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Journal articles on the topic 'Akute myeloid leukemia'

Author: Grafiati

Published: 28 June 2021

Last updated: 11 February 2022

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1

Suci Widyastiti, Nyoman, Ima Arum Lestarini, Yetty Movieta Nancy, Umi S Intansari, and R. Lindeman. "LEUKEMIA MEGAKARIOBLASTIK AKUT PADA SEORANG ANAK." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 14, no. 2 (March 15, 2018): 77. http://dx.doi.org/10.24293/ijcpml.v14i2.906.

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Acute Megakaryoblastic Leukemia (FAB AML M7) occurs in all age groups with two peaks in distribution. The one is in adults and theother in children 1 to 3 years of age especially in those with Down’s syndrome. The diagnosis of AML M7 requires more than 30% of thenucleated bone marrow cells being megakaryoblasts. The AML M7 was under diagnosed before the availability of monoclonal antibodies.The more common types of AML MO-M6 have to be excluded by morphological and cytochemical analysis whereas immunology is neededto exclude ALL. The megakaryocytic nature of the leukemia has to be proven by ultrastructural demonstration of platelet peroxidase or byimmunological demonstration of CD61, CD42, CD41 on the surface of the leukemic blasts. Megakaryocytic/megakaryoblastic leukemiasshow a wide morphologic spectrum. Cytoplasmic blebs and protrusions are the most prominent feature of many cases. The nuclei ofthese cells are round with more finely reticulated chromatin and with prominent nucleoli. The megakaryoblastic nature of these cells canbe suggested by morphology. Cytochemistry is of limited diagnostic value in megakaryoblastic leukemias. Usually it is used to excludethe more common types of leukemia. An eighteen months girl was admitted to hospital with anemia and hepatosplenomegaly. There isdismorphic - hypertelorism face and enlargement of neck lymph nodes. The laboratory examination found anemia, hyperleukocytosis with75 % blast cells. Morphologically the blast cells show prominent blebs and cytoplasmic budding resemble features of budding platelets.The cytochemistry staining for granulocyte and erythrocyte lineages were negative. The expressions of lymphoid and myeloid lineagesmarkers by immunoflowcytometry method were also negative. Cytogenetic examination was followed. The physical and laboratoryexamination result conclude a child with Acute Megakaryoblastic Leukemia. Cytogenetic examination was followed

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2

Nugraha, Ida Bagus Aditya, and Wayan Losen Adnyana. "Seorang Penderita Acute Myeloid Leukemia (AML) M4 yang Mengalami Tumor Lysis Syndrome." Jurnal Penyakit Dalam Udayana 1, no. 1 (June 30, 2017): 8–16. http://dx.doi.org/10.36216/jpd.v1i1.8.

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Tumor Lisis Sindrom (TLS) adalah suatu kondisi yang bersifat mengancam nyawa sering terjadi setelah pemberian kemoterapi pada keganasan hematologik seperti Akut Limfoblastik Leukemia atau high grade lymphoma, tetapi tumor lisis sindrom dapat juga terjadi pada kegananasan hematologik yang lain seperti Leukemia Limfoblastik Kronik, Akut Myeloid Leukemia, Multipel Myeloma, Hogkin Lymphoma dan low-intermediate Non Hodgkin Lymphoma, juga pada beberapa solid tumor seperti kanker paru, kanker mamae dan testis. Pada AML, dengan kadar sel darah putih < 25x10³/µLhanya 1% dilaporkan mengalami TLS. Berikut ini dipaparkan sebuah kasus TLS pada pasien AML (M4) yang sedang menjalani kemoterapi hari ke-2 dengan leukopenia. Kasus ini diangkat untuk lebih mengingatkan pentingnya kewaspadaan pada setiap kasus malignansi yang akan menjalani kemoterapi, sehingga kejadian TLS dapat dicegah serta monitoring dan manajemen komplikasi untuk mencegah akibat yang lebih buruk.

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Said, Burhanuddin, Maimun ZA, and Budiman Budiman. "LINEAGE SWITCH LEUKEMIA LIMFOBLASTIK AKUT MENJADI LEUKEMIA MIELOMONOSITIK AKUT PADA PEREMPUAN USIA 26 TAHUN (Lineage Switch From Acute Lymphoblastic Leukemia To Acute Myelomonocytic Leukemia at A 26 Years Old Woman)." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 21, no. 1 (April 15, 2018): 96. http://dx.doi.org/10.24293/ijcpml.v21i1.1266.

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A lineage switch from Acute Lymphoblastic Leukemia (ALL) to Acute Myeloid Leukemia (AML) is very rare. It was estimated between6− 9% of cases that occurred, especially lineage switch from ALL to Acute Myelomonoblastic Leukemia (AMMOL). The reviewers reporta case of a 26 years old women with the first clinical presentation were fever and double visions and diagnosed as B-Acute lymphoblasticleukemia ALL with CD13 and CD33 expression aberrations, based on Bone Marrow Aspiration (BMA) and immunoprephenotyping inHongkong Hospital. After induction therapy, in the second month, BMA was done and found 10% blast, so it couldn’t be assessed ascomplete remission. After two (2) months, she comes back to Indonesia to follow continuing the treatment. She was suffered from severeheadache and blurred vision. The blast cell morphology of BMA showed myeloblast 25% and monoblast 60%, consistent with the diagnosisof AMMOL. Moreover, both findings were quite specific for each common cell ALL and acute myelomonocytic leukemia. These findingssupport that this case is completely different leukemic clones occurred at each leukemic expression. Exogenic factor such as chemotherapyand endogenic factor due to chromosomal abnormalities is supposed to be the cause of this lineage switch during the treatment.

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Indrasari, Yulia Nadar, and Ana Murtasyidah. "ACUTE MEGAKARYOBLASTIC LEUKEMIA." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 25, no. 3 (April 25, 2019): 364. http://dx.doi.org/10.24293/ijcpml.v25i3.1503.

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Leukemia megakarioblastik akut (AMegL) dibagi dalam tiga kelompok berdasarkan patofiosiolgi, usia, respon terhadap terapi dan prognosis. Kelompok tersebut adalah AMegL yang terjadi pada anak-anak dengan sindrom Down (DS-AMegL), AMegL yang terjadi pada anak-anak yang tidak memiliki sindrom Down (non-DS-AMegL) dan AMegL pada orang dewasa non-DS (AMegL dewasa). AMegL pada anak tanpa sindrom Down juga disebut leukemia megakarioblastik pediatrik akut atau AMegL anak.1Dasar diagnosis AMegL atau AML M7 menurut FAB adalah adanya sel lini megakariosit 30% atau lebih dari seluruh sel.2 Sedangkan diagnosis AMegL menurut panduan WHO 2016 adalah leukemia akut dengan > 20% blast dimana > 50% adalah lini megakariosit. Sel megakariosit lebih jelas terlihat pada mikroskop elektron yang bereaksi positif terhadap platelet peroksidase2 atau menggunakan antibodi marker terhadap CD41/gpIIb, CD42b/gpIb, CD61/gpIIIa, faktor Von Willebrand dan pengecatan LAT.3 Temuan sitogenetika berbeda antara ketiga jenis AMegL sesuai dengan perbedaan patofisiologinya. WHO (2016) menyebutkan leukemia megakarioblastik akut ke dalam kriteria AML not otherwise specific (NOS). AmegL adalah leukemia akut dengan > 20% blast dimana > 50% adalah lini megakariosit. Kriteria ini mengeksklusi AML dengan mielodisplasia (acute myeloid leukemia with myelodysplasia related change; AMLMRC), AML yang berhubungan dengan terapi, dan AML dengan kelainan genetik rekuren, seperti AML dengan t(1;22)(p13.3;q13.1), inv(3)(q21.3q26.2), atau t(3;3)(q21.3;q26.2). DS-AMegL juga diklasifikasikan sendiri ke dalam Myeloid Leukemia associated Down Syndrome.3Prognosis AMegL pada pasien dewasa yang diobati jauh di bawah bentuk AMegL lainnya. Waktu kelangsungan hidup rata-rata hanya 18 hingga 41 minggu dengan tingkat kelangsungan hidup 5 tahun hanya 10-11 persen. Perbaikan besar dalam statistik ini kemungkinan akan membutuhkan pendekatan pengobatan baru yang diarahkan pada mekanisme yang mendasari penyakit ini.1

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Király, Péter Attila, Krisztián Kállay, Dóra Marosvári, Gábor Benyó, Anita Szőke, Judit Csomor, and Csaba Bödör. "Familiáris myelodysplasiás szindróma és akut myeloid leukaemia klinikai és genetikai háttere." Orvosi Hetilap 157, no. 8 (February 2016): 283–89. http://dx.doi.org/10.1556/650.2016.30375.

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Myelodysplastic syndrome and acute myeloid leukaemia are mainly sporadic diseases, however, rare familial cases exist. These disorders are considered rare, but are likely to be more common than currently appreciated, and are characterized by the autosomal dominant mutations of hematopoietic transcription factors. These syndromes have typical phenotypic features and are associated with an increased risk for developing overt malignancy. Currently, four recognized syndromes could be separated: familial acute myeloid leukemia with mutated CEBPA, familial myelodysplastic syndrome/acute myeloid leukemia with mutated GATA2, familial platelet disorder with propensity to myeloid malignancy with RUNX1 mutations, and telomere biology disorders due to mutations of TERC or TERT. Furthermore, there are new, emerging syndromes associated with germline mutations in novel genes including ANKRD26, ETV6, SRP72 or DDX41. This review will discuss the current understanding of the genetic basis and clinical presentation of familial leukemia and myelodysplasia. Orv. Hetil., 2016, 157(8), 283–289.

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ULAŞ, Beliz Bahar, and Pervin TOPÇUOĞLU. "New Agents in the Treatment of Acute Myeloid Leukemia." LLM Dergi 3, no. 4 (January 31, 2020): 67–75. http://dx.doi.org/10.5578/llm.68329.

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7

Telek, Béla, László Rejtő, Péter Batár, Zsófia Miltényi, Gyula Reményi, Zsófia Simon, Zsófia Ujj, et al. "Az akut myeloid leukaemia gyógyszeres kezelése. Jelenlegi lehetőségek, jövőbeli kilátások." Orvosi Hetilap 157, no. 22 (May 2016): 843–48. http://dx.doi.org/10.1556/650.2016.30433.

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Acute myelogenous leukemia is a heterogeneous disease. Recent molecular mutational analysis techniques have shed more light on different, genetically well characterised types of the disease. Treatment approach is uniform except for acute promyelocytic leukemia. Application of the “3 + 7” induction treatment has been the gold standard in the past 40 years. While the dose of cytarabine has not been changed, escalating daunorubicine dose in younger (<60 years) patients with good performance status to 90 mg/m2 had a positive impact on overall survival. High dose chemotherapy is tolerated poorly in patients older than 60 years of age and, as treatment is not curative in the elderly, improvement of overall survival and quality of life remains the main goal of management in these patients. Low intensity treatment is beneficial and can provide additional advantage over supportive care. Innovative and targeted therapy approaches might give promise to better management of patients with acute myelogenous leukemia. Orv. Hetil., 2016, 157(22), 843–848.

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Setiawan, Agus, Indarini Indarini, Lyana Setiawan, Siti Boedina Kresno, Nugroho Prayogo, and Arini Setiawati. "CASPASE-3 AKTIF DI LEUKEMIA MIELOSITIK AKUT (LMA) DAN LEUKEMIA LIMFOBLASTIK AKUT (LLA)." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 19, no. 3 (October 14, 2016): 141. http://dx.doi.org/10.24293/ijcpml.v19i3.411.

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Dysregulation of apoptosis plays an essential role either in leukemogenesis or treatment response. Caspase-3 is a cysteine protease that functions as the final common mediator of apoptosis. The expression of the active caspase-3 is presumed as a predictor of prognosis and is able to predict the chemotherapy sensitivity. The aim of this study is to identify and to know the profile of active caspase-3 in Acute Myeloid Leukaemia (AML) and Acute Lymphoblastic Leukaemia (ALL), to correlate its expression in marrow and peripheral blood mononuclear cells, and to verify the extent of its use as a complete remission predictor after induction treatment. The study subjects consisted of patients who were diagnosed as AML and ALL with marrow and peripheral blood examination performed at the Department of Clinical Pathology Dharmais Cancer Hospital and CiptoMangunkusumo Hospital. Based on this study, it is revealed that the active caspase-3 expression in mononuclear marrow cells was higher in AML compared to ALL (p=0.033), active caspase-3 expression in marrow showed a strong correlation (r=0.764; p=0.001) to peripheral blood mononuclear cells in ALL and a medium correlation (r=0.594; p=0.042) in AML. The expression of the active caspase-3 in ALL patients was lower in complete remission patients compared to the non-complete remission patients. Regarding to this study it is recommended to measure the active caspase-3 along with molecules integrating in apoptosis signaling pathways such as cytochrome-c and in the formation of apoptosome.

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9

DEMİRCİOĞLU, Sinan, Ayvaz YELER, and Ali DOĞAN. "Evaluation of Serum B12 Level in Patients with Acute Myeloid Leukemia." LLM Dergi 2, no. 4 (October 30, 2018): 89–92. http://dx.doi.org/10.5578/llm.67773.

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10

ÖCAL, Ramazan, Zübeyde Nur ÖZKURT, Mehmet Sezgin PEPELER, Gizem TOKER, and Münci YAĞCI. "Acute Myeloid Leukemia Presented with Severe Erythrodermia and Dermatopathic Lymphadenitis." LLM Dergi 1, no. 1 (January 15, 2017): 18–21. http://dx.doi.org/10.5578/llm.45471.

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11

Sativa, Shania Ocha. "PENGARUH GENETIK, GAYA HIDUP DAN LINGKUNGAN PADA KEJADIAN LEUKEMIA MIELOBLASTIK AKUT." JIMKI: Jurnal Ilmiah Mahasiswa Kedokteran Indonesia 8, no. 1 (February 26, 2020): 83–88. http://dx.doi.org/10.53366/jimki.v8i1.42.

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ABSTRAK Leukemia Mieloblastik Akut merupakan salah satu kelainan sel darah berupa keganasan yang ditandai dengan proliferasi dan pertumbuhan dari sel hematopoietik yang imatur di dalam sum-sum tulang dan darah. Pasien dengan AML memiliki gejala khas seperti mudah lelah, sulit bernapas atau sesak, perdarahan, dan tanda-tanda infeksi yang merupakan akibat dari kegagalan sumsum tulang. Penyakit ini dapat didiagnosis dengan pemeriksaan darah lengkap, analisis darah tepi, serta pemeriksaan sampel sumsum tulang. Insidensi penyakit ini tinggi pada orang dewasa. Hampir 80% kasus leukemia akut terjadi pada orang dewasa dan 20% kasus leukemia akut terjadi pada anak-anak. Kejadiannya meningkat seiring dengan bertambahnya usia seseorang. Oleh karena penyebab pasti dari leukemia belum diketahui, beberapa faktor risiko terkait pernyakit ini telah diidentifikasi. Beberapa faktor risiko absolut dan relatif dari leukemia akut dikelompokkan menjadi faktor genetik, gaya hidup dan lingkungan. Merokok, obesitas, konsumsi alkohol serta asupan makanan berpengaruh terhadap perkembangan dari leukemia sendiri. Faktor risiko lingkungan yang dapat menyebabkan AML ialah paparan benzen, radiasi ionisasi dosis tinggi, agen kemoterapetik, dan paparan zat atau bahan elektromagnetik. Kata Kunci: Faktor Risiko, Keganasan, Leukemia Mieloblastik Akut ABSTRACT Acute Myeloblastic Leukemia (AML) is a blood cell disorder in the form of malignancy characterized by the proliferation and growth of immature hematopoietic cells in the bone marrow and blood. Patients with AML have typical symptoms such as fatigue, difficulty breathing or tightness, bleeding, and signs of infection that result from bone marrow failure. The disease can be diagnosed by a complete blood count, peripheral blood analysis, and examination of bone marrow samples. The incidence of this disease is high in adults. Nearly 80% of cases of acute leukemia occur in adults and 20% of cases of acute leukemia occur in children. The incidence increases with age. Because the exact cause of leukemia is unknown, several risk factors associated with this disease have been identified. Some absolute and relative risk factors for acute leukemia are grouped into genetic, lifestyle and environmental factors. Smoking, obesity, alcohol consumption and food intake influence the development of leukemia itself. Environmental risk factors that can cause AML are benzene exposure, high dose ionizing radiation, chemotherapeutic agents, and exposure to substances or electromagnetic materials. Keywords: Risk Factor, Malignancy, Acute Myeloid Leukemia

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12

Tatar, Selim, and Kurtuluş Öngel. "A case diagnosis as acute myeloid leukemia on a Family Medicine Policlinic." Journal of Turkish Family Physician 10, no. 2 (June 25, 2019): 109–12. http://dx.doi.org/10.15511/tjtfp.19.00299.

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Biró, Adrienn, László Ternyik, Miklós Egyed, István Bálint, Veronika Czoma, Béla Kajtár, and Zsolt Káposztás. "Appendicitis képében jelentkező akut promyelocytás leukaemia kiújulása allogén csontvelő-transzplantációt követően." Orvosi Hetilap 161, no. 51 (December 20, 2020): 2171–74. http://dx.doi.org/10.1556/650.2020.31943.

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Összefoglaló. Az akut myeloid leukaemia ellátása primeren hematológiai feladat, relapsusa során is ritka a sebészeti szövődmény. Esettanulmányunkban egy 46 éves férfi beteget mutatunk be, akinél rutinvérvétel során felfedezett akut promyelocytás leukaemia miatt történt hematológiai kezelés. Alapbetegsége komplett molekuláris remisszióba jutott, ezt követően fenntartó kezeléseket kapott, de betegsége kiújult. Reindukciós kezelést követően fehérvérsejtszáma normalizálódott, de nem jutott molekuláris remisszióba. További kezelés után a férfi testvérétől gyűjtött őssejttel allogén csontvelő-transzplantáció történt. Közel egy éve molekuláris remisszióban volt a beteg, amikor jelentkeztek jobb alhasi panaszai neutropenia, a C-reaktív protein magas értéke és pozitív hasi ultrahang mellett. Akutan laparoszkópos módszerrel távolítottuk el a láthatóan gyulladt féregnyúlványt. A hisztológiai feldolgozás során az akut promyelocytás leukaemia manifesztációja igazolódott. Tekintettel arra, hogy közben csontvelői relapsus is kialakult, újabb reindukciós kezelés, és másik testvérétől vett őssejtekkel ismételten allogén csontvelő-transzplantáció történt. Az általunk ismert irodalomban appendicitis képében jelentkező akut promyelocytás leukaemia relapsusáról nem találtunk közleményt, ezért tartottuk esetünket publikációra érdemesnek. Orv Hetil. 2020; 161(51): 2171–2174. Summary. The treatment of acute myeloid leukemia is primarily hematological. Surgical complications are rare even during relapse. We present the case of a 46-year-old man who was diagnosed with acute promyelocytic leukemia after a routine blood test. Following hematological treatment, molecular remission was achieved, and he was on maintenance therapy, when his leukemia relapsed. He received re-induction treatment and his white blood cell count normalised, however, molecular remission was not reached. After further treatment, allogeneic bone marrow transplantation was performed with stem cells collected from his brother. He developed right lower quadrant abdominal pain with neutropenia, elevated C-reactive protein and abdominal ultrasound report showed thickened appendix after nearly one year of molecular remission. We performed en emergency laparoscopic appendicectomy to remove the inflamed appendix. Histology confirmed acute promyelocytic leukemia manifestation in the appendix. Given the repeated bone marrow relapse, he received re-induction treatment and allogeneic bone marrow transplantation again with stem cells collected from his another brother. To the best of our knowledge, no previous report in the literature can be found of appendicitis mimicking relapse of acute promyelocytic leukemia, thus, this case report holds merit for publication. Orv Hetil. 2020; 161(51): 2171–2174.

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Beytemür, Ozan. "Acute myeloid leukemia diagnosed with soft tissue mass in the right thigh." Joint Diseases and Related Surgery 26, no. 1 (March 16, 2015): 56–59. http://dx.doi.org/10.5606/ehc.2015.13.

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Mulatsih, Sri, Sunarto Sunarto, and Sutaryo Sutaryo. "Fusi Gen Translocation Ets Leukemia-Acute Myeloid Leukemia 1 (Tel-Aml1) Sebagai Faktor Prognosis pada Leukemia Limfoblastik Akut Anak." Sari Pediatri 10, no. 6 (November 29, 2016): 404. http://dx.doi.org/10.14238/sp10.6.2009.404-9.

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Fungsi fusi gen TEL-AML1 dalam leukemogenesis adalah mempengaruhi kunci proses pengaturan, termasuk kenaikan proses cell-renewal yang tidak terkontrol, menghentikan proliferasi dan diferensiasi yang menyebabkan resistensi terhadap proses apoptosis. Banyak studi menghasilkan data bahwa prognosis pasien leukemia limfoblastik akut (LLA) dengan fusi gena TEL-AML1 masih kontroversi, khususnya prognosis jangka panjang. Banyak penelitian yang menghubungkan adanya fusi gena ini dengan resistensi terhadap kemoterapi, dan lainnya menggunakan minimal residual disease (MRD) untuk melihat respons terhadap pengobatan. Adanya co-existences gena lain bisa memberikan kontribusi terhadap prognosis pasien LLA dengan fusi gen TEL-AML1. Dibutuhkan lebih banyak studi translasional untuk lebih memahami peran fusi gen dalam klinik. Pengetahuan mendasar mekanisme molekular pada leukemia sangat penting, khususnya dalam penanganan pasien. Pemahaman yang lebih baik tentang patogenesis leukemia bisa menghasilkan pengertian dan pengetahuan baru untuk menyusun strategi baru dalam penanganan pasien LLA yang didasarkan kaidah molekular

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TERZİ DEMİRSOY, Esra, Elif BİRTAŞ ATEŞOĞLU, Pınar TARKUN, Özgür MEHTAP, Ayfer GEDÜK, and Abdullah HACIHANEFİOĞLU. "Soluble Programme Death- Ligand 1(sPDL-1) Identify Acute Myeloid Leukemia Patients." LLM Dergi 2, no. 3 (July 16, 2018): 65–70. http://dx.doi.org/10.5578/llm.67519.

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ÖZÜLKER, Filiz, Tamer ÖZÜLKER, and Ebru ÖZGÖNENEL. "Myeloid Sarcoma as an Extramedullary Manifestation of Acute Myeloid Leukemia Detected with 18F-FDG PET/CT: Case Report." Turkiye Klinikleri Journal of Case Reports 24, no. 4 (2016): 306–9. http://dx.doi.org/10.5336/caserep.2015-47599.

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ANDIÇ, Neslihan, Beyhan DURAK ARAS, Eda TATLIPINAR, Sevgi ÖZPOLAT, Hava ÜSKÜDAR TEKE, Eren GÜNDÜZ, and Olga Meltem AKAY. "Del(6)(p22)In De Novo Acute Myeloid Leukemia As a Sole Genetic Abnormality." LLM Dergi 1, no. 2 (April 15, 2017): 55–57. http://dx.doi.org/10.5578/llm.57359.

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GÖREN ŞAHIN, Deniz, Eren GÜNDÜZ, Buket YURTERİ, Ahmet YEŞİLYURT, Neslihan ANDIÇ, Hava ÜSKÜDAR TEKE, and Olga Meltem AKAY. "Epigenetic Regulation of the 'Peroxisome Proliferator Actived Receptor-Gamma' Gene in Acute Myeloid Leukemia Patients." Turkiye Klinikleri Journal of Medical Sciences 39, no. 4 (2019): 375–80. http://dx.doi.org/10.5336/medsci.2019-66573.

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Mulatsih, Sri, and Silvia Meiliana. "Leukemia Limfoblastik Akut pada Anak Usia di Bawah Satu Tahun." Sari Pediatri 11, no. 3 (November 24, 2016): 219. http://dx.doi.org/10.14238/sp11.3.2009.219-22.

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Latar belakang. Angka kejadian leukemia limfoblastik akut (LLA) pada anak usia di bawah satu tahun sekitar 2%-5% dari seluruh pasien LLA dengan event-free survival (EFS) untuk 3 sampai 6 tahun hanya 22%-54%. Prognosis LLA pada anak di bawah usia 1 tahun dipengaruhi beberapa faktor, di antaranya usia pada saat diagnosis, angka leukosit awal yang tinggi, ekspresi CD10, ekspresi myeloid-associated antigen, translokasi 11q23/MLL (mixed-lineage leukemia) rearrangements, dan respon pada terapi awal.Tujuan. Memberikan gambaran klinis dan luaran terapi pasien LLA anak usia di bawah satu tahun.Metode. Laporan empat kasus LLA pada bayi mengenai perjalanan klinis, perawatan, dan hasil akhir pengobatan yang dirawat di Bagian Ilmu Kesehatan Anak RSUP Dr. Sardjito, Yogyakarta.Hasil. Telah dirawat empat kasus LLA anak usia di bawah satu tahun. Satu kasus drop out dari pengobatan dan satu kasus meninggal pada fase awal pengobatan karena syok septik. Pasien tersebut datang dengan jumlah leukosit 2400/μL, CD10+ (40%), dan imunofenotiping menunjukkan sel pre-B. Terapi yang diberikan adalah protokol risiko tinggi. Satu kasus yang sudah selesai pengobatan mempunyai jumlah leukosit awal 29.400/ μL, CD10+ (68%), dan imunofenotiping menunjukkan sel pre-B. Satu pasien masih dalam pengobatan. Keempat pasien mengalami komplikasi berupa perdarahan dan sepsis.Kesimpulan. Luaran terapi pasien LLA di bawah 1 tahun cukup baik, apabila dilakukan pendekatan terapi serta perawatan suportif yang optimal. Sangat perlu dilakukan pemeriksaan imunofenotiping, sitogenetik ataupun molekular untuk membantu stratifikasi risiko awal sehingga pengobatan dapat lebih tepat.

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Lunesia, Rangga, and Irza Wahid. "CHRONIC MIELOMONOSITIC LEUKEMIA PADA USIA MUDA." Jurnal Kesehatan Andalas 7 (July 29, 2018): 54. http://dx.doi.org/10.25077/jka.v7i0.828.

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Chronic Mielomonositic Leukemia (CMML) adalah keganasan heterogen yang ditandai dengan monositosis di darah perifer (>1x109/L), terdapat kelainan mielodisplastik dan mieloproliferatif di sumsum tulang, dan memiliki kecendrungan untuk bertransformasi menjadi leukemia myeloid akut. Angka kejadian CMML sangat jarang, di Indonesia tercatat hanya 2,5 % kasus dari keseluruhan MDS. Pengobatan pada MP-CMML dengan jumlah blast sedikit adalah pemberian terapi sitoreduktif yaitu hydroxyurea yang bertujuan mengontrol proliferasi myelomonositic sel dan mengurangi organomegali. Telah dilaporkan suatu kasus laki-laki 28 tahun dengan keluhan pucat. Pada pemeriksaan fisik ditemukan konjungtiva anemis dan splenomegali. Pemeriksaan laboratorium didapatkan hemoglobin 6.5 gr/dl, leukosit: 93.540/mm3, hitung jenis: 1/0/6/42/8/27. Pemeriksaan BMP menunjukkan aktivitas Granulopoeitik: meningkat, ditemukan mieloblast 3%, Promielosit 3%, monoblast 2%, Promonosit 1%, dominasi monosit 33%, ditemukan juga dysplasia seperti pseudo pelgerhuet, dengan kesan sesuai gambaran Chronic Mielomonositic Leukemia. Pada pasien ini dengan jumlah leukosit > 13 x 109/L termasuk kedalam MP-CMML diberikan terapi hydroxyurea. Follow up setelah pemberian terapi Hb 8.8 gr/dl, Leukosit 38.200/mm3, pada hitung jenis: 0/1/5/45/7/23.

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Kern, Wolfgang, and Susanne Schnittger. "Monitoring of minimal residual disease in acute myeloid leukemia Monitorisierung minimaler Resterkrankung bei akuter myeloischer Leukämie." LaboratoriumsMedizin 29, no. 5 (January 1, 2005): 343–67. http://dx.doi.org/10.1515/jlm.2005.048.

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Bedekovics, Judit, László Rejtő, Béla Telek, Miklós Udvardy, Anikó Újfalusi, Éva Oláh, Zsuzsa Hevessy, János Kappelmayer, Béla Kajtár, and Gábor Méhes. "Immunohistochemical demonstration of NPMc+ acute myeloid leukemia: biological and clinical features related to cytoplasmic nucleophosmin expression." Orvosi Hetilap 150, no. 22 (May 1, 2009): 1031–35. http://dx.doi.org/10.1556/oh.2009.28623.

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A nucleophosmin gén (NPM1) 12-es exonjának mutációja, jelenlegi ismereteink szerint, a leggyakoribb genetikai eltérés akut myeloid leukaemiában. Az eddigi beszámolók alapján kimutatásával a betegség sajátos biológiájú és kedvező lefolyású formája határozható meg, amely a leukaemiák WHO-osztályozásában 2008-tól külön csoportként kerül említésre. A mutáció hatására megváltozik a kódolt fehérje sejten belüli eloszlása, és az NPM fehérje a sejtmag helyett a citoplazmában halmozódik fel (NPMc+). Ez a jelenség, amely a kizárólag mutáns géntermék kapcsán figyelhető meg, szövettani vizsgálat keretében immunhisztokémiával is kimutatható. Jelen tanulmányunkban hazai körülmények között először vizsgáltuk az NPM-mutáció előfordulását felnőttkori AML-ben immunhisztokémia módszerével. A 2005 és 2008 között diagnosztizált összesen 41 eset részletes kiértékelése során 6 esetben (14,6%) észleltünk citoplazmikus reakciót, valamennyi de novo jelentkező és jellegzetes citogenetikai eltérést nem mutató AML-esetek közül került ki (6/23, 26,1%), egy kivételével nőbetegekben. A blasztsejtek alacsony CD34-, c-kit- és HLA-DR-expressziója alapján a NPMc+ AML a nem érintett esetektől jól elkülöníthetőnek bizonyult, ezek a markáns jellegzetességek az eddig közölt külföldi adatokkal teljes mértékben megegyeznek. Tapasztalataink alapján az NPM-mutáció immunhisztokémiai vizsgálata egyszerűen beépíthető a hétköznapi hematológiai diagnosztikai gyakorlatba.

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Harto, Aryo, and Chastine Fatichah. "SEGMENTASI DAN PEMISAHAN SEL DARAH PUTIH BERSENTUHAN MENGGUNAKAN K-MEANS DAN HIERARCHICAL CLUSTERING ANALYSIS PADA CITRA LEUKEMIA MYELOID AKUT." JUTI: Jurnal Ilmiah Teknologi Informasi 15, no. 2 (July 1, 2017): 162. http://dx.doi.org/10.12962/j24068535.v15i2.a599.

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MUTLAY, Feyza, Ömür Gökmen SEVİNDİK, Şerife SOLMAZ, Celal ACAR, Sema ALPÇAVUŞ, Ahmet SEYHANLI, Mehmet Ali ÖZCAN, et al. "Retrospective Evaluation of Patients with and without Primary Antifungal Prophylaxis During Remission Induction Chemotherapy in Patients with Acute Myeloid Leukemia." LLM Dergi 4, no. 1 (January 31, 2020): 1–9. http://dx.doi.org/10.5578/llm.69347.

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Arguni, Eggi, Sasmito Nugroho, Sri Mulatsih, and Sutaryo. "Petanda Imunofenotip CD10 Sendiri Atau Bersama CD3 Atau CD13/CD33 sebagai Faktor Prognosis Luaran Terapi Fase Induksi Leukemia Limfoblastik Akut Anak." Sari Pediatri 19, no. 5 (April 16, 2018): 260. http://dx.doi.org/10.14238/sp19.5.2018.260-6.

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Latar belakang. Kegagalan terapi masih menjadi penyumbang terbesar bagi mortalitas anak dengan leukemia limfoblastik akut (LLA). Ekspresi CD10 menentukan diferensiasi sebagian besar leukemia sel B. Petanda imunofenotip untuk LLA sel T, yaitu CD3, dan myeloid antigen, yaitu CD13/CD33, dengan jumlah kecil juga terekspresi pada B-ALL. Tujuan. Mengetahui pengaruh ekspresi CD10 sendiri atau bersama dengan CD3 atau CD13/CD33 terhadap luaran terapi fase induksi LLA anak.Metode. Desain penelitian menggunakan nested case-control. Sampel penelitian merupakan pasien LLA anak yang baru terdiagnosis di INSKA RSUP Dr Sardjito Yogyakart Januari 2006-Desember 2009, dilengkapi pemeriksaan imunofenotip saat penegakan diagnosis. Analisis bivariat dan multivariat digunakan untuk menentukan faktor prognosis independen terhadap luaran terapi. Hasil. Seratus enam puluh tujuh pasien diikutsertakan dalam penelitian ini. Faktor usia dan ekspresi CD10 merupakan faktor prognosis independen yang menentukan luaran terapi fase induksi. Kelompok usia <1 tahun dan >10 tahun akan mengalami gagal remisi (OR 3,1; IK95%: 1,271-7,625; p=0,013), dan LLA anak dengan CD10 negatif akan mengalami gagal remisi 2,7 kali lebih tinggi dibanding CD10 positif (IK95%: 1,171-6,232; p=0,020). Kesimpulan. CD10 negatif merupakan faktor prognosis independen terhadap kejadian gagal remisi. Ekspresi imunofenotip CD10 bersama CD3 dan CD13/CD33, bukan merupakan faktor prognosis bagi luaran terapi fase induksi.

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AKKUŞ, Erman, Eda Büşra BABAYİĞİT, Sinem CİVRİZ BOZDAĞ, Meltem KURT YÜKSEL, Pervin TOPÇUOĞLU, and Selami Koçak TOPRAK. "A Case of Acute Myeloid Leukemia Transformed from Myelodisplastic Syndrome Which Relapsed with der(1) t(1;19) Chromosomal Abnormality After Allogenic Transplantation." LLM Dergi 4, no. 1 (January 31, 2020): 18–21. http://dx.doi.org/10.5578/llm.67424.

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Mahul, P., Marie-Antoinette Piens, D. Guyotat, J. Godard, E. Archimbaud, B. Bui-Xuan, and J. Motin. "Disseminated Geotrichum capitatum Infection in a Patient with Acute Myeloid Leukemia: Disseminierte Geotrichum capitatum-Infektion bei einem Patienten mit akuter myeloischer Leukamie." Mycoses 32, no. 11 (April 24, 2009): 573–77. http://dx.doi.org/10.1111/j.1439-0507.1989.tb02184.x.

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GÖKMEN, Ayla, Ender SOYDAN, Zafer GÖKGÖZ, Ozan ÖZKUMUR, Şahika ŞEN, Önder ARSLAN, and Muhit ÖZCAN. "Intensive Sequential Chemotherapy with Etoposide, Mitoxantrone and Ctarabine (EMA) as Salvage in Patients with Acute Myeloid Leukemia Relapsing After Allogeneic Stem Cell Transplantation a Retrospective Analysis." LLM Dergi 3, no. 3 (December 10, 2019): 51–54. http://dx.doi.org/10.5578/llm.68966.

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Septiantoro, Bayu Prio, Dyah Aryani Perwitasari, and Indra Pradipta. "Penggunaan Sefepim Untuk Demam Neutropenia Pada AML di RSUP Dr. Kariadi Semarang." Medica Hospitalia : Journal of Clinical Medicine 7, no. 1 (May 18, 2020): 23–26. http://dx.doi.org/10.36408/mhjcm.v7i1.423.

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Latar belakang: Demam neutropenia merupakan salah satu efek samping kemoterapi yang paling serius, karena adanya infeksi dapat berkembang dengan cepat dan dapat mengancam jiwa. Antibiotik yang diindikasikan untuk profilaksis pada pasien demam neutropenia diantaranya adalah sefepim. Penelitian ini bertujuan untuk mengetahui durasi kebutuhan sefepim terhadap perbedaan rejimen kemoterapi AML, serta luaran terapinya di RSUP Dr. Kariadi, Semarang. Metode: Penelitian ini menggunakan rancangan deskriptif dengan pengambilan data secara restrospektif dari bulan Juni 2018 hingga April 2019 di satu ruangan rawat inap RSUP Dr. Kariadi, Semarang. Kriteria inklusi adalah pasien usia 18-64 tahun dengan diagnosa AML yang mengalami demam neutropenia dengan riwayat pernah menjalani kemoterapi, mendapatkan terapi antibiotik sefepim. Kriteria eklusi dalam penelitian ini yaitu pasien yang alergi terhadap sefepim, yang tidak melanjutkan pengobatannya, dengan program cangkok sumsum tulang dan dengan adanya diagnosa sepsis/septik syok sebelum diberikannya sefepim. Hasil: Total sebanyak 15 pasien memenuhi kriteria inklusi. Durasi pemberian sefepim yang paling banyak adalah kelompok dengan pemberian 8-14 hari (46,7%), selanjutnya ?7 hari (33,3%), sedangkan pemberian selama >14 hari tidak ditemukan. Pasien yang meninggal pada penelitian ini sebanyak 3 pasien (20%), dengan 2 pasien diantaranya teridentifikasi mengalami sepsis karena sefepim yang resisten akibat patogen ESBL E. coli, sedangkan satu lainnya tidak diketahui patogen penyebabnya. Kesimpulan: Pasien dengan rejimen intensif rata-rata memerlukan durasi terapi yang lebih lama. Munculnya patogen ESBL khususnya E. coli mempunyai luaran yang jelek dan angka kematian yang lebih tinggi, sehingga kita sarankan untuk menggunakan karbapenem daripada sefepim untuk kondisi ini. Kata kunci: Demam neutropenia, leukemia myeloid akut, sefepim Backgound: Febrile neutropenia is one of the most serious side effects of chemotherapy, because the infection can develop rapidly which can be life-threatening. Cefepime is drug of choice that indicated for prophylaxis in patients with febrile neutropenia. The aim of this study was to determine the duration of the cefepime needs of differences in AML chemotherapy regimens, and the outcomes in Dr. Kariadi General Hospital Center, Semarang. Method: The study used descriptive design with retrospective data collection from June 2018 to April 2019 in an inpatient room at Dr. Kariadi General Hospital Center, Semarang. The inclusion criteria are patients aged 18-64 years old with diagnosis of AML who has febrile neutropenia with a history of having undergone chemotherapy with cefepime prophylaxis. The exclusion criteria in this study were allergy to cefepime, patients who did not continue their treatment, bone marrow transplant programs and diagnosis of sepsis / septic shock before the administration of cefepime. Result: A total of 15 patients met the inclusion criteria. The most duration of cefepime was in the group with 8-14 days (46,7%), then ?7 days (33,3%), whereas> 14 days were not found. The patients who died in this study were 3 patients (20%), with 2 patients identified as having sepsis due to the pathogen ESBL E. coli cefepime resistant, while the other one did not know the causative pathogen. Conclusion: Patients with an intensive regimen require a longer duration therapy. The emergence of ESBL pathogens especially E. coli has poor outcomes and a higher mortality rate, so we recommend using carbapenem rather than cefepime for this condition. Keywords: Febrile neutropenia, acute myeloid leukemia, cefepime

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Steidl, Christian, Rainer Schabla, Ulrich Germing, Barbara Hildebrandt, Thomas Noesslinger, Michael Pfeilstoecker, Aristoteles Giagounidis, et al. "Sequential Cytogenetic Analyses of 577 Patients with Myelodysplastic Syndromes: Correlations between Initial Karyotype, Cytogenetic Dynamics, and Clinical Course." Blood 106, no. 11 (November 16, 2005): 2531. http://dx.doi.org/10.1182/blood.v106.11.2531.2531.

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Abstract Myelodysplastic syndromes are dynamic diseases presenting with different clinical courses ranging from almost stable courses to rapid progression to acute myeloid leukemias. Karyotype is one of the most important prognostic factors and defines subgroups of favorable, intermediate and adverse prognosis. So far, comparably low attention has been payed on karyotypic changes occuring in sequential cytogentic examinations during the course of the disease. We retrospectively examined karyotypes of 577 patients with MDS or AML with previous history of MDS and at least two successfully performed metaphase analyses. The cytogenetic and clinical data was collected from 5 different centres of the “Kompetenznetz Akute und Chronische Leukaemien” (Duesseldorf, Duisburg, Freiburg, Goettingen, Vienna). Compared to the inital karyotype, karyotype evolution was defined as acquisition of additional aberrations, expansion of an aberrant clone by more than 20% or development of a completely aberrant karyotype after a former mosaic karyotype. According to these criteria, we found karyotype evolution in 155 cases (27%). 2–8 cytogenetic examinations have been performed per case. In 121 cases additional aberrations occured and in 34 cases the aberrant clone expanded in a subsequent analysis. In the group of patients with expansion of the aberrant clone the most frequent karyotypes were 5q- (9x) and +8 (7x). The most frequent aberrant karyotypes later acquiring additional aberrations were complex (22x) and karyotypes with two aberrations (11x), but in the vast majority of cases additional aberrations occurred on basis of a normal karyotype (70x). The most frequent additional aberrations were −7/7q- (23x), 5q- (11x) and +8 (11x). In the group of initially normal karyotypes patients with karyotype evolution had a shorter survivial (p<0.05). In summary, partial or complete momosomy 7 is the most frequent additional aberration in sequential cytogenetic analyses, indicating progression of disease. Due to their genetic instability complex karyotypes or karyotypes with 2 aberrations typically acquire additional anomalies in the course, whereas karyotypes with 5q- and +8 tend to have comparably stable courses. Furthermore, we show that also cases with a normal karyotype can harbour genetic instability as in 12% of all cases a normal karyotype evolved into an aberrant karyotype which was associated with a worse prognosis compared to stable normal karyotypes. Subgroup analyses are necessary to address correlations with therapy, time to AML progression, and the dependency on examination intervals.

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Haferlach, T., C. Schoch, and W. Hiddemann. "Die neue WHO-Klassifikation zur Einteilung der akuten myeloischen Leukamien (AML): Vorteile und Probleme im Vergleich zur FAB (French-American-British)-Klassifikation. The New WHO Classification for Acute Myeloid Leukemias: Comparison to the FAB Classification." Laboratoriums Medizin 26, no. 1-2 (February 2002): 19–22. http://dx.doi.org/10.1046/j.1439-0477.2002.02002.x.

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Haferlach, T., C. Schoch, and W. Hiddemann. "Die neue WHO-Klassifikation zur Einteilung der akuten myeloischen Leukamien (AML): Vorteile und Probleme im Vergleich zur FAB (French-American-British)-Klassifikation/The New WHO Classification for Acute Myeloid Leukemias: Comparison to the FAB Classification." LaboratoriumsMedizin 26, no. 1/2 (January 1, 2002): 19–22. http://dx.doi.org/10.1515/labmed.2002.004.

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Keskin, Mehmet Zeynel, and Yusuf Özlem İlbey. "Massive Hematuria in an Acute Myeloid Leukemia Patient That Required Transcatheter Embolization." Journal of Tepecik Education and Research Hospital, 2020. http://dx.doi.org/10.5222/terh.2020.34635.

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35

Hartoyo, Vinson, and Andree Kurniawan. "Pendekatan Diagnostik Terhadap Leukemia Akut." Medicinus 6, no. 1 (August 4, 2018). http://dx.doi.org/10.19166/med.v6i1.1138.

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Acute leukemia is the most common form of cancer in children, comprises approximately 30 percents of all childhood malignancies, with acute lymphoblastic leukemia (ALL) being five times more common than acute myeloid leukemia (AML)1. Despite the advance in the treatment of acute lymphobalstic leukemia, five-year event free survival rate still remain quite low in group of patient with advanced age of onset (40% or below in later age)2,3,4. A case of 17 year old girl presented with 3 day onset of profuse bleeding from her nostril, ear, gums and gastrointestinal tract (melena and hematemesis). Blood count and peripheral blood smear revealed a pancytopenia with 26% blast count lymphocyte dominant, and reticulocyte percentage of 0.26% which is signalling a bone marrow failure. The patient was planned to undergo a bone marrow transplant before finally died on third day of care.

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Kayser, Sabine, and Richard F. Schlenk. "Genetische und immunzytometrische Diagnostik bei der akuten myeloischen Leukämie und ihre Bedeutung für die Wahl der Therapiestrategie/Genetic and immunophenotypical diagnostics for acute myeloid leukemia and their implication on treatment strategy." LaboratoriumsMedizin 36, no. 1 (January 1, 2012). http://dx.doi.org/10.1515/jlm-2011-0005.

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ZusammenfassungBei der akuten myeloischen Leukämie (AML) spielen zyto- und molekulargenetische Veränderungen eine zentrale Rolle in der Pathogenese, sind unverzichtbar für die diagnostische Kategorisierung, stellen die wichtigsten Faktoren für die Vorhersage des Therapieansprechens und der klinischen Prognose dar und werden zunehmend für spezifische Genotyp-adaptierte Induktions- und Konsolidierungsstrategien genutzt. Insbesondere für die AML-Entitäten Core-binding-factor AML, charakterisiert durch die t(8;21) und die inv(16)/t(16;16), und AML mit

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