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Frontiers of Medicine 2017年第3期11卷 440-444页

作者： Zhan Su Fengyu Wu Weiyu Hu Xiaodan Liu Shaoling Wu Xianqi Feng Zhongguang Cui Jie Yang Zhenguang Wang Hongzai Guan Hongguo Zhao Wei Wang Chunting Zhao Jun Peng Department of Haematology Qilu Hospital Shandong University Jinan 250012 China Department of Haematology The Affiliated Hospital of Qingdao University Qingdao 266000 China PET/CT Center The Affiliated Hospital of Qingdao University Qingdao 266000China Department of Hepatobiliary Surgery The Affiliated Hospital of Qingdao University Qingdao 266000 China Department of Haematology Qingdao University Medical College Qingdao 266071 China

philadelphia chromosome-positive acute myeloid leukemia is controversial and difficult to distinguish from the blast phase of chronic myeloid leukemia. As a myeloid neoplasm, rare cases of this leukemia manifest multiple soft-tissue tumors or bone lyric lesions. In this paper, we describe a 49-year-old male patient who had an abrupt onset with sharp chest pain, fever, fatigue, emaciation, and splenomegaly. 18F-fluoro-deoxy-glucose positron emission tomography/computed tomography （18F-FDG PET/CT） result showed diffuse and uneven hypermetabolic lesions in the bone marrow with peripheral bone marrow expansion, multiple soft tissue neoplasms with high 18F-FDG uptake, and lyric bone lesions. Bone marrow smear and biopsy detected aberrant blast cells expressing myeloid rather than lymphoid immunophenotype marker. For the existence of philadelphia chromosome and BCR-ABL1 fusion gene together with complex chromosome abnormalities, a diagnosis of philadelphia-positive acute myeloid leukemia was made, although the type （de novo or blast crisis） remained unclear.

关键词： philadelphia chromosome acute myeloid leukemia mass osteolysis positron emission tomography

Efficacy and prognostic factors of imatinib plus CALLG2008 protocol in adult patients with newly diagnosed philadelphia chromosome-positive acute lymphoblastic leukemia

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Frontiers of Medicine 2017年第2期11卷 229-238页

作者： Yinjun Lou Yafang Ma Chenyin Li Sansan Suo Hongyan Tong Wenbin Qian Wenyuan Mai Haitao Meng Wenjuan Yu Liping Mao Juyin Wei Weilei Xu Jie Jin Institute of Hematology Department of Hematology the First Affiliated Hospital College of Medicine Zhejiang University Hangzhou 310003 China Key Laboratory of Hematopoietie Malignancies Zhejiang Province Hangzhou 310003 China

A CALLG2008 protocol was developed by the Chinese Acute Lymphoblastic Leukemia Cooperative Group for adult acute lymphoblastic leukemia （ALL）. We retrospectively analyzed 153 newly diagnosed adult patients with philadelphia chromosome （Ph）-positive ALL enrolled into imatinib （400 mg/d） plus CALLG2008 regimen between 2009 and 2015. The median age was 40 years （range, 18-68 years）, with 81 （52.3%） males. The overall hematologic complete remission （CR） rate was 96.7% after induction. With a median follow-up of 24.2 months, the estimated 3-year overall survival （OS） and event-free survival （EFS） rates were 49.5% （95% confidence interval （CI）： 38.5%-59.5%） and 49.2% （95% CI： 38.3%-59.2%）, respectively. Fifty-eight （36 with haploidentical donor） patients underwent allogeneic hematopoietic stem call transplantation （allo-HSCT） in first CR. Among the patients in CR1 after induction, both the 3-year OS and EFS were significantly better in the allo-HSCT group than in the without alIo-HSCT group （73.2%, 95% CI： 58.3%-83.5% vs. 22.2%, 95% CI： 8.7%-39.6% and 66.5%, 95% CI： 50.7%-78.2% vs. 16.1%, 95% CI： 5.1%-32.7%, respectively）. Multivariate analysis showed that alIo-HSCT and achievement of major molecular response were associated with favorable OS or EFS independently. Interestingly, in the alIo-HSCT cohort, the donor type （haploidentical versus matched donors） had no significant impact on EFS or OS. All these results suggested that imatinib plus CALLG2008 was an effective protocol for Ph-positive ALL. Haploidentical donors can also be a reasonable alternative expedient donor pool.

关键词： philadelphia chromosome acute lymphoblastic leukemia imatinib CALLG2008

Administration of imatinib in the first 90 days after allogeneic hematopoietic cell transplantation in patients with philadelphia chromosome-positive acute lymphoblastic leukemia

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Chinese Medical Journal 2011年第2期124卷 246-252页

作者： CHEN Huan LIU Kai-yan XU Lan-ping LIU Dai-hong CHEN Yu-hong SHI Hong-xia HAN Wei ZHAN Xiao-hui WANG Yu ZHAO Ting HUANG Xiao-jun Peking University Institute of Hematology Peking University People's Hospital Beijing 100044 China

Background Relapse happens frequently after allogeneic hematopoietic cell transplantation （alIo-HCT） in the patients with philadelphia chromosome-positive acute lymphoblastic leukemia （Ph^＋ ALL）. Detection of the minimal residual disease （MRD） before and after alIo-HCT is associated with higher relapse rate. Early administration of imatinib after alIo-HCT may prevent recurrent Ph^＋ ALL. The aim of this study was to evaluate the safety and efficacy of imatinib in preventing hematological relapse when imatinib was administrated in the first 90 days after alIo-HCT. Methods Patients with Ph^＋ ALL that underwent alIo-HCT were enrolled in a prospective study. A TaqMan-based real-time quantitative polymerase chain reaction （RQ-PCR） technique was used to detect the MRD （bcr-abl transcript levels）. Imatinib therapy was initiated prior to 90 days after alIo-HCT if the patient＇s absolute neutrophil count （ANC） was above 1.0×10^9/L （without granulocyte colony-stimulating factor （G-CSF） administration） and the platelet count was greater than 50.0×10^9/L, or if the bcr-abl transcript levels were elevated in two consecutive tests, or if the bcr-abl transcript levels were 〉10.2 after the initial engraftment. The initial daily dose of imatinib was 400 mg/d for adults and 260 mg/m^2 for children （younger than 17 years）. Imatinib was administered for at least I month and the bcr-abl TaqMan results were negative for 3 consecutive tests, or complete molecular remission （CR^mol） was sustained for at least 3 months. Results From May 2005 to October 2008, 29 patients were enrolled in this study, of whom, 19 patients were male and 10 were female. The median age of the enrolled patients was 33 years （range 6-50 years）. Imatinib therapy was started at a median time of 60 days （range 20-122 days） post HCT （only one patient started Imatinib therapy at 122nd day after HCT）. Twenty-five adult patients could tolerate a dose of 300-400 mg/d of imatinib, and three children tolerated a dose of 260 mg

关键词： philadelphia chromosome acute lymphoblastic leukemia allogeneic hematopoietic cell transplantation minimal residual disease

Chronic myeloid leukemia-from the philadelphia chromosome to specific target drugs:A literature review

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World Journal of Clinical Oncology 2021年第2期12卷 69-94页

作者： Mariana Miranda Sampaio Maria Luísa Cordeiro Santos Hanna Santos Marques Vinícius Lima de Souza Gonçalves Glauber Rocha Lima Araújo Luana Weber Lopes Jonathan Santos Apolonio Camilo Santana Silva Luana Kauany de SáSantos Beatriz Rocha Cuzzuol Quézia Estéfani Silva Guimarães Mariana Novaes Santos Breno Bittencourt de Brito Filipe Antônio França da Silva Márcio Vasconcelos Oliveira Cláudio Lima Souza Fabrício Freire de Melo Instituto Multidisciplinar em Saúde Universidade Federal da BahiaVitória da Conquista 45029-094BahiaBrazil Campus Vitória da Conquista Universidade Estadual do Sudoeste da BahiaVitória da Conquista 45083-900BahiaBrazil

Chronic myeloid leukemia(CML)is a myeloproliferative neoplasm and was the first neoplastic disease associated with a well-defined genotypic anomaly―the presence of the philadelphia *** advances in cytogenetic and molecular assays are of great importance to the diagnosis,prognosis,treatment,and monitoring of *** discovery of the breakpoint cluster region(BCR)-Abelson murine leukemia(ABL)1 fusion oncogene has revolutionized the treatment of CML patients by allowing the development of targeted drugs that inhibit the tyrosine kinase activity of the BCR-ABL *** kinase inhibitors(known as TKIs)are the standard therapy for CML and greatly increase the survival rates,despite adverse effects and the odds of residual disease after discontinuation of *** therapeutic alternatives,the subsequent TKIs lead to faster and deeper molecular remissions;however,with the emergence of resistance to these drugs,immunotherapy appears as an alternative,which may have a cure potential in these *** this background,this article aims at providing an overview on CML clinical management and a summary on the main targeted drugs available in that context.

关键词： Chronic myeloid leukemia Breakpoint cluster region-Abelson murine leukemia Immunotherapy Tyrosine kinase inhibitors philadelphia chromosome Diagnosis

A novel t(3;12)(q21;p13) translocation in a patient with accelerated chronic myeloid leukemia after imatinib and nilotinib therapy

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Cancer Biology & Medicine 2013年第1期10卷 47-51页

作者： Ayda Bennour Ikram Tabka Yosra Ben Youssef Zahra Kmeira Abderrahim Khelif Ali Saad Halima Sennana Department of Cytogenetics Molecular Genetics and Reproductive Biology Farhat Hached University Teaching Hospital Department of Clinical Hematology Farhat Hached Hospital

The acquisition of secondary chromosomal aberrations in chronic myeloid leukemia (CML) patients with philadelphia chromosome-positive (Ph+) karyotype signifies clonal evolution associated with the progression of the disease to its accelerated or blastic phase. Therefore, these aberrations have clinical and biological significance. T(3;12)(q26;p13), which is a recurrent chromosomal aberration observed in myeloid malignancies, is typically associated with dysplasia of megakaryocytes, multilineage involvement, short duration of any blastic phase, and extremely poor prognosis. We have identified a recurrent reciprocal translocation between chromosomes 3 and 12 with different breakpoint at bands 3q21 in the malignant cells from a 28-year-old man. The patient was initially diagnosed as having Ph+ CML in the chronic phase. The t(3;12)(q21;p13) translocation occurred 4 years after the patient was first diagnosed with CML while undergoing tyrosine kinase inhibitor therapy. We confirmed the t(3;12)(q21;p13) translocation via fluorescence in situ hybridization assay by using whole-chromosome paint probes for chromosomes 3 and 12. Our findings demonstrate that, similar to other recurrent translocations involving 3q26 such as t(3;3) and t(3;21), the t(3;12)(q21;p13) translocation is implicated not only in myelodysplastic syndrome and acute myeloid leukemia but also in the progression of CML. These findings extend the disease spectrum of this cytogenetic aberration.

关键词： philadelphia chromosome t(3 12)(q21 p13) chronic myeloid leukemia accelerated phase fluorescence in situhybridization

Damage Mechanism of CK2 and IKAROS in philadelphia Like Acute Lymphoblastic Leukemia

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Journal of Biosciences and Medicines 2024年第4期12卷 49-59页

作者： Ignacio Vélez-Rodríguez Victoria Carranza-Aranda Facultad Mexicana de Medicina Universidad La Salle Tlalpan M&#233xico Hospital General de Mé xico Cuauht&#233moc M&#233xico

Acute lymphoblastic leukemia (ALL) is characterized by immature and poorly differentiated B lymphocytes in large numbers in the blood. B cells are distinct from the cell types involved in their development (common lymphoid progenitor cells, pro-B cells, pre-B cells, and mature cells). The process of B cell maturation depends on precise communication within the cell: signals activate specific genes that are essential for proper development. Errors in this intricate signaling network can lead to issues with B cell function and contribute to disease. B-lineage acute lymphoid leukemias, malignancies of precursor-stage B lymphoid cells inhibit lymphoid differentiation, leading to abnormal cell proliferation and survival. The process of developing leukemia (leukemogenesis) can be triggered by an overproduction of both hematopoietic stem cells (the cells that form all blood cells) and the immature versions of white blood cells called lymphoblasts. Acute lymphoblastic leukemia (ALL) with the presence of the philadelphia chromosome (ALL Ph) is classified as a high-risk manifestation of the disease, this chromosome is the product of the reciprocal translocation, whose product is a BCR-ABL fusion protein. It is a highly active tyrosine kinase that can transform hematopoietic cells into cytokine-independent. Hyperphosphorylation cascades inhibit the differentiating function of IKZF1 as a tumor suppressor gene which leads to an abnormal proliferation of B cells due to the presence of the philadelphia chromosome;it inhibits the differentiating process, leukemogenesis involving immature B cells in the bloodstream can result from the uncontrolled growth and division of hematopoietic stem cells and immature lymphoblasts (the precursors to B cells).

关键词： Acute Lymphoblastic Leukemia IKAROS Dephosphorylation philadelphia chromosome CK2

Clonal evolution analyses of a chronic myeloid leukemia patient with hematopoietic stem cell transplantation based on deep sequencing

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Holistic Integrative Oncology 2023年第1期2卷 85-92页

作者： Fuhua Yang Ping Wang Jia Wan Xiaoqing Jia An Zhou Yuan Zhang Jiani Song Qiang Gong Wei-Dong Li Jieping Chen Department of Genetics School of Basic Medical SciencesTianjin Medical UniversityTianjin 300070China Tianjin Key Laboratory of Retinal Functions and Diseases Tianjin Branch of National Clinical Research Center for Ocular DiseaseEye Institute and School of OptometryTianjin Medical University Eye HospitalTianjin 300384China Department of Hematology Southwest HospitalArmy Medical UniversityChongqing 400038China

Background The philadelphia(Ph)chromosome is the hallmark chromosome aberration in chronic myeloid leukemia(CML),which confers the cancer phenotype of the ***,how the Ph chromosome forms and the genetic clonal evolution structure after targeted Ph treatment are still *** In this study,we performed genome sequencing and clonal evolution analyses in a series of bone marrow specimens and skin biopsy from a CML patient who had received hematopoietic stem cell transplantation from her sister,then relapsed(lymphoid blast crisis),and received Ph-targeted *** The Ph chromosome was the“driver”clonal change in the original CML and the *** the patient and her sister had micro-deletions in the BCR gene region;however,the patient had a frameshift BRIP1 mutation that may account for the malfunctioning homologous recombination DNA repair of the BCR gene region and formation of the Ph *** We found that the BCR-ABL1 translocation was the driving force of the patient’s CML and *** malfunctioning double-strand DNA break repair caused by the BRIP1 mutation could be the cause of Ph chromosome formation in the patient.

关键词： philadelphia chromosome Clonal evolution DNA repair Homologous recombination Targeted therapy

Acute Priapism: A Revealing Inaugural Mode of Chronic Myeloid Leukemia. A Case Report and Review of the Literature

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Open Journal of Urology 2022年第5期12卷 237-241页

作者： Dimitri Mbethe Adrien Mougougou Steevy Ndang Ngou Milama Said Mohamed Moudouni Izoudine Bissiriou Giscard Smith Olagui Jean Massandé Mouyendi Urology Department of the University Hospital of Libreville Libreville Gabon Urology Department of the Mohamed 6 University Hospital of Marrakech Marrakesh Morocco Urological and Visceral Surgery Department Omar Bongo Ondimba Armed Forces Instruction Hospital Libreville Gabon

Priapism is a painful and prolonged erection occurring without any sexual stimulation and not resulting in ejaculation. It most often occurs in patients with sickle cell disease. We report here the case of acute recurrent priapism revealing inaugural mode of CML in a 22-year-old patient with no particular pathological history. The study of the onco-hematological karyotype revealed a karyotype with 46 chromosomes with a clonal chromosomal anomaly: The t (9;22) “philadelphia chromosome”. The evolution was favorable under imatinib.

关键词： Priapism Chronic Myeloid Leukaemia philadelphia chromosome