1.Chronic neutrophilic leukemia.
Ui Soon PARK ; Sung Hyun PARK ; Myung Ju AHN ; Woong Soo LEE
Korean Journal of Medicine 2003;64(4):482-483
No abstract available.
Leukemia, Neutrophilic, Chronic*
2.A case of chronic neutrophilic leukemia.
Hee Sun JEON ; Hyoun Tae KIM ; Ae Ja PARK ; Hyoun Dae KIM ; Young Soon LEE ; Yong Sung KIM ; Sang Jae LEE ; Soon Hyun SHINN
Korean Journal of Hematology 1992;27(2):369-375
No abstract available.
Leukemia, Neutrophilic, Chronic*
3.Splenic rupture in primary amyloidosis with chronic neutrophilic leukemia.
Blood Research 2015;50(1):5-5
No abstract available.
Amyloidosis*
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Leukemia, Neutrophilic, Chronic*
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Splenic Rupture*
4.A Case of Acute Myeloid Leukemia Transformed from JAK2 V617F-Positive Chronic Neutrophilic Leukemia.
Jae Hee LEE ; Jung Sook HA ; Nam Hee RYOO ; Dong Seok JEON ; Jae Ryong KIM
Laboratory Medicine Online 2012;2(2):101-104
Chronic neutrophilic leukemia (CNL) is a rare myeloproliferative neoplasm (MPN) characterized by persistent peripheral blood neutorphilia, bone marrow hypercellularity of neutrophilic granulocyte proliferation and hepatosplenomegaly. Acquired somatic mutation, JAK2 V617F, is the only molecular marker known to have association with classic BCR-ABL1 negative MPNs. However, JAK2 V617F has been detected occasionally in other MPNs such as CNL or other disease entities. We experienced a case of CNL with JAK2 V617F mutation. The patient was diagnosed according to the 2008 WHO classification criteria, and developed AML 9 months after the diagnosis of CNL. The JAK2 V617F was detected in the bone marrow throughout the clinical course. More cases are needed to establish the role of JAK2 V617F in the pathogenesis, prognosis and disease course of CNL.
Bone Marrow
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Granulocytes
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Humans
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Leukemia, Myeloid, Acute
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Leukemia, Neutrophilic, Chronic
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Neutrophils
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Prognosis
5.Leukemia Cutis in Chronic Neutrophilic Leukemia Associated with Colony Stimulating Factor 3 Receptor Mutation: Clinical Severity Paralleled with Hematologic Abnormality
Osung KWON ; Joonsoo PARK ; Hyun CHUNG ; Kyung Duck PARK
Annals of Dermatology 2019;31(6):673-677
Cutaneous lesions of leukemia cutis (LC) by chronic neutrophilic leukemia (CNL) have been merely reported due to the rare occurrences of CNL. Furthermore cutaneous lesions in relation to clinical severity have been far less studied. A 70-year-old man presented with multiple violaceous papules and excoriations on both lower extremities. The diagnosis was LC based on histologic and laboratory evaluation and the origin was elaborated as CNL with the confirmation of colony stimulating factor 3 receptor (CSF3R) mutation. Interestingly, the patient presented clinical severity in a parallel manner to the hematologic abnormality. To the best of our knowledge, there has been no reported case of CSF3R confirmed LC in CNL featuring explicit skin eruption in relation to laboratory findings.
Aged
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Colony-Stimulating Factors
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Diagnosis
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Humans
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Leukemia
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Leukemia, Neutrophilic, Chronic
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Lower Extremity
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Skin
6.A Case of Transition of Polycythemia Vera to Chronic Neutrophilic Leukemia.
Seung Soon LEE ; Joon Ho MOON ; Jun Wook HA ; Young Kyung LEE ; Jin Seok AHN ; Dae Young ZANG ; Hyo Jung KIM
The Korean Journal of Internal Medicine 2004;19(4):285-288
Chronic Neutrophilic Leukemia (CNL) is a rare myeloproliferative disorder characterized by a persistent increase of mature peripheral neutrophils, myeloid hyperplasia in bone marrow, hepatosplenomegaly, elevated neutrophil alkaline phosphatase (NAP) and absence of Philadelphia chromosome, with no evidence of infection or malignancy sufficient to mimic a leukemoid reaction. CNL has been associated with multiple myelomas in many reported cases, but transition of Polycythemia Vera (PV) to CNL is very rare. An 81-year-old female patient, who had undergone intermittent phlebotomy following the diagnosis of PV 8 years previously, was admitted to our hospital due to lower back pain. A physical examination showed a splenomegaly 2cm below the costal margin, with tenderness of the thoracic and lumbar spine area. A peripheral blood examination showed a WBC count of 91, 800/micro L (neutrophil 88%) with a rare immature form, hemoglobin of 9.1 g/dL and a platelet count of 1, 661, 000/micro L. Her NAP score was 58. The bone marrow examination showed 95% cellularity, with an M: E ratio of 10: 1, increased megakaryocytes with normal morphology and the absence of myelofibrosis. Chromosomal studies showed no Philadelphia chromosome. A radiological examination showed compression fractures of the vertebrae and spinal cord compression. No underlying disease causing a leukemoid reaction was detected. With iron replacement, the hemoglobin level failed to increase over 12 g/dL. Therefore, it was concluded to be a transition of PV to CNL. After administration of hydroxyurea and vertebroplasty, the symptom improved and the WBC count was sustained below 40, 000/micro L.
Aged
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Aged, 80 and over
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Female
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Humans
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Leukemia, Neutrophilic, Chronic/*etiology
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Polycythemia Vera/*complications
8.A case of chronic neutrophilic leukemia.
Sun Chang HONG ; Ji Hoon KIM ; Jung Min LEE ; Jun Oh CHUNG ; Yun Kwon KIM ; So Yon KIM ; Gyeong In LEE
Korean Journal of Medicine 2006;71(3):328-332
Chronic neutrophilic leukemia (CNL) is a rare myeloproliferative disorder characterized by clonal proliferation of mature neutrophils, hepatosplenomegaly, elevated leukocyte alkaline phosphatase score (ALP score) and a negative Philadelphia chromosome. To date, approximately 150 cases have been reported in the literature, including some cases presenting with a 'leukemic' state reflected by a neutrophilic reaction. The term 'true' CNL, recently introduced by Reilly, highlights the need for more experience with CNL cases to improve the diagnostic criteria. In Korea, about 10 cases have been reported in the literature and some of those cases did not meet the WHO diagnostic criteria for CNL. We present a typical case of CNL in a 66-year-old man who complained of general weakness and weight loss. On admission, the white blood cell count from the peripheral blood was 175,600/L with 80% segmented neutrophils. The cytogenic study was negative for the Philadelphia chromosome and had a normal karyotype.
Aged
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Alkaline Phosphatase
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Humans
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Karyotype
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Korea
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Leukemia, Neutrophilic, Chronic*
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Leukocyte Count
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Leukocytes
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Myeloproliferative Disorders
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Neutrophils
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Philadelphia Chromosome
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Weight Loss
9.Current strategies in the diagnosis and management of chronic neutrophilic leukemia.
Altangerel OTGONBAT ; Mingfeng ZHAO
Chinese Medical Journal 2014;127(24):4258-4262
OBJECTIVETo review the implications for diagnosis, pathogenesis and potential for new therapeutic option for chronic neutrophilic leukemia (CNL).
DATA SOURCESData cited in this review were obtained mainly from PubMed and Medline from 1993 to 2013 and highly regarded older publications were also included. The terms "chronic neutrophilic leukemia" and "diagnosis" were used for the literature search.
STUDY SELECTIONWe identified, retrieved and reviewed the information on the clinical and laboratory features, the new genetic findings, prognosis and disease evolution and management of CNL.
RESULTSThe discovery of high-frequency granulocyte-colony stimulating factor receptor (CSF3R) mutations in CNL identifies a new major diagnostic criterion, and lends more specificity to the World Health Organization (WHO) diagnostic criteria for CNL, which are variably applied in routine clinical practice.
CONCLUSIONSIn patients for whom the cause of neutrophilia is not easily discerned, the incorporation of CSF3R mutation testing can be a useful point-of-care diagnostic to evaluate the presence of a clonal myeloid disorder, as well as providing the potential for genetically informed therapy. The oncogenic CSF3R mutations are molecular markers of sensitivity to inhibitors of the SRC family-TNK2 and JAK kinases and may provide a new avenue for therapy.
Carrier Proteins ; genetics ; Female ; Humans ; Leukemia, Neutrophilic, Chronic ; diagnosis ; genetics ; Male ; Mutation ; Nuclear Proteins ; genetics ; Receptors, Colony-Stimulating Factor ; genetics
10.CSF3R, ASXL1,SETBP1, JAK2 V617F and CALR mutations in chronic neutrophilic leukemia.
Yajuan CUI ; Bing LI ; Qian JIANG ; Zefeng XU ; Tiejun QIN ; Peihong ZHANG ; Yue ZHANG ; Zhijian XIAO
Chinese Journal of Hematology 2014;35(12):1069-1073
OBJECTIVETo observe the CSF3R, ASXL1, SETBP1, JAK2 V617F and CALR mutations in patients with chronic neutrophilic leukemia (CNL).
METHODSTwelve suspected "CNL" patients were retrospectively reviewed according the WHO criteria (2008). CSF3R,ASXL1,SETBP1 and CALR mutations were sequenced, and JAK2 V617F was tested by allele specific (AS)-PCR.
RESULTS6 of 12 cases were diagnosed as CML, and all of the 6 carried. 4 of 6 patients also had ASXL1 and SETBP1 mutations and one had a CALR mutation (c.1154-1155insTTGTC). Two patients with monoclonal gammopathy with uncertain significance (MGUS) combined with CNL-like symptoms had no CSF3R, ASXL1, SETBP1, JAK2 V617F or CALR mutation. The same results were also seen in other 4 cases with secondary neutrophilic leukocytosis.
CONCLUSIONCSF3R, ASXL1 and SETBP1 mutations differential diagnosis of CNL, and should be included in the diagnostic protocol so as to improve diagnostic accuracy for CNL.
Carrier Proteins ; Humans ; Janus Kinase 2 ; Leukemia, Neutrophilic, Chronic ; Mutation ; Nuclear Proteins ; Polymerase Chain Reaction ; Receptors, Colony-Stimulating Factor ; Repressor Proteins ; Retrospective Studies