Myeloid/lymphoid neoplasms associated with eosinophilia and PCM1-JAK2 is a provisional entity in WHO 2016. Prior case reports have shown quite a few clinical presentations in different patients with this chromosome translocation,characterized by eosinophilia in combination with myelodysplastic/ myeloproliferative neoplasms, acute myeloid leukemia(AML) and rarely,
Critical Role of PET-Scan in Unravelling the Dual Pathology- Review of Litera...AnonIshanvi
Simultaneous presentation of two lymphatic haematological malignancies is extremely rare. Adequate and optimal diagnostic steps including various imaging techniques and histopathological biopsies are required unpin the exact diagnoses to be able to deliver the best management strategies
Critical Role of PET-Scan in Unravelling the Dual Pathology- Review of Litera...daranisaha
Simultaneous presentation of two lymphatic haematological malignancies is extremely rare. Adequate and optimal diagnostic steps including various imaging techniques and histopathological biopsies are required unpin the exact diagnoses to be able to deliver the best management strategies...
Critical Role of PET-Scan in Unravelling the Dual Pathology- Review of Litera...JohnJulie1
Simultaneous presentation of two lymphatic haematological malignancies is extremely rare. Adequate and optimal diagnostic steps including various imaging techniques and histopathological biopsies are required unpin the exact diagnoses to be able to deliver the best management strategies...
Critical Role of PET-Scan in Unravelling the Dual Pathology- Review of Litera...NainaAnon
Simultaneous presentation of two lymphatic haematological malignancies is extremely rare. Adequate and optimal diagnostic steps including various imaging techniques and histopathological biopsies are required unpin the exact diagnoses to be able to deliver the best management strategies...
The simultaneous occurrence of two lymphatic malignancies in
one patient is extremely rare with an incidence rate of 1.4–6.5
cases/1,000,000 individuals [8]. Co-existence of MM and other
lymphoid malignancies like Chronic Lymphocytic Leukemia (CLL)
[9], MM and Hodgkin’s Disease (HD) [10], MM and Lympho
Plasmacytic Lymphoma (LPL) [11] has been reported. However,
there are less than 5 reported cases in PubMed of simultaneous
presentation of DLBCL and MM
Critical Role of PET-Scan in Unravelling the Dual Pathology- Review of Litera...EditorSara
Simultaneous presentation of two lymphatic haematological malignancies is extremely rare. Adequate and optimal diagnostic steps including various imaging techniques and histopathological biopsies are required unpin the exact diagnoses to be able to deliver the best management strategies...
Critical Role of PET-Scan in Unravelling the Dual Pathology- Review of Litera...semualkaira
Simultaneous presentation of two lymphatic haematological malignancies is extremely rare. Adequate and optimal diagnostic steps including various imaging techniques and histopathological biopsies are required unpin the exact diagnoses to be able to deliver the best management strategies...
Critical Role of PET-Scan in Unravelling the Dual Pathology- Review of Litera...semualkaira
Simultaneous presentation of two lymphatic haematological malignancies is extremely rare. Adequate and optimal diagnostic steps including various imaging techniques and histopathological biopsies are required unpin the exact diagnoses to be able to deliver the best management strategies...
Critical Role of PET-Scan in Unravelling the Dual Pathology- Review of Litera...AnonIshanvi
Simultaneous presentation of two lymphatic haematological malignancies is extremely rare. Adequate and optimal diagnostic steps including various imaging techniques and histopathological biopsies are required unpin the exact diagnoses to be able to deliver the best management strategies
Critical Role of PET-Scan in Unravelling the Dual Pathology- Review of Litera...daranisaha
Simultaneous presentation of two lymphatic haematological malignancies is extremely rare. Adequate and optimal diagnostic steps including various imaging techniques and histopathological biopsies are required unpin the exact diagnoses to be able to deliver the best management strategies...
Critical Role of PET-Scan in Unravelling the Dual Pathology- Review of Litera...JohnJulie1
Simultaneous presentation of two lymphatic haematological malignancies is extremely rare. Adequate and optimal diagnostic steps including various imaging techniques and histopathological biopsies are required unpin the exact diagnoses to be able to deliver the best management strategies...
Critical Role of PET-Scan in Unravelling the Dual Pathology- Review of Litera...NainaAnon
Simultaneous presentation of two lymphatic haematological malignancies is extremely rare. Adequate and optimal diagnostic steps including various imaging techniques and histopathological biopsies are required unpin the exact diagnoses to be able to deliver the best management strategies...
The simultaneous occurrence of two lymphatic malignancies in
one patient is extremely rare with an incidence rate of 1.4–6.5
cases/1,000,000 individuals [8]. Co-existence of MM and other
lymphoid malignancies like Chronic Lymphocytic Leukemia (CLL)
[9], MM and Hodgkin’s Disease (HD) [10], MM and Lympho
Plasmacytic Lymphoma (LPL) [11] has been reported. However,
there are less than 5 reported cases in PubMed of simultaneous
presentation of DLBCL and MM
Critical Role of PET-Scan in Unravelling the Dual Pathology- Review of Litera...EditorSara
Simultaneous presentation of two lymphatic haematological malignancies is extremely rare. Adequate and optimal diagnostic steps including various imaging techniques and histopathological biopsies are required unpin the exact diagnoses to be able to deliver the best management strategies...
Critical Role of PET-Scan in Unravelling the Dual Pathology- Review of Litera...semualkaira
Simultaneous presentation of two lymphatic haematological malignancies is extremely rare. Adequate and optimal diagnostic steps including various imaging techniques and histopathological biopsies are required unpin the exact diagnoses to be able to deliver the best management strategies...
Critical Role of PET-Scan in Unravelling the Dual Pathology- Review of Litera...semualkaira
Simultaneous presentation of two lymphatic haematological malignancies is extremely rare. Adequate and optimal diagnostic steps including various imaging techniques and histopathological biopsies are required unpin the exact diagnoses to be able to deliver the best management strategies...
Bone Marrow Histology is a Pathognomonic Clue to Each of the JAK2V617F, MPL,5...asclepiuspdfs
According to the World Health Organization and Clinical Laboratory Molecular and Pathological criteria bone marrow pathology in JAK2V617F mutated trilinear myeloproliferative neoplasm (MPN) patients essential thrombocythemia (ET) and polycythemia vera are indistinguishably featured by clustered medium to large pleomorphic megakaryocytes and increased cellularity (60–90%) due to increased erythropoiesis and megakaryopoiesis. MPL515 mutated ET is the second distinct clonal MPN characterized by thrombocythemia in a normocellular bone marrow showing clustered increased large to giant mature megakaryocytes with staghorn-like hyperlobulated nuclei. Calreticulin (CALR) mutated hypercellular thrombocythemia associated with prefibrotic megakaryocytic, granulocytic myeloproliferation (MGM) recently became the third distinct MPN featured by dense clusters of immature megakaryocytes with cloud-like nuclei. Bone marrow pathology in newly diagnosed MPN patients appears to be a pathognomonic clue for diagnostic differentiation between JAK2V617F mutated trilinear MPN, MPL515 normocellular thrombocythemia, and CALR thrombocythemia with MGM characteristics followed by secondary reticulin fibrosis. Their natural histories clearly differ featured by an increase of erythro/granulopoiesis and cellularity in JAK2V617F, decrease of erythropoiesis and cellularity in MPL515 and increase of dual megakaryo/granulopoiesis and cellularity in CALR mutated MPN.
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Peripheral T-Cell Lymphomas: Progress in TreatmentEditorSara
Peripheral T-Cell Lymphomas (PTCL) arises from mature T-cells and they represent an extremely heterogeneous group. They are sub-classified into three major groups based on clinical presentation and localization, namely the nodal, extra nodal and leukemic PTCL. This review focuses on nodal PTCL which are the most frequently encountered entities...
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Peripheral T-Cell Lymphomas (PTCL) arises from mature T-cells and they represent an extremely heterogeneous group. They are sub-classified into three major groups based on clinical presentation and localization, namely the nodal, extra nodal and leukemic PTCL. This review focuses on nodal PTCL which are the most frequently encountered entities...
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Leiomyosarcoma (LMS) metastasis in the central nervous system is extremely rare. Metastatic LMSs have been described in the orbit, meninges, and skull base, however there are no reports of LMS metastasis into the cavernous sinuswith primary origin from lower extremity and long silent disease period of 7 years..
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Colorectal or bowel cancer is one of the major cause of cancer worldwide. Research has shown that 15 to 20 % colorectal cancer patients are also diagnosed with synchronous liver metastases (LM) at presentation and about one third eventually develop liver lesions (Leporrier, Maurel, Chiche, Bara, Segol, and Launoy, 2006; Manfredi, Lepage, Hatem, Coatmeur, Faivre, and Bou-vier, 2006)...
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Neulasta Onpro kit eliminates need for additional clinic visit after chemotherapy. Given the racially diverse population in our institution, we investigated acceptance of Onpro kit among patients on chemotherapy.Single-institution, retrospective review conducted in patients with GI tumors who received Onpro kit within 1 hour of completion of systemic chemotherapy from Jan 2014 through Jan 2018...
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Acute promyelocytic leukemia(APL),a specific characteristic of t(15;17) chromosomal translocation,molecular gene analyses are conclusive in vivo evidence that oncogenic pml/RARa fusion plays a crucial role in APL leukemogenesis [1-3]. Since the introduction of initial 13-cis retinoic acid(13-cis RA)[4],and currently all-trans RA(ATRA) [5] and tamibarotene [6],RA plus chemotherapy or RA plus As2O3 regimen is currently the standard of care [7]...
Hairy Cell Leukemia (HCL) is a rare subtype of B-cell chronic lymphoid leukemia which was first described by Bertha Bouroncle in 1958 [1]. The annual incidence of HCL is approximately 0.3 cases per 100,000 and the disease comprises 2-3% of all leukaemia?s in the Western world [2,3]...
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Malignmesotelioma can be causedbyserozalleaves of pleura, pericard, peritoneum, tunicavaginalisor testis. Inthe United States, about 2500 newcases of mesothelioma are reported each year. Most frequent type is pleural mesotelioma, second frequent type is peritoneal mesotelioma. The annual incidence of malignant peritoneal mesothelioma is one in about 1,000,000 people...
STAT-6 In Hodgkin Lymphoma Pathobiology and Treatment-Review of the Literaturedaranisaha
Classical Hodgkin Lymphoma (cHL), consists of rare neoplastic Hodgkin and Reed-Sternberg cells (HRS) residing in a prominent inflammatory background. HRS show deregulated activation of multiple signaling pathways and transcription factors. The activation of these pathways and factors is partly mediated through interactions of HRS with various other types of cells in the microenvironment, but also through genetic lesions...
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mortality, and public health costs than all illicit drugs combined. The
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combined into a single substance use disorder (SUD) on a continuum
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Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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Cardiac conduction defects can occur due to various causes.
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
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Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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A 43-Year-Old Male with PCM1-JAK2 Gene Fusion Experienced T-Lymphoblastic Lymphoma, Myelofibrosis, and Acute Myeloid Leukemia
1. Clinics of Oncology
ISSN: 2640-1037
Case Report
A 43-Year-Old Male with PCM1-JAK2 Gene Fusion Experienced
T-Lymphoblastic Lymphoma, Myelofibrosis, and Acute Myeloid
Leukemia
Tsai CC1
, Su YCMD1
, Chen BJ2
, Hsieh SM3
, Whang-Peng J4
, Chao TY*1,5
1
Division of Hematology and Oncology, Department of Internal medicine, Taipei Medical University-Shuang Ho Hospital, New Taipei
City, Taiwan, (R.O.C.)
2
Department of Pathology, Taipei Medical University-Shuang Ho Hospital, New Taipei City,Taiwan, (R.O.C.)
3
Department of Clinical Pathology, Taipei Medical University-Shuang Ho Hospital,Taiwan, (R.O.C.)
4
Cancer Center, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan, (R.O.C.)
5
International Ph.D. Program in Medicine, College of Medicine, Taipei Medical University, Taipei City, Taiwan,(R.O.C.)
Volume 2 Issue 3- 2020
Received Date: 25 Jan 2020
Accepted Date: 08 Feb 2020
Published Date: 12 Feb 2020
2. Keywords
PCM1-JAK2, T-lymphoblas-
tic lymphoma, myelofibrosis,
acute myeloid leukemia
*Corresponding Author (s): Tsu Yi Chao MD, Division of Hematology and Oncology, Depart-
ment of Internal medicine, Taipei Medical University-Shuang Ho Hospital, New Taipei City,
23561, Taiwan, (R.O.C.), E-mail: 10575@s.tmu.edu.tw
clinicsofoncology.com
Citation: Chao TY, A 43-Year-Old Male with PCM1-JAK2 Gene Fusion Experienced T-Lymphoblastic
Lymphoma, Myelofibrosis, and Acute Myeloid Leukemia. Clinics of Oncology. 2020; 2(3): 1-4
1. Abstract
Myeloid/lymphoid neoplasms associated with eosinophilia and PCM1-JAK2 is a provisional entity in
WHO 2016. Prior case reports have shown quite a few clinical presentations in different patients with
this chromosome translocation,characterized by eosinophilia in combination with myelodysplastic/
myeloproliferative neoplasms, acute myeloid leukemia(AML) and rarely, T-lymphoblastic
lymphoma(T-LBL) or B-acute lymphoblastic leukemia(B-ALL). We herein reported a case who
initially was diagnosed as T-LBL with myelofibrosis. He developed AML after chemotherapy for
T-LBL. We used fluorescence in situ hybridization (FISH) analysis proves the presence of PCM1-JAK2
fusion in his tumor cells. Our case with the unique feature of AML transformation from initial T-LBL
provides a further evidence in support of the provisional entity of myeloid/lymphoid neoplasm with
PCM1-JAK2.
3. Introduction
Molecular genetic abnormalities, such as PDGFRA, PDGFRB,
FGFR1, in myeloid/lymphoid neoplasms associated with
eosinophilia is one of the category of myeloid neoplasms in WHO
classification 2008. In 2016, the WHO introduced a new provisional
entity PCM1-JAK2 into this category [1]. The first description
of a patient with t(8;9)(p22;p24) was reported by Stewart et al in
1990 [2]. Reiter et al used reverse transcription-PCR and FISH to
identify the recurrent PCM1-JAK2 fusion gene in patients with
t(8;9)(p21-23;p23-24) in 2005[3]. Since then there have been at
least 33 patients reported with a lymphoid or myeloid neoplasm
associated with t(8;9)(p22;p24);PCM1-JAK2[4, 5]. These patients’
characteristics are very similar to those with rearrangements of
PDGFRA, PDGFRB, or FGFR1 with regard to epidemiology,
clinical features, and genetic changes [5]. This disease entity is
rare and characterized by a combination of eosinophilia with the
bone marrow findings of left-shifted erythroid predominance,
lymphoid aggregates, and often myelofibrosis, at times mimicking
primary myelofibrosis. Even rarer, it can present as T- or B-acute
lymphoblastic leukemia (ALL)[4]. There is a marked male
predominance with a genderratio of 27:5. The age range is wide,
from 12 to 75 years old with a median of 47. Clinical features often
include hepatosplenomegaly[3, 4]. We report herein a 43-year-
old man, who has t(8;9)(p22;p24);PCM1-JAK2, experienced
T-lymphoblastic lymphoma(T-LBL), gradually progressive to
myelofibrosis after initial treatment and finally developed blastic
transformation into acute myeloid leukemia(AML).
4. Material and Methods
4.1. Case Report
A 43-year-old Taiwanese man sought for medical attention
due to multiple enlarged clustered lymph nodes in bilateral
3. Volume 2 Issue 3 -2020 Case Report
clinicsofoncology.com 3
a platelet of 38 x10^9 /L, leukoblastosis (band 9%, metamyelocyte
5%, myelocyte 13%, promyelocyte 24%)and blast cells around 10%.
A bone marrow biopsydisplayed blastic transformation into AML,
accompanied by increase in eosinophils and myelofibrosis grade
2 (0-3) by reticulin and Masson-Trichrome stains (Figure 1). In
consideration of the previous T-LBL and MPN-like morphology
with increased eosinophils and further blastic transformation in the
bone marrow, myeloid/lymphoid neoplasm with eosinophilia and
gene rearrangement was considered. Cytogenetic study of the bone
marrow aspirates showed 46,XY,t(8;9)(p22;p24), andfluorescence
in situ hybridization (FISH)analysisshowed PCM1-JAK2fusion
(Figure 2). Other recurrent genetic abnormalities of AML were
negative, including AML1-ETO(RUNX1-RUNX1T1), CBFB-
MYH11 and MLL-PTD fusion transcripts; NPM1, FLT3-ITD
and FLT3-TKD mutations. The patient then recieved induction
and consolidation treatment with I3A7 and HiDAC while the
manuscript was being prepared.
5. Discussion
Myeloid/lymphoid neoplasms with eosinophilia and PCM1-
JAK2 is a new provisional entity in WHO 2016 classification of
myeloid neoplasms. Prior case reports have shown quite a few
clinical presentations in different patients with this chromosome
translocation, characterized by eosinophilia in combination with
myeloproliferative neoplasms, myelodysplastic/myeloproliferative
neoplasms, AML and rarely, T-LBL or B-ALL. The present case
initially presented as T-LBL, and finally became an AML, with
progressive bone marrow fibrosis. The presentation is unique in
this category.
JAK2 is a non-receptor tyrosine kinase essential for such hormone-
like cytokines as growth hormone (GH), prolactin (PRL),
erythropoietin(EPO), thrombopoietin (TPO) and the family of
cytokinesthatsignalthroughtheIL-3receptor.JAK2pointmutation,
such as V617F, accounts for some MPN [6]. The protein PCM-1
localizes to cytoplasmic granules known as “centriolar satellites”
which is involved in microtubule organization in interphase [7].
Although the functions of each gene have been discovered partially,
what effects of this fusion gene for leukaemogensis is still unclear.
In recent years, many gene mutations and chromosome
abnormalities have been discovered with correlation to
leukaemogenesis via multiple steps toward the development of
AML. The gene mutations or chromosome abnormalities act
together to induce progression from normal haematopoietic stem/
progenitor cells to clonal, preleukamic stem/progenitor cells, to
overtly transformed leukaemic cells[8].
In T-LBL, the leukemogenic events are mostly caused by
translocation placing the proto-oncogene under control of a T
cell receptor (TCR) promoter or enhancer, or transcription factor
juxtaposition to TCR loci. Oncogenic fusion proteins are less
common in the leukaemogenesis but indeedpresent.ETV6-JAK2
is one of them, and is found in B- and T-LBL [1, 9]. Perhaps,
PCM1-JAK2could also forms the fusion protein leading to the
leukemogenic event.
Although why the fusion gene PCM1-JAK2 develops a broad
spectrum of clinical presentation is not clear,yetthe fact that the
blast crisis can be myeloid or lymphoid implies that this disease
might derive from a pluripotent stem cell [10, 11]. The interaction
between the each function of PCM1 and JAK2 within a fusion gene
should be clarified in the future. Based on the emerging findings
of genetic mutations which contribute to the multiple steps
toward the development of lymphoid and myeloid leukemia, we
propose that other oncogenesmay also play a role, e.g. interaction
with PCM1-JAK2 fusion protein on the final progression of this
neoplasm toward myeloid or lymphoid neoplasms.
In our case, though, the patient develop AML after chemotherapy, it
is difficult to distinguished novo AML from t-AML. Because t(8;9)
(p22;p24) existed from the first diagnosis of T-LBL, it may support
the notion that this translocation dictate the final transformation
of AML.
In summary, we reported a case with PCM1-JAK2 fusion, who
presented initially with T-LBL with progression to myelofibrosis
after chemotherapy and finally with blastic transformation to AML.
Our case provides a further evidence in support of the provisional
entity of myeloid/lymphoid neoplasm with PCM1-JAK2 reported
in the 2016 WHO categories of myeloid neoplasms and acute
leukemia.
6. Acknowledgements
We thank Yung -Cheng Su for funding this study and the molecular
laboratory in Taipei Medical University-Shuang Ho Hospital for
performing the fluorescence in situ hybridization.
References
1. Arber DA, Orazi A, Hasserjian R, Thiele J, Borowitz MJ, Le Beau MM
et al. The 2016 revision to the World Health Organization classification of
myeloid neoplasms and acute leukemia. Blood. 2016; 127: 2391-405.
2. Stewart K, Carstairs KC, Dube ID, Keating A. Neutrophilic myelofibrosis
presenting as Philadelphia chromosome negative BCR nonrearranged
chronic myeloid leukemia. American Journal of Hematology. 1990; 34:
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3. Reiter A, Walz C, Watmore A, Schoch C, Blau I, Schlegelberger B et
al., The t(8;9)(p22;p24) Is a Recurrent Abnormality in Chronic and Acute
Leukemia that Fuses PCM1 to JAK2. Cancer Res. 2005; 65: 2662-7.
4. Bain BJ, Ahmad S. Should myeloid and lymphoid neoplasms with
PCM1-JAK2 and other rearrangements of JAK2 be recognized as specific
entities? Br J Haematol. 2014; 166: 809-17.
5. Patterer V, Schnittger S, Kern W, Haferlach T, Haferlach C. Hematologic
malignancies with PCM1-JAK2 gene fusion share characteristics with
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PDGFRA, PDGFRB, and FGFR1. Ann Hematol. 2013; 92: 759-69.
6. Yamaoka K, Saharinen P, Pesu M, Et Holt V, Silvennoinen O, O’Shea JJ.
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microtubule organization depends on PCM-1. J Cell Biol. 2002; 159: 255-
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8. Swerdlow SH, Campo E. WHO classifications of tumours of
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9. Rabin KR, Margolin J, Poplack DG. Molecular Genetics of ALL, in The
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10. Robyn J, Lemery S, McCoy JP, Kubofcik J, Kim YJ, Pack S et al.,
Multilineage involvement of the fusion gene in patients with FIP1L1/
PDGFRA-positive hypereosinophilic syndrome. Br J Haematol. 2006; 132:
286-92.
11. Chaffanet M, Popovici C, Leroux D, Jacrot M, Adelaide J, Dastugue
N et al. t(6;8), t(8;9) and t(8;13) translocations associated with stem
cell myeloproliferative disorders have close or identical breakpoints in
chromosome region 8p11-12. Oncogene. 1998; 16: 945-9.
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Volume 2 Issue 3 -2020 Case Report