scholarly journals Pseudo-Chediak-Higashi anomaly in a case of acute myeloid leukemia: electron microscopic studies

Blood ◽  
1979 ◽  
Vol 54 (4) ◽  
pp. 863-871 ◽  
Author(s):  
M Tulliez ◽  
JP Vernant ◽  
J Breton-Gorius ◽  
M Imbert ◽  
C Sultan
Keyword(s):  
Electron Microscopy ◽  
Lymph Nodes ◽  
Acute Promyelocytic Leukemia ◽  
Myeloid Leukemia ◽  
Promyelocytic Leukemia ◽  
Myelogenous Leukemia ◽  
Electron Microscopic ◽  
Microscopic Studies ◽  
Acute Myelogenous ◽  
Chediak Higashi Syndrome

Abstract The formation and fine structure of giant granules in neutrophil promyelocytes of a patient with a variant of acute myelogenous leukemia were investigated by electron microscopy. The patient presented with large lymph nodes and disseminated intravascular coagulation (DIC). By light microscopy, numerous giant granules, resembling those of Chediak- Higashi syndrome (CHS), were present, but Auer bodies could not be found. By electron microscopy, these giant granules were seen to be formed by fusion of azurophilic granules, as in CHS; however, they were different from the large granules of CHS, since they contained numerous microcrystalline structures like those of Auer bodies. However, the crystalline cores of these granules exhibited a periodicity different from that of Auer bodies of acute promyelocytic leukemia. This clinical and hematologic syndrome (giant granules, enlarged lymph nodes, and DIC may represent a variant of acute promyelocytic leukemia.

scholarly journals Pseudo-Chediak-Higashi anomaly in a case of acute myeloid leukemia: electron microscopic studies

Blood ◽  
1979 ◽  
Vol 54 (4) ◽  
pp. 863-871
Author(s):  
M Tulliez ◽  
JP Vernant ◽  
J Breton-Gorius ◽  
M Imbert ◽  
C Sultan
Keyword(s):  
Electron Microscopy ◽  
Lymph Nodes ◽  
Acute Promyelocytic Leukemia ◽  
Myeloid Leukemia ◽  
Promyelocytic Leukemia ◽  
Myelogenous Leukemia ◽  
Electron Microscopic ◽  
Microscopic Studies ◽  
Acute Myelogenous ◽  
Chediak Higashi Syndrome

The formation and fine structure of giant granules in neutrophil promyelocytes of a patient with a variant of acute myelogenous leukemia were investigated by electron microscopy. The patient presented with large lymph nodes and disseminated intravascular coagulation (DIC). By light microscopy, numerous giant granules, resembling those of Chediak- Higashi syndrome (CHS), were present, but Auer bodies could not be found. By electron microscopy, these giant granules were seen to be formed by fusion of azurophilic granules, as in CHS; however, they were different from the large granules of CHS, since they contained numerous microcrystalline structures like those of Auer bodies. However, the crystalline cores of these granules exhibited a periodicity different from that of Auer bodies of acute promyelocytic leukemia. This clinical and hematologic syndrome (giant granules, enlarged lymph nodes, and DIC may represent a variant of acute promyelocytic leukemia.

scholarly journals Accelerated myeloblast destruction and abnormal lysosome disruption in cultured bone marrow: association with indolent acute myelogenous leukemia

Blood ◽  
1976 ◽  
Vol 48 (1) ◽  
pp. 23-32 ◽  
Author(s):  
RF Branda ◽  
HS Jacob ◽  
SD Douglas ◽  
CF Moldow ◽  
RR Puumala
Keyword(s):  
Bone Marrow ◽  
Acute Myelogenous Leukemia ◽  
Myelogenous Leukemia ◽  
Leukemic Cells ◽  
Electron Microscopic ◽  
Granule Formation ◽  
Microscopic Studies ◽  
Acute Myelogenous ◽  
Primary Granules

Abstract Despite no chemotherapy and a marrow morphologically typical of frank relapse, an acute myelogenous leukemia (AML) patient survived for nearly 1 yr. During this time she remained asymptomatic and maintained nearly normal levels of platelets and hemoglobin. Cytochemical and electron microscopic studies of her bone marrow in liquid culture revealed on several occasions a unique maturational sequence in that leukemic cells differentiated to form morphologically abnormal primary granules which appeared to rupture and cause cytolysis of these cells. In these cultures, blasts rapidly disappeared and were replaced by more mature granulocytes, in contrast to observations in cultures derived from five other patients with AML in relapse which showed persistently elevated blast counts with no evidence of maturation in vitro. These findings support the concept that in AML cell maturation is regularly impaired and in some cases also aberrant. In addition, the abnormal granule formation with autolysis of the leukemic cells observed in one patient may explain both the early cell death in vitro and this patient's relatively indolent clinical course. Similar in vitro studies may help predict atypical clinical courses in patients with AML and facilitate design of appropriate chemotherapy.

Establishment of baseline toxicity expectations with standard frontline chemotherapy in acute myelogenous leukemia

Blood ◽  
2007 ◽  
Vol 110 (10) ◽  
pp. 3547-3551 ◽  
Author(s):  
Ehab Atallah ◽  
Jorge Cortes ◽  
Susan O'Brien ◽  
Sherry Pierce ◽  
Mary Beth Rios ◽  
...  
Keyword(s):  
Adverse Events ◽  
Myeloid Leukemia ◽  
Febrile Episode ◽  
Promyelocytic Leukemia ◽  
Myelogenous Leukemia ◽  
Control Group ◽  
Intensive Chemotherapy ◽  
Serious Adverse Events ◽  
Acute Myelogenous ◽  
Grade 3

Abstract The rates of expected serious adverse events in patients with acute leukemia on chemotherapy far exceed those in patients with solid tumors. Regulatory authorities require similar reporting criteria, which overburden the investigators and infrastructure with unnecessary documentation. To establish a baseline for expected toxicities before and during leukemia therapy, we reviewed 1534 adults with acute myeloid leukemia (AML; excluding acute promyelocytic leukemia) from 1990 to 2006 who received frontline intensive chemotherapy; 723 (47%) were 60 years or older. Prior to therapy, grade 3/4 cytopenias were observed in 86% of patients. All patients developed one or more grade 3/4 cytopenias during therapy, and more than 90% had a febrile episode. Admission to the intensive care unit, mechanical ventilation, and dialysis were required in 28%, 16%, and 7%, respectively. Mortality during induction, 2-week mortality, and 6-week mortality were 20%, 5%, and 16%, respectively. Grade 3/4 renal or hepatic toxicities were observed in 3% and 22% of patients, respectively. Other grade 3 or 4 toxicities were also common before treatment and during therapy. This paper establishes a baseline toxicity rate for patients with AML during induction therapy, and this could be used as a control group for future reference. Guidelines for reporting adverse events in leukemia studies should be revisited.

scholarly journals Accelerated myeloblast destruction and abnormal lysosome disruption in cultured bone marrow: association with indolent acute myelogenous leukemia

Blood ◽  
1976 ◽  
Vol 48 (1) ◽  
pp. 23-32
Author(s):  
RF Branda ◽  
HS Jacob ◽  
SD Douglas ◽  
CF Moldow ◽  
RR Puumala
Keyword(s):  
Bone Marrow ◽  
Acute Myelogenous Leukemia ◽  
Myelogenous Leukemia ◽  
Leukemic Cells ◽  
Electron Microscopic ◽  
Granule Formation ◽  
Microscopic Studies ◽  
Acute Myelogenous ◽  
Primary Granules

Despite no chemotherapy and a marrow morphologically typical of frank relapse, an acute myelogenous leukemia (AML) patient survived for nearly 1 yr. During this time she remained asymptomatic and maintained nearly normal levels of platelets and hemoglobin. Cytochemical and electron microscopic studies of her bone marrow in liquid culture revealed on several occasions a unique maturational sequence in that leukemic cells differentiated to form morphologically abnormal primary granules which appeared to rupture and cause cytolysis of these cells. In these cultures, blasts rapidly disappeared and were replaced by more mature granulocytes, in contrast to observations in cultures derived from five other patients with AML in relapse which showed persistently elevated blast counts with no evidence of maturation in vitro. These findings support the concept that in AML cell maturation is regularly impaired and in some cases also aberrant. In addition, the abnormal granule formation with autolysis of the leukemic cells observed in one patient may explain both the early cell death in vitro and this patient's relatively indolent clinical course. Similar in vitro studies may help predict atypical clinical courses in patients with AML and facilitate design of appropriate chemotherapy.

Therapy-related myelodysplastic syndrome–acute myelogenous leukemia in patients treated for acute promyelocytic leukemia: an emerging problem

Blood ◽  
2002 ◽  
Vol 99 (3) ◽  
pp. 822-824 ◽  
Author(s):  
Roberto Latagliata ◽  
Maria Concetta Petti ◽  
Susanna Fenu ◽  
Marco Mancini ◽  
Maria Antonietta Aloe Spiriti ◽  
...  
Keyword(s):  
Acute Promyelocytic Leukemia ◽  
Acute Myelogenous Leukemia ◽  
Residual Disease ◽  
Prognostic Score ◽  
Allogeneic Bone Marrow Transplantation ◽  
Survival Rates ◽  
Promyelocytic Leukemia ◽  
Myelogenous Leukemia ◽  
Allogeneic Bone ◽  
Acute Myelogenous

Abstract The use of all-trans retinoic acid (ATRA) in combination with chemotherapy has markedly improved the prognosis for patients with acute promyelocytic leukemia (APL); the higher complete remission (CR) and survival rates now reported in this disease almost approach those obtained for other highly curable hematologic malignancies. Of 77 patients with APL who were consecutively treated at a single institution and who achieved CR after induction and consolidation therapy, 5 (6.5%) acquired therapy-related myelodysplasia (tMDS), acute myelogenous leukemia (AML), or both (tMDS–AML). Of these, 3 of 46 (6.5%) patients received front-line chemotherapy with or without ATRA and acquired tMDS–AML while in first remission of APL. Two underwent repeated chemotherapy cycles with ATRA because of APL relapse and acquired tMDS–AML while in the second or third remission of APL. In 2 patients, clinical and biologic characteristics of tMDS–AML were as expected for postalkylating forms (long latency, MDS phase preceding AML, karyotypic aberrations involving chromosomes 5 or 7), even though one of them had not previously received alkylating drugs. Three of the 5 patients died shortly after tMDS–AML diagnosis, one is alive with tMDS, and one is alive and in CR after allogeneic bone marrow transplantation. The occurrence of tMDS–AML after successful therapy for APL is an emerging problem. The availability of prognostic score systems at initial diagnosis and monitoring of residual disease by polymerase chain reaction might allow better tailoring of treatment intensity in APL to spare unnecessary toxicity and to minimize the risk for tMDS–AML in patients who are presumably cured.

scholarly journals Specific expression of the annexin VIII gene in acute promyelocytic leukemia

Blood ◽  
1992 ◽  
Vol 79 (7) ◽  
pp. 1802-1810 ◽  
Author(s):  
KS Chang ◽  
G Wang ◽  
EJ Freireich ◽  
M Daly ◽  
SL Naylor ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Acute Promyelocytic Leukemia ◽  
Dna Sequence ◽  
Acute Myelogenous Leukemia ◽  
Lymphoblastic Leukemia ◽  
Fusion Transcript ◽  
Promyelocytic Leukemia ◽  
Myelogenous Leukemia ◽  
Specific Expression ◽  
Acute Myelogenous

Abstract Since the translocation breakpoint t(15;17) (q22;q21) in acute promyelocytic leukemia (APL) occurs within the retinoic acid receptor- alpha (RARA) gene, the expression of many genes normally regulated by RARA may be affected by this translocation. To identify genes that may be aberrantly expressed in APL, a subtraction cDNA library of an APL patient with t(15;17) was constructed. A cDNA, pRD1, specifically expressed in APL was identified. DNA sequence analysis of pRD1 showed that this gene is similar to the DNA sequence of annexin VIII, a gene which encodes a vascular anticoagulant. The annexin VIII gene was assigned to chromosome 10, which indicates that specific expression of this gene in APL is not directly involved in the t(15;17) breakpoint region. We have analyzed the expression of annexin VIII gene in nine t(15;17)-positive APL patients and one APL patient with a chromosome 17q-abnormality. We found that all APL samples expressed high levels of the annexin VIII gene. Expression of the annexin VIII gene in all other leukemias, including acute myelogenous leukemia, chronic myelogenous leukemia, chronic lymphocytic leukemia, and acute lymphoblastic leukemia, was undetectable, except in one patient with acute myelogenous leukemia in which a very low level of expression was detected. Annexin VIII is highly expressed in the APL cell line, NB4. Its expression was significantly reduced after 8 hours of all-trans retinoic acid (ATRA) treatment, whereas the expression of RARA increased several-fold within 4 hours postinduction. Thus, increased expression of RARA preceded the downregulation of annexin VIII after ATRA induction, suggesting an inverse relationship between RARA and annexin VIII expression. Since increased expression of the fusion transcript was seen after ATRA induction and an APL without a t(15;17) translocation expressed high levels of annexin VIII, it appears that increased expression of annexin VIII in APL is not related to the fusion transcript. Therefore, dysregulation of the RARA gene may be related to the overexpression of annexin VIII in APL.

scholarly journals An Electron Microscopic Study of the Bone Marrow of the Rat in an Experimental Myelogenous Leukemia

Blood ◽  
1972 ◽  
Vol 39 (1) ◽  
pp. 99-112 ◽  
Author(s):  
LI-TSUN CHEN ◽  
EVELYN E. HANDLER ◽  
EUGENE S. HANDLER ◽  
LEON WEISS
Keyword(s):  
Electron Microscopy ◽  
Bone Marrow ◽  
Myelogenous Leukemia ◽  
Leukemic Cells ◽  
Intercellular Spaces ◽  
Electron Microscopic ◽  
Sinus Wall ◽  
Acute Myelogenous ◽  
Viruslike Particles ◽  
Rat Bone

Abstract Alterations in the vascular sinus and hematopoietic compartment of rat bone marrow were observed with electron microscopy during the pathogenesis of an acute myelogenous leukemia. As the disease progresses, the sinus wall becomes damaged and disintegrates; normal hemic elements disappear, and the marrow compartment becomes packed with leukemic myeloblasts. Viruslike particles are present in intercellular spaces and appear to bud from leukemic cells.

scholarly journals Fournier’s gangrene as an initial manifestation of acute promyelocytic leukemia: A case report and review of the literature

2019 ◽  
Vol 7 ◽  
pp. 2050313X1983442 ◽  
Author(s):  
Anahita Mostaghim ◽  
Muhammad Dhanani ◽  
Robin R Ingalls
Keyword(s):  
Acute Promyelocytic Leukemia ◽  
Acute Myelogenous Leukemia ◽  
Case Reports ◽  
Fournier’S Gangrene ◽  
Promyelocytic Leukemia ◽  
Myelogenous Leukemia ◽  
Fournier's Gangrene ◽  
Initial Manifestation ◽  
Surgical Services ◽  
Acute Myelogenous

Fournier’s gangrene is classically associated with diabetes mellitus and alcohol use disorder. While it is associated with chemotherapy, there are few case reports of Fournier’s gangrene as the initial presentation of acute myelogenous leukemia. A 38-year-old male presented with progressive scrotal swelling and hematochezia. Blood cell count showed depression of all cell lines without myeloblasts. He received broad-spectrum antibiotics and underwent surgical debridement once. Urgent bone marrow biopsy confirmed acute promyelocytic leukemia. The patient was started on chemotherapy. He was discharged without relapse of the infection. This is the fourth case of acute myelogenous leukemia presenting as Fournier’s gangrene in the literature and the only case to have survived. This brings forth a possible diagnostic consideration in patients without obvious predisposing risk factors for Fournier’s gangrene, particularly in those with pancytopenia. Coordination with surgical services as well as hematology/oncology specialists is imperative to survival of these dual diagnosis patients.

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