d.In November 2015,she developed dyspnea with pancytopenia while IM treatment was continued for 42 mo.A chromosome study using a bone marrow sample showed a 46,XX karyotype with t(11;19)(q23;p13.1)in 22 of 26 analyzed metaphase cells.Fluorescence in situ hybridization using the locus-specific indicator(11q23)gene break-apart probe showed positive rearrangement in 82%of interphase cells.Reverse-transcription polymerase chain reactions subsequently confirmed the KMT2A/ELL transcript.She achieved complete response with incomplete neutrophil recovery with two decitabine treatment cycles.After the third cycle of decitabine,the disease relapsed,and she refused further treatment.She died of hemorrhagic stroke 5 mo after diagnosis.To the best of our knowledge,this is the first report of AML with KMT2A gene rearrangements in a patient with a GIST receiving IM treatment.CONCLUSION Physicians should consider the potential risks of developing hematologic malignancies,including therapy-related AML,in patients with GISTs receiving IM treatment.展开更多
文摘BACKGROUND Acute myeloid leukemia(AML)is one of the most common types of leukemia in adults.However,AML is relatively rare in the population overall,accounting for only about 1 percent of all cancers.Treatment for AML can be very effective for some patients,yet it leaves others with serious and even life-threatening side effects.Chemotherapy is still the primary treatment for most AML,but over time,leukemia cells become resistant to chemotherapy drugs.In addition,stem cell transplantation,targeted therapy,and immunotherapy are currently available.At the same time,with the progression of the disease,the patient may have corresponding complications,such as coagulation dysfunction,anemia,granulocytopenia,and repeated infection,so transfusion supportive therapy will be involved in the overall treatment regime.To date,few articles have reported on blood transfusion treatment options for patients with ABO subtypes AML-M2.Blood transfusion therapy is an important supportive treatment for AML-M2,and accurate determination of patients'blood type is one of the most important steps in the treatment process.In this study,we explored blood typing and supportive treatment strategies for a patient with A2 subtype AML-M2 to provide the basis for treatment for all patients.CASE SUMMARY In order to determine the blood type of the patient,serological and molecular biological methods were used for reference tests,and the genetic background was studied to determine the patient's final blood type and select the appropriate blood products for infusion treatment.According to the results obtained by serological and molecular biological methods,the blood type of the patient was A2 subtype;the genotype was A02/001;the irregular antibody screening was negative,and anti-A1 was found in the plasma.According to the overall treatment plan,active anti-infection,elevated cells,component blood transfusion support,and other rescue and supportive treatments were given,and the patient successfully passed the stage of myelosuppression after chemotherapy.Re-examination of bone marrow smears showed that AL was in complete remission of bone marrow signs,and minimal residual leukemia lesions suggested no cells with obvious abnormal immunophenotype(residual leukemia cells<10-4).CONCLUSION The infusion of patients with A2 subtype AML-M2 with A irradiated platelets and O washing red blood cells can meet the needs of clinical treatment.
文摘BACKGROUND The Janus kinase 2(JAK2) V617 F mutation is common in patients with breakpoint cluster region-Abelson1(BCR-ABL1)-negative myeloproliferative neoplasms,including polycythemia vera, essential thrombocythemia and primary myelofibrosis, but is rarely detected in BCR-ABL1-positive chronic myeloid leukemia(CML) patients. Here, we report a CML patient with both a BCR-ABL1 rearrangement and JAK2 V617 F mutation.CASE SUMMARY A 45-year-old Chinese woman was admitted to our department with a history of significant thrombocytosis for 20 d. Color Doppler ultrasound examination showed mild splenomegaly. Bone marrow aspiration revealed a karyotype of 46,XX, t(9;22)(q34;q11.2) in 20/20 metaphases by cytogenetic analysis,rearrangement of BCR-ABL1(32.31%) by fluorescent polymerase chain reaction(PCR) and mutation of JAK2 V617 F(10%) by PCR and Sanger DNA sequencing.The patient was diagnosed with CML and JAK2 V617 F mutation. Following treatment with imatinib for 3 mo, the patient had an optimal response and BCRABL1(IS) was 0.143%, while the mutation rate of JAK2 V617 F rose to 15%.CONCLUSION Emphasis should be placed on the detection of JAK2 mutation when CML is diagnosed to distinguish JAK2 mutation-positive CML and formulate treatment strategies.
基金supported by grants from the Foundation of Science and Technology of Wuhan City(No.201161038339)Health Department of Hubei Province of China(No.QJX2010-4)+1 种基金Natural Science Foundation of Hubei Province of China(No.2011CDB205)National"Twelfth Five-Year"Plan for Science&Technology Support(No.2012BAI11B00)
文摘Myeloid-derived suppressor cells （MDSCs） play a crucial role in T cell dysfunction, which is related to poor outcome in patients with severe trauma. Cyclooxygenase-2 （Cox-2） contributes to immune disorder in trauma and infection via production of prostaglandin E2. However, the role of Cox-2 in the accumulation and function of MDSCs after traumatic stress has not been fully elucidated. In the present study, we treated murine trauma model with NS398, a selective Cox-2 inhibitor. Then the percentages of CD1 lb＋/Gr-l＋ cells, proliferation and apoptosis of CD4＋ T cells were determined. Ar- ginase activity and arginase-1 （Arg-1） protein expression of splenic CDllb＋/Gr-I＋ cells, and de- layed-type hypersensitivity （DTH） response were analyzed. The results showed that Cox-2 blockade significantly decreased the percentages of CD1 lb＋/Gr-l＋ cells in the spleen and bone marrow 48 and 72 h after traumatic stress. NS398 inhibited arginase activity and down-regulated the Arg-1 expression of splenic CD1 lb＋/Gr-l＋ ceils. Moreover, NS398 could promote proliferation and inhibit apoptosis of CD4＋ T cells. It also restored DTH response of traumatic mice. Taken together, our data revealed that Cox-2 might play a pivotal role in the accumulation and function of MDSC after traumatic stress.
文摘Spurred by better understanding of disease biology,improvements in molecular diagnostics,and the development of targeted therapies,the treatment of acute myeloid leukemia(AML)has undergone significant evolution in recent years.Arguably,the most exciting shift has come from the success of treatment with the B-cell lymphoma-2 inhibitor venetoclax.When given in combination with a hypomethylating agent or low dose cytarabine,venetoclax demonstrates high response rates,some of which are durable.In spite of this,relapses after venetoclax treatment are common,and much interest exists in elucidating the mechanisms of resistance to the drug.Alterations in leukemic stem cell metabolism have been identified as a possible escape route,and clinical trials focusing on targeting metabolism in AML are ongoing.This review article highlights current research regarding venetoclax treatment and resistance in AML with a focus on cellular metabolism.
文摘BACKGROUND Acute myeloid leukemia(AML)harboring 11q23 translocations is classified as therapy-related AML in patients who have undergone prior treatment with cytotoxic agents.There have been only a few reports of AML that subsequently developed during imatinib mesylate(IM)treatment for gastrointestinal stromal tumors(GISTs).CASE SUMMARY A 63-year-old woman was diagnosed with a hepatic GIST recurrence in April 2012;she was administered IM 400 mg/d.In November 2015,she developed dyspnea with pancytopenia while IM treatment was continued for 42 mo.A chromosome study using a bone marrow sample showed a 46,XX karyotype with t(11;19)(q23;p13.1)in 22 of 26 analyzed metaphase cells.Fluorescence in situ hybridization using the locus-specific indicator(11q23)gene break-apart probe showed positive rearrangement in 82%of interphase cells.Reverse-transcription polymerase chain reactions subsequently confirmed the KMT2A/ELL transcript.She achieved complete response with incomplete neutrophil recovery with two decitabine treatment cycles.After the third cycle of decitabine,the disease relapsed,and she refused further treatment.She died of hemorrhagic stroke 5 mo after diagnosis.To the best of our knowledge,this is the first report of AML with KMT2A gene rearrangements in a patient with a GIST receiving IM treatment.CONCLUSION Physicians should consider the potential risks of developing hematologic malignancies,including therapy-related AML,in patients with GISTs receiving IM treatment.
