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1

Whitehead, VM, DS Rosenblatt, MJ Vuchich, JJ Shuster, A. Witte, and D. Beaulieu. "Accumulation of methotrexate and methotrexate polyglutamates in lymphoblasts at diagnosis of childhood acute lymphoblastic leukemia: a pilot prognostic factor analysis." Blood 76, no. 1 (July 1, 1990): 44–49. http://dx.doi.org/10.1182/blood.v76.1.44.44.

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Abstract Lymphoblasts in bone marrow samples, obtained from 43 children with acute lymphoblastic leukemia at diagnosis, were incubated with 1.0 mumols/L [3H] methotrexate for 24 hours in vitro. Nonexchangeable methotrexate and methotrexate polyglutamates were separated and quantitated. Event-free survival at 5 years was 38% +/- 9% for all 43 patients (27 failures), and 44% +/- 10% for the 35 with non-T, non-B- cell acute lymphoblastic leukemia (20 failures). Of these 35 children, those whose lymphoblasts accumulated more than 100 pmol methotrexate and 500 pmol methotrexate polyglutamates per billion cells experienced better 5-year event-free survival than those whose lymphoblasts did not (65% +/- 12% v 22% +/- 9%, P = .010). This difference characterized “good-risk” patients who were female (P = .014), less than age 7 at diagnosis (P = .005), or had low initial white blood cell counts (less than 20 X 10(9)/L, P = .018). Findings were similar for the 43 children with acute lymphoblastic leukemia and for the “good-risk” children in this total group. Thus, the ability of lymphoblasts to accumulate methotrexate and form methotrexate polyglutamates may be important to the curative properties of current therapy of acute lymphoblastic leukemia in children, particularly for “good-risk” patients. In such patients, inherent rather than acquired drug resistance may be the initial event leading to treatment failure.
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2

Whitehead, VM, DS Rosenblatt, MJ Vuchich, JJ Shuster, A. Witte, and D. Beaulieu. "Accumulation of methotrexate and methotrexate polyglutamates in lymphoblasts at diagnosis of childhood acute lymphoblastic leukemia: a pilot prognostic factor analysis." Blood 76, no. 1 (July 1, 1990): 44–49. http://dx.doi.org/10.1182/blood.v76.1.44.bloodjournal76144.

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Lymphoblasts in bone marrow samples, obtained from 43 children with acute lymphoblastic leukemia at diagnosis, were incubated with 1.0 mumols/L [3H] methotrexate for 24 hours in vitro. Nonexchangeable methotrexate and methotrexate polyglutamates were separated and quantitated. Event-free survival at 5 years was 38% +/- 9% for all 43 patients (27 failures), and 44% +/- 10% for the 35 with non-T, non-B- cell acute lymphoblastic leukemia (20 failures). Of these 35 children, those whose lymphoblasts accumulated more than 100 pmol methotrexate and 500 pmol methotrexate polyglutamates per billion cells experienced better 5-year event-free survival than those whose lymphoblasts did not (65% +/- 12% v 22% +/- 9%, P = .010). This difference characterized “good-risk” patients who were female (P = .014), less than age 7 at diagnosis (P = .005), or had low initial white blood cell counts (less than 20 X 10(9)/L, P = .018). Findings were similar for the 43 children with acute lymphoblastic leukemia and for the “good-risk” children in this total group. Thus, the ability of lymphoblasts to accumulate methotrexate and form methotrexate polyglutamates may be important to the curative properties of current therapy of acute lymphoblastic leukemia in children, particularly for “good-risk” patients. In such patients, inherent rather than acquired drug resistance may be the initial event leading to treatment failure.
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3

Madabhavi, Irappa, Mitul Modi, Malay Sarkar, Sandeep K S, Mansi Shah, and Vinay Sakaleshpura Mallikarjuna. "Cancrum Oris(Noma): An Early Sign of Acute Lymphoblastic Leukemia Relapse." American Journal of Clinical Pathology 152, Supplement_1 (September 11, 2019): S49. http://dx.doi.org/10.1093/ajcp/aqz113.030.

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Abstract Cancrum oris is an infectious disease, which involves the orofacial tissues and adjacent neighboring structures in its fulminant course. Cancrum oris can occur rarely in chemotherapy-induced neutropenic patients with acute lymphoblastic leukemia. This rare case report reveals that cancrum oris can be a sign of acute lymphoblastic leukemia relapse. It is characterized by gangrenous lesions on skin with fine-needle aspiration cytology smear from the lesion showing infiltration of lymphoblasts. Cancrum oris can occur rarely in chemotherapy-induced neutropenic patients with acute lymphoblastic leukemia, but the presentation as an early sign of extramedullary disease relapse has not been documented in literature. Here we report a case of cancrum oris in a 27-year-old woman who presented with redness and swelling of the upper lip and infranasal area. She had a known case of acute lymphoblastic leukemia diagnosed 6 months back and was on regular multiagent chemotherapy for the same. Clinical examination revealed gangrenous lesions on infranasal, intranasal, and area involving the upper lip. Complete blood count, bone marrow aspiration, and cytology did not show any lymphoblasts. Blood culture and swab culture from the gangrenous area were sterile. Patient did not get better even after 7 days of broad-spectrum antibiotic treatment. With a high degree of clinical suspicion of isolated extramedullary relapse, fine-needle aspiration cytology from marginal and gangrenous area was taken and revealed infiltration of soft tissues by lymphoblasts. After receiving four cycles of multiple chemotherapy drugs, the skin lesions resolved. Treatment of cancrum oris involves the correction of the underlying immune status, antibiotics, and surgical reconstruction. The rare possibility of relapse of acute lymphoblastic leukemia presenting as cancrum oris should be kept in mind in patients with acute lymphoblastic leukemia on chemotherapy with skin manifestations.
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4

Salzberg, Dana B., Amy K. Keating, Jian-zhe Cao, Susan Sather, Kimberley Hill, Adil Anwar, and Douglas K. Graham. "Ectopic Expression of Mer Receptor Tyrosine Kinase in Childhood T Cell Acute Lymphoblastic Leukemia." Blood 104, no. 11 (November 16, 2004): 4310. http://dx.doi.org/10.1182/blood.v104.11.4310.4310.

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Abstract Tyrosine kinases play an important role in normal cellular growth and differentiation. Deregulation of tyrosine kinase activity can result in cellular transformation leading to the development of human cancer. The Mer receptor tyrosine kinase, initially cloned from a human B lymphoblastoid cell line, is expressed in a spectrum of hematopoetic, epithelial, and mesenchymal cell lines. Interestingly, while the RNA transcript of Mer is detected in numerous T and B lymphoblastic cell lines, Mer RNA is not found in normal human thymocytes, lymphocytes or in PMA/PHA stimulated lymphocytes. We have developed an anti-human Mer monoclonal antibody to further study the ectopic Mer expression in lymphoblasts. The antibody detects several forms of the Mer protein including a fully glycosylated 205 kD Mer protein in monocytes and a less glycosylated 170–180 kD Mer protein in acute lymphoblastic leukemia (ALL) cell lines. We analyzed lymphoblasts from 16 T cell ALL patients diagnosed between July 1995 and July 2004 at The Children’s Hospital, Denver for Mer protein surface expression. Of the T cell ALL patient samples, we found that 9/16 (56%) were positive for Mer protein surface expression. Although we were not able to statistically evaluate the clinical outcomes relative to Mer expression due to the study sample number, there was a statistically significant association between positive expression of Mer and lack of surface expression of CD3 (p = 0.035). We found that 7/9 (78%) of the Mer positive lymphoblasts lacked CD3 surface expression, while only 1/6 (17%) of the Mer negative samples lacked CD3 surface expression (see figure). Lymphoblasts that lack surface expression of CD3 represent an immature phenotype and have been associated with a decreased event free survival as compared with surface positive CD3 lymphoblasts. Further investigation of the ectopic expression of Mer in lymphoblasts may reveal the use of this novel Mer glycosylated protein as a prognostic marker and possibly a future therapeutic target in the treatment of childhood leukemia. Figure Figure
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5

Homans, AC, EN Forman, and BE Barker. "Use of monoclonal antibodies to identify cerebrospinal fluid lymphoblasts in children with acute lymphoblastic leukemia." Blood 66, no. 6 (December 1, 1985): 1321–25. http://dx.doi.org/10.1182/blood.v66.6.1321.1321.

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Abstract The identification of small numbers of leukemic cells in the cerebrospinal fluid (CSF) presents a diagnostic problem in the treatment of children with acute lymphoblastic leukemia (ALL). We adapted a latex sphere rosetting technique to allow us to identify simultaneously cell surface markers and cell morphology in 199 CSF samples from 34 patients and 14 control subjects. In patients without leukemic meningitis, the majority of CSF lymphocytes (69%) were found to be mature T cells positive for OKT11. A much smaller number of cells (8%) were found to be B cells positive for la. In these children, only 3% of CSF lymphoid cells expressed the common acute lymphoblastic leukemia antigen (CALLA). Similar results were found in the control subjects. By contrast, 28 CSF samples from nine children with varying numbers of CSF lymphoblasts had much greater proportions of CALLA- and la-positive CSF cells (24% to 96%). Leukemic meningitis was present in one of these patients and later developed in four others. However, three patients with small numbers of lymphoblasts present but with low proportions of CALLA-positive CSF cells (less than 5%) subsequently had normal CSF examinations. We found the use of this rosetting technique valuable in providing information complementary to that obtained from cell morphology alone about the possible malignant nature of small numbers of lymphoblast-like CSF cells seen on cytocentrifuge preparations in children with ALL.
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6

Homans, AC, EN Forman, and BE Barker. "Use of monoclonal antibodies to identify cerebrospinal fluid lymphoblasts in children with acute lymphoblastic leukemia." Blood 66, no. 6 (December 1, 1985): 1321–25. http://dx.doi.org/10.1182/blood.v66.6.1321.bloodjournal6661321.

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The identification of small numbers of leukemic cells in the cerebrospinal fluid (CSF) presents a diagnostic problem in the treatment of children with acute lymphoblastic leukemia (ALL). We adapted a latex sphere rosetting technique to allow us to identify simultaneously cell surface markers and cell morphology in 199 CSF samples from 34 patients and 14 control subjects. In patients without leukemic meningitis, the majority of CSF lymphocytes (69%) were found to be mature T cells positive for OKT11. A much smaller number of cells (8%) were found to be B cells positive for la. In these children, only 3% of CSF lymphoid cells expressed the common acute lymphoblastic leukemia antigen (CALLA). Similar results were found in the control subjects. By contrast, 28 CSF samples from nine children with varying numbers of CSF lymphoblasts had much greater proportions of CALLA- and la-positive CSF cells (24% to 96%). Leukemic meningitis was present in one of these patients and later developed in four others. However, three patients with small numbers of lymphoblasts present but with low proportions of CALLA-positive CSF cells (less than 5%) subsequently had normal CSF examinations. We found the use of this rosetting technique valuable in providing information complementary to that obtained from cell morphology alone about the possible malignant nature of small numbers of lymphoblast-like CSF cells seen on cytocentrifuge preparations in children with ALL.
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7

Loghavi, Sanam, Jeffery L. Kutok, and Jeffrey L. Jorgensen. "B-Acute Lymphoblastic Leukemia/Lymphoblastic Lymphoma." American Journal of Clinical Pathology 144, no. 3 (September 1, 2015): 393–410. http://dx.doi.org/10.1309/ajcpan7bh5dnywzb.

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8

Indriastuti, Endah, and Arifoel Hajat. "CHRONIC MYELOGENEOUS LEUKEMIA TRANSFORMATION INTO ACUTE LYMPHOBLASTIC LEUKEMIA." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 25, no. 2 (April 13, 2019): 240. http://dx.doi.org/10.24293/ijcpml.v25i2.1395.

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Introduction : Chronic myelogeneous leukemia (CML) is a myeloproliferative neoplasm that can progress into various conditions. Transformation of CML into acute lymphoblastic leukemia (ALL) is a rare case. Case : A 22-year-old male with history of CML since 2014 and positive BCR-ABL p210 in 2017 came with complaint of weakness. Physical examination showed hepatosplenomegaly. CBC results Hb 7.1 g/dL, WBC 290,620/μL, platelet 434,000/μL. Blood smear evaluation (BSE) suggested CML blastic crisis dd AML-M5. Patient’s condition got worse. CBC result showed WBC 96,770/μL and platelet 7,000/μL in 2 weeks later. BSE was dominated by mononuclear cells with scanty blue cytoplasm, no granules, no auer rods, loose chromatine and indistinct nucleoli, suggesting lymphoblasts with a proportion of 60%. Bone marrow aspiration (BMA) and immunophenotyping was done to confirm BSE. The BMA result was dominated by lymphoblast, consistent with ALL. The immunophenotyping result was CD10+, CD34+(0,99%), CD79a+, HLA-DR+, and CD20+. Molecular examination showed positive RUNX1 and NRAS while negative FLT3, NPM1 and del(5q). Discussion : BCR-ABL gene can be found both in CML and ALL. CML transformation into ALL had been reported to be related with deletion of a transcription gene. Diagnosis of ALL can be established by BMA and immunophenotyping. CD34+ expression of lymphoblast in ALL can be varied, but in this case was minimal. Conclusion : Patient with history of CML showed an ALL picture based on BSE, BMA and immunophenotyping suggesting CML transformation into ALL although CD34+ expression was minimal.
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9

Volchkov, E. V., Yu V. Olshanskaya, and N. V. Myakova. "Prognostic markers of lymphoblastic lymphoma." Pediatric Hematology/Oncology and Immunopathology 19, no. 4 (December 22, 2020): 198–204. http://dx.doi.org/10.24287/1726-1708-2020-19-4-198-204.

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Lymphoblastic lymphoma (LBL) is the second most common non-Hodgkin's lymphoma in childhood. According to modern concepts LBL and acute lymphoblastic leukemia (ALL) are considered as manifestations of the same disease given the similar morphological substrate of the tumor – T and B lymphoblasts. The standard for the treatment of LBL is currently ALL-like riskadapted treatment protocols that allow achieving overall and event-free survival rates of 80–90%. The division into risk groups is based on the stage of the disease and the response to induction therapy. However, the problem of relapse/refractory course of the disease remains a serious problem due to the lack of sufficiently effective therapeutic options. Currently, there is a sufficient amount of clinical data that reliably shows that a number of molecular biological factors can be used to create a new system of into risk groups stratification of patients with LBL. This review focuses on the analysis of various factors that may be responsible for the prognosis of LBL in children.
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10

Katik, Banu, Anja Selig, Janna Velder, Elvira E. Shults, Thomas Wieder, Guenter Henze, Hans-Guenther Schmalz, and Aram Prokop. "New Pinostilbene Analogues Overcome Anthracycline Resistance in Acute Lymphoplastic Leukemia Ex Vivo." Blood 108, no. 11 (November 16, 2006): 4403. http://dx.doi.org/10.1182/blood.v108.11.4403.4403.

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Abstract Anthracylines play a very important role in the treatment of acute lymphoblastic leukemia (ALL) and relapsed ALL in childhood, however resistance to anthracyclines leads to a poor prognosis. In the present study, we have synthesized two new pinostilbene analogues, i.e. trans-3,4′-dihydroxy-5-methoxystilbene and (E)-resveratrol 4′-O-ß-D-glucopyranoside, which are able to overcome anthracycline resistance in childhood acute lymphoblastic leukemia (ALL) ex vivo and induce apoptosis in established leukemia cell lines via mitochondrial pathway. Apoptosis induction has been investigated by flowcytometric measurement of DNA-fragmentation [LC 50: 10 μM for (1) and (2)], mitochondrial membrane potential reduction and phosphatedylserin-staining on cell membrane surface. Cell death by necrosis could be excluded by a lactatdehydrogenase-release assay. For the first time we analysed the antileukemic and chemopreventive potentials of the pinostilbene analogues (1) and (2) ex vivo in a significant number of primary lymphoblasts of patients suffering from childhood ALL. Patients: Primary lymphoblasts isolated from 22 children with de novo ALL (median: 6.8 years; range 0,6–16.9 years) and relapsed ALL (median:7.2 years) were tested for ex vivo drug response with the anthracyclines daunorubicin (10 μmol/l) and doxorubicin (10 μmol/l) and two new pinostilbene analogues (1) and (2) (10μmol/l), according to their LC50 values in established cell lines. We could demonstrate in these primary cells that the pinostilbenes (1) and (2) were even more effective as compared with the anthracyclines. Out of 22 patients 14 were female (14 de novo ALL) and 8 were male (6 de novo ALL, 2 relapsed ALL). Within these cell populations following immunologic subgroups were found: c-ALL, pre-B-ALL, pro-B-ALL, T-ALL and pre-T-ALL. Results: Daunorubicin induced apoptosis in 6 out of 22 lymphoblast populations (response rate 27,3 %). A similar response rate was observed after treatment with doxorubicin: only 5 of 22 lymphoblast populations responded (22,7%). Nevertheless, far higher response rates were observed for (1) with 11/15 (73,3 %; p<0.005) and for (2) with 15/17 (88,2%; p<0.0002, all p-values by t-test). Interestingly, treatment of daunorubicin-resistant lymphoblasts resulted in significant apoptosis induction in 6 out of 10 cell populations after treatment with compound (1) (response rate 60 %) and in 6/6 after treatment with compound (2) (response rate 100%). Furthermore, pinostilbene (2) showed significant synergistic activity with daunorubicin in 2 of 3 lymphoblast populations. We clearly demonstrated that the ex vivo treatment of lymphoblasts from children with de novo and relapsed ALL with the new pinostilbenes (1) and (2) induced significantly higher response rates than daunorubicin or doxorubicin treatment. In conclusion, the high ex vivo sensitivity of anthracycline resistant leukemia cells to pinostilbene treatment reveals the great proapoptotic and chemopreventive potential of this new class of antileukemic agents.
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11

Hussain, Shah, Sufyan Ahmad, and Fatima Javed. "PANCYTOPENIA AS INITIAL PRESENTATION OF ACUTE LYMPHOBLASTIC LEUKEMIA AND ITS ASSOCIATIONWITH BONE MARROWRESPONSE." International Journal of Advanced Research 10, no. 02 (February 28, 2022): 133–38. http://dx.doi.org/10.21474/ijar01/14185.

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Objective:The objective of this study is to determine the frequency of pancytopenia and bone marrow response to treatment of acute lymphoblastic leukemia. Materials And Methods:This is a cross sectional study carried out at Medical Oncology Department, Hayatabad Medical Complex, Peshawar. A total of 120 patients were included in the study. Venous blood sample was obtained from patients and sent to the laboratory of the hospital for assessment of red blood cells, white blood cells, and platelets. Reports were assessed and levels were noted. If levels were lower than normal, then patients were labeled as having pancytopenia was labeled.Patients were advised treatment i.e drug regimen including weekly intravenous vincristine, daunorubicin, weekly intrathecal methotrexate and daily dexamethosone for 4 weeks). After 4 weeks they underwent bone marrow aspiration. All samples were sent to the laboratory of the hospital for assessment of bone marrow response i.e M1 (less than 5% lymphoblasts), M2 (5% to 25% Lymphoblasts)& M3 (more than 25% Lymphoblasts). Results:Pancytopenia was recorded in 35 (29.16%) patients presenting with acute lymphoblastic leukemia. Out of these thirty-five patients, 21 (60%) were male and 14(40%) were female. Out the 21 males, 20 (95.24%)hadM1 responsewhile01(4.76%)patienthadM2response. Out of the14female patients,12(85.71 %)hadM1 response, 1(7.14 %) had M2 and 1(7.14%) had M3 response. Out of the 85 patients who did not have pancytopenia, 50 (58.8%) were male and 35 (41.2%) were female. Out of the 50 males withoutpancytopenia,36(72%) hadM1,10(20%)hadM2and4(8%) hadM3response.Among the 35 female patients, 31(88.57%) had M1, 2(5.71%) had M2 and 2(5.71%) had M3 response. Conclusion:The study concluded that although pancytopenia is a fairly common presentation of acute lymphoblastic leukemia but there is no significant difference in the outcome of patients receiving treatment for acute lymphoblastic leukemia in association with presence or absence of pancytopenia as initial presentation or with respect to duration of the disease.
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12

Kurzer, Jason H., and Olga K. Weinberg. "Identification of early B cell precursors (stage 1 and 2 hematogones) in the peripheral blood." Journal of Clinical Pathology 71, no. 9 (May 25, 2018): 845–50. http://dx.doi.org/10.1136/jclinpath-2018-205172.

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Differentiating malignant B-lymphoblasts from early benign B cell precursors (hematogones) is a vital component of the diagnosis of B-lymphoblastic leukaemia. It has been previously reported that only late-stage B cell precursors circulate in the peripheral blood. Consequently, flow cytometric detection of cells with immunophenotypic findings similar to earlier stage precursors in the peripheral blood justifiably raises concern for involvement by B-lymphoblastic leukaemia. We report here, however, that benign early B cell precursors can indeed be detected in the peripheral blood, thus complicating the interpretation of flow cytometric findings derived from these sample types. A retrospective search of our collective databases identified 13 cases containing circulating early stage B cell precursors. The patients ranged in age from 15 days to 85 years old. All positive cases demonstrated that the earlier B cell precursors were associated with later stage precursors, a finding that could help differentiate these cells from B-lymphoblastic leukaemia.
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13

Li, Yan, Rui Zhu, Lei Mi, Yihui Cao, and Di Yao. "Segmentation of White Blood Cell from Acute Lymphoblastic Leukemia Images Using Dual-Threshold Method." Computational and Mathematical Methods in Medicine 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/9514707.

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We propose a dual-threshold method based on a strategic combination of RGB and HSV color space for white blood cell (WBC) segmentation. The proposed method consists of three main parts: preprocessing, threshold segmentation, and postprocessing. In the preprocessing part, we get two images for further processing: one contrast-stretched gray image and one H component image from transformed HSV color space. In the threshold segmentation part, a dual-threshold method is proposed for improving the conventional single-threshold approaches and a golden section search method is used for determining the optimal thresholds. For the postprocessing part, mathematical morphology and median filtering are utilized to denoise and remove incomplete WBCs. The proposed method was tested in segmenting the lymphoblasts on a public Acute Lymphoblastic Leukemia (ALL) image dataset. The results show that the performance of the proposed method is better than single-threshold approach independently performed in RGB and HSV color space and the overall single WBC segmentation accuracy reaches 97.85%, showing a good prospect in subsequent lymphoblast classification and ALL diagnosis.
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14

Khabirova, Eleonora, Laura Jardine, Tim H. H. Coorens, Simone Webb, Taryn D. Treger, Justin Engelbert, Tarryn Porter, et al. "Single-cell transcriptomics reveals a distinct developmental state of KMT2A-rearranged infant B-cell acute lymphoblastic leukemia." Nature Medicine 28, no. 4 (March 14, 2022): 743–51. http://dx.doi.org/10.1038/s41591-022-01720-7.

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AbstractKMT2A-rearranged infant ALL is an aggressive childhood leukemia with poor prognosis. Here, we investigated the developmental state of KMT2A-rearranged infant B-cell acute lymphoblastic leukemia (B-ALL) using bulk messenger RNA (mRNA) meta-analysis and examination of single lymphoblast transcriptomes against a developing bone marrow reference. KMT2A-rearranged infant B-ALL was uniquely dominated by an early lymphocyte precursor (ELP) state, whereas less adverse NUTM1-rearranged infant ALL demonstrated signals of later developing B cells, in line with most other childhood B-ALLs. We compared infant lymphoblasts with ELP cells and revealed that the cancer harbored hybrid myeloid–lymphoid features, including nonphysiological antigen combinations potentially targetable to achieve cancer specificity. We validated surface coexpression of exemplar combinations by flow cytometry. Through analysis of shared mutations in separate leukemias from a child with infant KMT2A-rearranged B-ALL relapsing as AML, we established that KMT2A rearrangement occurred in very early development, before hematopoietic specification, emphasizing that cell of origin cannot be inferred from the transcriptional state.
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15

Wei, E., V. Bellamkonda, and J. Polski. "Primary Chronic Myelogenous Leukemia Blast Crisis with Precursor B Lymphoblastic Leukemia, a Case Report." American Journal of Clinical Pathology 158, Supplement_1 (November 1, 2022): S108. http://dx.doi.org/10.1093/ajcp/aqac126.228.

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Abstract Introduction/Objective Primary chronic myelogenous leukemia (CML) blast crisis at the initial disease presentation is rare. Most CML blast crisis cases present with increased myeloblasts with a minority of patients showing lymphoblastic leukemia. Differentiating primary CML lymphoblast crisis from de novo acute lymphoblastic leukemia may represent a diagnostic challenge to both pathologists and treating clinicians. This distinction is important as it has significant implications on patient management. Methods/Case Report A 15-year-old male patient was admitted to our University Hospital for hyperleukocytosis. Patient reportedly had weight loss with occasional sweats and cervical lymphadenopathy. She was found to have massive splenomegaly. Peripheral blood showed hyperleukocytosis with predominance of granulocytes at all maturation stages ranging from blast to segmented neutrophils with increased blasts. Subsequent bone marrow findings were consistent with extensive involvement by B-lymphoblastic leukemia. Ten-color Flow cytometry showed approximately 30% blasts with rare lymphocytes and monocytes. The blasts revealed precursor B-lymphoblastic immunophenotypic expression of CD45, CD10, CD19, CD20, CD22, CD34, CD38, CD200, HLA-DR and TdT expression. The results were similar to that of peripheral blood. Granulocytes showed abnormal maturation pattern with increased immature precursors and partial expression of CD4 and CD56 with no abnormalities detected in lymphocytes. In this case, while the bone marrow findings are consistent with B-lymphoblastic leukemia, the peripheral blood findings are consistent with blast phase of chronic myeloid leukemia. Further evaluation by cytogenetic and molecular studies confirmed the presence of Philadelphia chromosome, p210 transcripts, and rearrangement of BCR-ABL1, which supported the impression of precursor B-lymphoblastic leukemia in primary blast phase of CML. The patient was treated with tyrosine kinase inhibitor combined chemotherapy and went into remission. She has been followed up without significant complications for a year. Results (if a Case Study enter NA) NA. Conclusion The diagnosis of CML in primary lymphoblastic crisis is rare and needs to be systemically excluded before giving the diagnosis of de novo BCR-ABL1-positive acute lymphoblastic leukemia. If the patient does not have splenomegaly or previous leukocytosis, it needs cytological examination and extensive molecular analyses.
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16

Thomas, Deborah A., and Hagop M. Kantarjian. "Lymphoblastic Lymphoma." Hematology/Oncology Clinics of North America 15, no. 1 (February 2001): 51–95. http://dx.doi.org/10.1016/s0889-8588(05)70200-8.

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17

Cortelazzo, Sergio, Maurilio Ponzoni, Andrés J. M. Ferreri, and Dieter Hoelzer. "Lymphoblastic lymphoma." Critical Reviews in Oncology/Hematology 79, no. 3 (September 2011): 330–43. http://dx.doi.org/10.1016/j.critrevonc.2010.12.003.

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18

Cortelazzo, Sergio, Andrés Ferreri, Dieter Hoelzer, and Maurilio Ponzoni. "Lymphoblastic lymphoma." Critical Reviews in Oncology/Hematology 113 (May 2017): 304–17. http://dx.doi.org/10.1016/j.critrevonc.2017.03.020.

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19

Kadin, M. "Lymphoblastic Lymphoma." ASH Image Bank 2004, no. 1118 (November 18, 2004): 101233. http://dx.doi.org/10.1182/ashimagebank-2004-101233.

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20

Kadin, M. "Lymphoblastic Lymphoma." ASH Image Bank 2004, no. 1118 (November 18, 2004): 101234. http://dx.doi.org/10.1182/ashimagebank-2004-101234.

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21

Kadin, M. "Lymphoblastic Lymphoma." ASH Image Bank 2004, no. 1130 (November 30, 2004): 101255. http://dx.doi.org/10.1182/ashimagebank-2004-101255.

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22

Belsky, Jennifer A., Anthony N. Audino, and Samir B. Kahwash. "Separating Lymphoblastic Lymphoma Involving Marrow From Lymphoblastic Leukemia." Journal of Pediatric Hematology/Oncology 41, no. 8 (November 2019): 658–59. http://dx.doi.org/10.1097/mph.0000000000001588.

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23

Abou Chakra, Rim, Bernard Najib, Wael Abdallah, Mira Akiki, Lea El Khoury, Ali Atoui, Malak Moubarak, and David Atallah. "B-Cell Lymphoblastic Lymphoma in Relapse Presenting as a Uterine Mass: A Case Report and Review of Literature." Case Reports in Oncology 14, no. 2 (June 17, 2021): 868–73. http://dx.doi.org/10.1159/000515196.

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B-cell lymphoblastic lymphoma (LBL) is a highly aggressive malignant proliferation of lymphoblasts of B-origin grouped with acute lymphoblastic leukemia. Multiple studies demonstrated the various sites of involvement in adult LBL. The involvement of the uterus as a site of relapse for such disease is rare. We herein report the case of relapsed B-cell LBL mimicking endometrial sarcoma. The patient is a 56-year-old female patient known to have B-cell LBL on chemotherapy. She presented with abdominal pain and fever. Positron emission tomodensitometry-computed tomography showed the presence of a uterine mass with bilateral iliac lymph node involvement. She underwent surgery with mass removal and pathology showed relapsed B-cell LBL.
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Smith, SD, P. McFall, R. Morgan, M. Link, F. Hecht, M. Cleary, and J. Sklar. "Long-term growth of malignant thymocytes in vitro." Blood 73, no. 8 (June 1, 1989): 2182–87. http://dx.doi.org/10.1182/blood.v73.8.2182.2182.

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Abstract We report a new methodology for the long-term growth of malignant T- lymphoblasts from patients with T-cell acute lymphoblastic leukemia (T- ALL) and T-cell lymphoblastic lymphoma (T-LL). When malignant cells were cultured in the presence of insulin-like growth factor I under hypoxic conditions, cellular proliferation occurred that resulted in the establishment of immortal cell lines from ten of 12 patient tumors. Authenticity of each cell line was verified by a direct comparison of the immunophenotype, karyotype, and immunogenotype with the patient's tumor cells. This improved method of cell culture permits frequent establishment of cell lines from patients with T-ALL/T-LL, thereby aiding in analysis of thymocyte transformation and neoplasia.
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25

Smith, SD, P. McFall, R. Morgan, M. Link, F. Hecht, M. Cleary, and J. Sklar. "Long-term growth of malignant thymocytes in vitro." Blood 73, no. 8 (June 1, 1989): 2182–87. http://dx.doi.org/10.1182/blood.v73.8.2182.bloodjournal7382182.

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We report a new methodology for the long-term growth of malignant T- lymphoblasts from patients with T-cell acute lymphoblastic leukemia (T- ALL) and T-cell lymphoblastic lymphoma (T-LL). When malignant cells were cultured in the presence of insulin-like growth factor I under hypoxic conditions, cellular proliferation occurred that resulted in the establishment of immortal cell lines from ten of 12 patient tumors. Authenticity of each cell line was verified by a direct comparison of the immunophenotype, karyotype, and immunogenotype with the patient's tumor cells. This improved method of cell culture permits frequent establishment of cell lines from patients with T-ALL/T-LL, thereby aiding in analysis of thymocyte transformation and neoplasia.
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26

Whitehead, VM, MJ Vuchich, SJ Lauer, D. Mahoney, AJ Carroll, JJ Shuster, DW Esseltine, C. Payment, AT Look, and J. Akabutu. "Accumulation of high levels of methotrexate polyglutamates in lymphoblasts from children with hyperdiploid (greater than 50 chromosomes) B-lineage acute lymphoblastic leukemia: a Pediatric Oncology Group study." Blood 80, no. 5 (September 1, 1992): 1316–23. http://dx.doi.org/10.1182/blood.v80.5.1316.bloodjournal8051316.

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Hyperdiploidy (greater than 50 chromosomes, or a DNA index greater than 1.16) confers a favorable prognosis in B-lineage acute lymphoblastic leukemia of childhood. Children with B-lineage acute lymphoblastic leukemia whose lymphoblasts at diagnosis accumulate high levels of methotrexate (MTX) and MTX polyglutamates (MTXPGs) in vitro experience a better event-free survival than those whose lymphoblasts do not (Blood 76:44, 1990). Lymphoblasts from 13 children with hyperdiploidy (greater than 50 chromosomes) accumulated high levels of MTX-PGs (1,095 and 571 to 2,346 pmol/10(9) cells [median and 25% to 75% intraquartile range]). These levels were higher than those in B-lineage lymphoblasts from 19 children with other aneuploidy (326 and 159 to 775 pmol/10(9) cells) and 15 children with diploidy (393 and 204 to 571 pmol/10(9) cells) (P = .0015). Chromosomal trisomies in hyperdiploid cases were highly nonrandom. Chromosome 9 was not one of the chromosomes involved in trisomies, even though this chromosome contains the gene for folate polyglutamate synthetase, which is the enzyme required for MTXPG synthesis. The correlation between MTXPG level and percentage of S- phase cells was weak, suggesting that increased levels of MTXPGs could not be attributed to elevated proportions of cells in active DNA synthesis. The ability of hyperdiploid lymphoblasts to accumulate high levels of MTXPGs may increase their sensitivity to MTX cytotoxicity, accounting in part for the improved outlook for hyperdiploid patients treated with regimens that emphasize MTX as a primary component of continuation therapy.
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27

Finn, Laura S., Douglas S. Hawkins, Joe C. Rutledge, and Kathleen Patterson. "Evaluation of Early Marrow Response in Childhood Aneuploid Acute Lymphoblastic Leukemia: Flow Cytometric DNA Analysis versus Standard Morphology." Pediatric and Developmental Pathology 7, no. 1 (January 2004): 39–47. http://dx.doi.org/10.1007/s10024-003-2017-x.

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Despite improved survival rates for childhood acute lymphoblastic leukemia (ALL), the relapse rate remains at 20–30%. Early peripheral blood and bone marrow (BM) responses have been associated with more favorable outcomes; all current children's cancer group (CCG) protocols for ALL require BM evaluation at days 7 and 14 with subsequent therapy based on the results. Morphologic interpretation of aspirate smears during induction chemotherapy is challenging, as the samples are often hypocellular, excessively friable, and cytologically altered by drugs. We have shown discordancy of day 7 and 14 BM lymphoblast counts using morphologic and flow cytometric immunophenotypic analyses (FC). The aim of our study was to determine the utility, reliability, and cost effectiveness of lymphoblast enumeration using DNA content analysis by flow cytometry (DNA-FC) and to further demonstrate the subjectivity of morphologic review. All new cases of ALL had DNA-FC and FC analyses. The percentage of lymphoblasts as determined by both methods was compared for 82 aneuploid cases. Three pathologists independently reviewed aspirate smears from 39 bone marrow samples of aneuploid ALL that were obtained during early induction. These results were compared among themselves and with the results obtained by DNA-FC. We found excellent correlation between the percentage of lymphoblasts as determined by DNA-FC and FC (R2= 0.97) over a range of 0 to 99%. Pathologic review agreed with the DNA-FC, on average, 68%. The sensitivity, specificity, and positive and negative predictive values of morphologic review, averaged 53, 84, 78, and 63%, respectively, when using DNA-FC as the “gold standard.” All three pathologists achieved agreement of lymphoblast percentage by morphology in 72%. In our laboratory, the use of DNA-FC equates to one-sixth the time and one-half the price of FC per exam. We have shown a strong correlation between blast counts determined by DNA-FC and FC. DNA-FC is an objective, economical, and reliable method to assess early response in induction marrows from aneuploid ALL where morphology is often uninterpretable. This test is highly reproducible and available at most pediatric institutions. Prospective studies need to be employed to evaluate the effect of more definitive methods (DNA-FC and FC) of assessing the early response in bone marrows on prognosis.
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Hirzel, Alicia C., Aaron Cotrell, Robert Gasparini, and Vathany Sriganeshan. "Precursor B-Cell Acute Lymphoblastic Leukemia/Lymphoma with L3 Morphology, Philadelphia Chromosome, MYC Gene Translocation, and Coexpression of TdT and Surface Light Chains: A Case Report." Case Reports in Pathology 2013 (2013): 1–4. http://dx.doi.org/10.1155/2013/679892.

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Acute lymphoblastic leukemia is predominantly found in children. It is a neoplasm of precursor cells or lymphoblasts committed to either a B- or T-cell lineage. The immature cells in B-acute lymphoblastic leukemia/lymphoma can be small or medium sized with scant or moderate cytoplasm and typically express B-cell markers such as CD19, cytoplasmic CD79a, and TdT without surface light chains. These markers, along with cytogenetic studies, are vital to the diagnosis, classification, and treatment of these neoplasms. We present an unusual case of a precursor B-cell ALL, in an 82-year-old woman, who presented with pancytopenia and widespread lymphadenopathy. The cells show L3 morphology (Burkitt-like lymphoma) with coexpression of TdT and surface light chains in addition to an MYC gene translocation and Philadelphia chromosome.
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29

Chiaretti, Sabina, Gina Zini, and Renato Bassan. "DIAGNOSIS AND SUBCLASSIFICATION OF ACUTE LYMPHOBLASTIC LEUKEMIA." Mediterranean Journal of Hematology and Infectious Diseases 6, no. 1 (October 24, 2014): e2014073. http://dx.doi.org/10.4084/mjhid.2014.073.

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Acute lymphoblastic leukemia (ALL) is a disseminated malignancy of B- or T-lymphoblasts which imposes a rapid and accurate diagnostic process to support an optimal risk-oriented therapy and thus increase the curability rate. The need for a precise diagnostic algorithm is underlined by the awareness that both ALL therapy and related success rates may vary greatly in function of ALL subset, from standard chemotherapy in patients with standard-risk ALL, to allotransplantation (SCT) and targeted therapy in high-risk patients and cases expressing suitable biological targets, respectively. This review offers a glimpse on how best identify ALL and the most relevant ALL subsets.
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30

Xu, Jie, and Shaoying Li. "Unusual T-Lymphoblastic Blast Phase of Chronic Myelogenous Leukemia." Case Reports in Hematology 2014 (2014): 1–5. http://dx.doi.org/10.1155/2014/304359.

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T-lymphoblastic leukemia/lymphoma (T-ALL) presenting as blast phase of chronic myelogenous leukemia (CML-BP) is rare. In patients without history of CML, it is difficult to differentiate between CML-BP or de novo T-ALL. Here we reported 2 unusual cases of T-ALL presenting as CML-BP. Case 1 was a 24-year-old female with leukocytosis. Besides T-lymphoblasts (32%), her marrow exhibited some morphologic features of CML. Multiple remission or relapsing marrow had never demonstrated morphologic features of CML. Despite of imatinib treatment and stem cell transplant, she died 2.5 years later. Case 2, a 66-year-old male with diffuse lymphadenopathy, showed T-ALL in a lymph node and concurrent CML chronic phase (CML-CP) in his marrow. Same BCR-ABL1 fusion transcript with minor breakpoint was present in both the lymph node and marrow specimens. Although both cases did not have a history of CML, both cases represented T-lymphoblastic CML-BP with unusual features: Case 1 is unusual in that it presented as T-ALL with some CML morphologic feature but never showed CML-CP in her subsequent marrows biopsies; Case 2 is the first reported case of T-lymphoblastic CML-BP harboring BCR-ABL1 transcript with a minor breakpoint.
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31

Matherly, LH, JW Taub, Y. Ravindranath, SA Proefke, SC Wong, P. Gimotty, S. Buck, JE Wright, and A. Rosowsky. "Elevated dihydrofolate reductase and impaired methotrexate transport as elements in methotrexate resistance in childhood acute lymphoblastic leukemia." Blood 85, no. 2 (January 15, 1995): 500–509. http://dx.doi.org/10.1182/blood.v85.2.500.500.

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Abstract A retrospective study of clinical resistance to methotrexate (MTX) was performed on 29 archival specimens of frozen lymphoblasts obtained from children with acute lymphoblastic leukemia (ALL), including 19 at initial presentation and 10 at first relapse. Blasts were assayed for dihydrofolate reductase and MTX transport by flow cytometry using the fluorescent methotrexate analog, PT430 (Rosowsky et al, J Biol Chem 257:14162, 1982). In contrast to tissue culture cells, patient blasts were often heterogeneous for dihydrofolate reductase content. Of the 19 specimens at initial diagnosis, 7 exhibited dual blast populations, characterized by threefold to 10-fold differences in relative dihydrofolate reductase; the dihydrofolate reductase-overproducing populations comprised 12% to 68% of the total blasts for these specimens. Remission duration intervals for patients exhibiting dual blast populations were notably shorter than for patients expressing a single blast population with lower dihydrofolate reductase ( < or = 9 months v > or = 15 months, respectively), a difference that was statistically significant (P = .045). There was no apparent correlation between expression of increased dihydrofolate reductase at diagnosis and known patient and disease prognostic features (immunophenotype, age, sex, and white blood count). For the relapsed patients, 4 of 10 exhibited dual lymphoblast populations with elevated dihydrofolate reductase. The majority of the patient lymphoblast specimens were entirely competent for MTX transport and, likewise, expressed immunoreactive reduced folate carriers by indirect immunofluorescence staining with specific antiserum to the transporter. Three patients (2 at relapse and 1 at diagnosis) exhibited heterogeneous expression of imparied MTX transport (14% to 73% of blasts). In only 1 of these patients did the majority of the lymphoblasts (73%) show impaired MTX transport and for this specimen, immunoreactive carrier proteins were virtually undetectable. These results suggest that heterogeneous expression of elevated dihydrofolate reductase and impaired MTX transport are important modes of resistance in childhood ALL patients undergoing chemotherapy with MTX and that these parameters may serve as predictive indices of clinical response to MTX.
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32

Matherly, LH, JW Taub, Y. Ravindranath, SA Proefke, SC Wong, P. Gimotty, S. Buck, JE Wright, and A. Rosowsky. "Elevated dihydrofolate reductase and impaired methotrexate transport as elements in methotrexate resistance in childhood acute lymphoblastic leukemia." Blood 85, no. 2 (January 15, 1995): 500–509. http://dx.doi.org/10.1182/blood.v85.2.500.bloodjournal852500.

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A retrospective study of clinical resistance to methotrexate (MTX) was performed on 29 archival specimens of frozen lymphoblasts obtained from children with acute lymphoblastic leukemia (ALL), including 19 at initial presentation and 10 at first relapse. Blasts were assayed for dihydrofolate reductase and MTX transport by flow cytometry using the fluorescent methotrexate analog, PT430 (Rosowsky et al, J Biol Chem 257:14162, 1982). In contrast to tissue culture cells, patient blasts were often heterogeneous for dihydrofolate reductase content. Of the 19 specimens at initial diagnosis, 7 exhibited dual blast populations, characterized by threefold to 10-fold differences in relative dihydrofolate reductase; the dihydrofolate reductase-overproducing populations comprised 12% to 68% of the total blasts for these specimens. Remission duration intervals for patients exhibiting dual blast populations were notably shorter than for patients expressing a single blast population with lower dihydrofolate reductase ( < or = 9 months v > or = 15 months, respectively), a difference that was statistically significant (P = .045). There was no apparent correlation between expression of increased dihydrofolate reductase at diagnosis and known patient and disease prognostic features (immunophenotype, age, sex, and white blood count). For the relapsed patients, 4 of 10 exhibited dual lymphoblast populations with elevated dihydrofolate reductase. The majority of the patient lymphoblast specimens were entirely competent for MTX transport and, likewise, expressed immunoreactive reduced folate carriers by indirect immunofluorescence staining with specific antiserum to the transporter. Three patients (2 at relapse and 1 at diagnosis) exhibited heterogeneous expression of imparied MTX transport (14% to 73% of blasts). In only 1 of these patients did the majority of the lymphoblasts (73%) show impaired MTX transport and for this specimen, immunoreactive carrier proteins were virtually undetectable. These results suggest that heterogeneous expression of elevated dihydrofolate reductase and impaired MTX transport are important modes of resistance in childhood ALL patients undergoing chemotherapy with MTX and that these parameters may serve as predictive indices of clinical response to MTX.
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33

Whitehead, VM, MJ Vuchich, SJ Lauer, D. Mahoney, AJ Carroll, JJ Shuster, DW Esseltine, C. Payment, AT Look, and J. Akabutu. "Accumulation of high levels of methotrexate polyglutamates in lymphoblasts from children with hyperdiploid (greater than 50 chromosomes) B-lineage acute lymphoblastic leukemia: a Pediatric Oncology Group study." Blood 80, no. 5 (September 1, 1992): 1316–23. http://dx.doi.org/10.1182/blood.v80.5.1316.1316.

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Abstract Hyperdiploidy (greater than 50 chromosomes, or a DNA index greater than 1.16) confers a favorable prognosis in B-lineage acute lymphoblastic leukemia of childhood. Children with B-lineage acute lymphoblastic leukemia whose lymphoblasts at diagnosis accumulate high levels of methotrexate (MTX) and MTX polyglutamates (MTXPGs) in vitro experience a better event-free survival than those whose lymphoblasts do not (Blood 76:44, 1990). Lymphoblasts from 13 children with hyperdiploidy (greater than 50 chromosomes) accumulated high levels of MTX-PGs (1,095 and 571 to 2,346 pmol/10(9) cells [median and 25% to 75% intraquartile range]). These levels were higher than those in B-lineage lymphoblasts from 19 children with other aneuploidy (326 and 159 to 775 pmol/10(9) cells) and 15 children with diploidy (393 and 204 to 571 pmol/10(9) cells) (P = .0015). Chromosomal trisomies in hyperdiploid cases were highly nonrandom. Chromosome 9 was not one of the chromosomes involved in trisomies, even though this chromosome contains the gene for folate polyglutamate synthetase, which is the enzyme required for MTXPG synthesis. The correlation between MTXPG level and percentage of S- phase cells was weak, suggesting that increased levels of MTXPGs could not be attributed to elevated proportions of cells in active DNA synthesis. The ability of hyperdiploid lymphoblasts to accumulate high levels of MTXPGs may increase their sensitivity to MTX cytotoxicity, accounting in part for the improved outlook for hyperdiploid patients treated with regimens that emphasize MTX as a primary component of continuation therapy.
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34

Zhang, QiGuo, Jian Ouyang, and Jianyong Li. "Acute Lymphoblastic Leukemia with Mature Appearing Lymphocytes: First Chinese Case Report and Literature Review." Blood 112, no. 11 (November 16, 2008): 4896. http://dx.doi.org/10.1182/blood.v112.11.4896.4896.

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Abstract Objective: To increase the knowledge and understanding of acute lymphoblastic leukemia with maturation(ALLm). Method: One ALLm case with clinical manifestation, bone marrow morphology, immunophenotype and cytogenetic results were presented and related literatures were reviewed. Result: The patient was a fifty-five year old women, the haematological feature was Pancytopenia. There were 12% lymphoblasts and 82.5% mature appearing lymphocytes in the bone marrow smear. The mature appearing leukemic cells could not be separated clearly by gating. However, the immunophenotypes of mature-appearing leukemic cells(Low FSC and Low CD45) and lymphoblasts were the same. Both results were CD33+CD34+CD19+CD22+HLA−DR+CD5−CD7−CD10−CD13−CD14−CD15−CD20−CD25−CD45−CD71−CD11b−CD103−CD117−. Bone marrow biopsy showed hypercellularity with diffuse infiltration of lymphocytes, The results were CD34++,TdT++,Pax-5+++,CD43++,CD3+(scatter),CD5+(scatter),CD20−,CD10+,CyclinD1−, lymphoblasts Ki67+, mature-appearing leukemic cells ki-67-. FISH analysis of the bone marrow revealed about 1% cells with a signal pattern suggesting loss of one copy of chromosome 8. After VDP, MA, AAG and HAG regimens Complete remission was not achieved. Conclusion: ALLm is a special morphological variant of acute lymphoblastic leukemia, most mature appearing cells are in resting G0 phase and this could be the reason why ALLm has a poor response to chemotherapy.
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35

Levkut, Martin, Peter Major, Lucia Kottferová, and Mikuláš Levkut. "B-cell lymphoblastic leukaemia in a guinea-pig – a case report." Acta Veterinaria Brno 90, no. 2 (2021): 221–23. http://dx.doi.org/10.2754/avb202190020221.

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In this case report, lymphoblastic leukaemia is described in a five-year-old female guinea pig. Clinical examination revealed lymphadenopathy, mainly with increased size of the popliteal lymph nodes. Lymphoblast cells were determined haematologically. Postmortem findings were hepatomegaly and splenomegaly. Histopathological examination of liver, spleen and lymph nodes revealed tumour cells of lymphoblastic type. These cells showed considerable cellular pleomorphism. The protein markers CD3 and CD20 and paired box 5 (PAX5) transcription factor were traced immunohistochemically. Immunophenotypization using PAX5 showed nuclear positivity of this marker, but CD3 and CD20 (not interspecies cross-reactivity for guinea pig) demonstrated no positive reaction in the tumour cells. CD3-positive cells were found only in guinea pig tissue sections used as control. PAX5 in guinea pigs appears as a beneficial and preferred marker for B-cell derived tumours.
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36

Whitehead, V. Michael, David S. Rosenblatt, Mary-Jane Vuchich, and Denise Beaulieu. "Methotrexate Polyglutamate Synthesis in Lymphoblasts from Children with Acute Lymphoblastic Leukemia." Developmental Pharmacology and Therapeutics 10, no. 6 (1987): 443–48. http://dx.doi.org/10.1159/000457776.

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37

Hong, Ruey-Long, Ssu-Wen Shen, Ming-Tseh Lin, Hwei-Fang Tien, Chin-Hsin Yang, and Yao-Chang Chen. "Lymphoblast colony-culture assay in acute lymphoblastic leukemia: A quantitative approach." Leukemia Research 17, no. 5 (May 1993): 463–70. http://dx.doi.org/10.1016/0145-2126(93)90103-r.

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38

Mohd Safuan, Syadia Nabilah, Mohd Razali Md Tomari, Wan Nurshazwani Wan Zakaria, Mohd Norzali Haji Mohd, and Nor Surayahani Suriani. "Computer aided system for lymphoblast classification to detect acute lymphoblastic leukemia." Indonesian Journal of Electrical Engineering and Computer Science 14, no. 2 (May 1, 2019): 597. http://dx.doi.org/10.11591/ijeecs.v14.i2.pp597-607.

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Acute lymphoblastic leukemia (ALL) is a disease that is detected by the presence of lymphoblast cell. Basically, lymphoblast cell is the abnormal cell of lymphocyte which is one of the White Blood Cell (WBC) types. Early prevention is suggested as this disease can be fatal and caused death. Traditionally, ALL is detected by using manual analysis which is challenging and time consuming. It can also yield inaccurate result as it is highly dependent on the pathologist’s skills. Industry has come out with hematology counter which is fast, accurate and automated. However, these machines are costly and cannot be afforded by some countries. For that reason, Computer Aided System (CAS) will be a great help to the pathologist for assisting purposes and it also can act as second opinion for the pathologist. This system contains six main steps which are color space correction, WBC segmentation, post processing, clumped area extraction, feature extraction and lymphoblast classification. Firstly, color space correction is apply by using l*a*b* color space to standardize the image’s intensity. Next, WBC segmentation is made to prune out WBC region using color space analysis with Otsu thresholding. However, segmented image contains noises that need to be eliminated and it is accomplished by applying morphological filter with Connected Component Labelling (CCL). There is an overlapping WBC which need to be separated by using Watershed method to extract the individual cells. Next, feature extraction is made to collect the cell’s data to be fed into the classifier. Classifier used in this system to classify lymphoblast is Support Vector Machine (SVM) and this system is able to achieve 96.69% of accuracy.
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39

Granados Romero, Francisco Fabian, and Enma maría Guadamud Lorenti. "Acute lymphoblastic leukemia." Journal of America health 1, no. 1 (January 2, 2018): 1–5. http://dx.doi.org/10.37958/jah.v1i1.1.

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Acute lymphoblastic leukemia is the most common hematologic neoplasm in pediatric age. Acute lymphoblastic leukemia (ALL) comprises 80% of all acute leukemias in this age group. Although the etiology is unknown, some genetic, viral and environmental predisposing factors have been detailed. The clinical manifestations are usually the result of bone marrow by leukemic cells (anemia, thrombopenia and neutropenia). The diagnosis is made by morphological, cytogenetic and molecular analysis of bone marrow aspirate. The treatment lasts about two years. The prognosis of children with acute lymphoblastic leukemia has improved brilliantly in recent decades thanks to new drugs and treatment tailored to patients' risk.
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40

Alvarnas, Joseph C., Patrick A. Brown, Patricia Aoun, Karen Kuhn Ballen, Naresh Bellam, William Blum, Michael W. Boyer, et al. "Acute Lymphoblastic Leukemia." Journal of the National Comprehensive Cancer Network 10, no. 7 (July 2012): 858–914. http://dx.doi.org/10.6004/jnccn.2012.0089.

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41

Nizzamani, Ghulam Shah, Zaheer Ahmed Nizamani, Amin Fahim, and Ikram Uddin Ujjan. "ACUTE LYMPHOBLASTIC LEUKEMIA." Professional Medical Journal 23, no. 03 (March 10, 2016): 12–316. http://dx.doi.org/10.29309/tpmj/2016.23.03.1480.

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Objectives: The aim of the present study is to evaluate the frequencyof chromosomal abnormalities in childhood acute lymphoblastic leukemia at a tertiarycare hospital of Sindh. Study design: Observation study. Place of study: Isra UniversityHospital, Hyderabad and Oncology Unit Liaquat University of Medical and Health Sciences,Jamshoro. Duration of study: From January 2014 to March 2015. Materials and Methods:Cytogenetic analysis was conducted on peripheral blood and bone marrow samples of 100diagnosed cases of acute lymphoblastic leukemia (ALL). Peripheral blood and bone marrowsamples were collected and putted into sodium heparinized bottles. Cytogenetic analysiswas performed by karyotyping according to the ISCN guidelines for human cytogeneticnomenclature using cytovision-+ system for image analysis. Data was analyzed on statistic8.1 USA and expressed as means, percentage and chi-square with P-value of ≤ 0.05 beingdefined significant. Results: Chromosomal abnormalities were found in 53% of the ALLcases. Numerical abnormalities were found in 71% whereas 35% cases showed structuralabnormalities. 29% cases of ALL showed diploidy and aneuploidy was found in 69% of casesand 2% cases were unknown. Highest number of patients 51% showed hyperploidy followedby 12% cases of hypoploidy and 6% showed pseudoploidy. Chromosomal translocationst(9; 22) (q34; q11) and t(8; 22) (q24; q11) were noted in 6% each and t(8; 14) (q22; q32)were seen in 5% of the cases of childhood ALL. Conclusion: The present study reportschromosomal abnormalities in 53% of cases. Numerical abnormalities were found in 71%whereas 35% cases showed structural abnormalities.
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42

Schrappe, Martin. "Acute lymphoblastic leukemia." HemaSphere 2 (June 2018): 1. http://dx.doi.org/10.1097/hs9.0000000000000078.

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43

Kantarjian, Hagop, and Elias Jabbour. "Acute Lymphoblastic Leukemia." Oncology Times 43, no. 17 (September 5, 2021): 1,11,12,18–18. http://dx.doi.org/10.1097/01.cot.0000791796.99084.b2.

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44

Pui, Ching-Hon, Mary V. Relling, and James R. Downing. "Acute Lymphoblastic Leukemia." New England Journal of Medicine 350, no. 15 (April 8, 2004): 1535–48. http://dx.doi.org/10.1056/nejmra023001.

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45

Litzow, Mark R. "Acute lymphoblastic leukemia." Hematology 19, no. 4 (May 24, 2014): 246–47. http://dx.doi.org/10.1179/1024533214z.000000000281.

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46

Ulmer, Lynn D., and Lori Larson. "Acute Lymphoblastic Leukemia." Laboratory Medicine 27, no. 11 (November 1, 1996): 720–22. http://dx.doi.org/10.1093/labmed/27.11.720.

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47

Loyola, Inés, Patricia Cadahía, and Ariana Trastoy. "Hypergranular lymphoblastic leukaemia." British Journal of Haematology 182, no. 4 (May 9, 2018): 466. http://dx.doi.org/10.1111/bjh.15264.

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48

Gale, Robert Peter, Dieter Hoelzer, and Hagop M. Kantarjian. "Acute Lymphoblastic Leukemia." American Journal of Clinical Oncology 14, no. 1 (February 1991): 90. http://dx.doi.org/10.1097/00000421-199102000-00027.

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49

Creevy, J. "Acute lymphoblastic leukaemia." Journal of Wound Care 6, no. 10 (November 2, 1997): 456. http://dx.doi.org/10.12968/jowc.1997.6.10.456.

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50

Hoelzer, Dieter, Nicola Gökbuget, Oliver Ottmann, Ching-Hon Pui, Mary V. Relling, Frederick R. Appelbaum, Jacques J. M. van Dongen, and Tomasz Szczepański. "Acute Lymphoblastic Leukemia." Hematology 2002, no. 1 (January 1, 2002): 162–92. http://dx.doi.org/10.1182/asheducation-2002.1.162.

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Abstract This is a comprehensive overview on the most recent developments in diagnosis and treatment of acute lymphoblastic leukemia (ALL). Dr. Dieter Hoelzer and colleagues give an overview of current chemotherapy approaches, prognostic factors, risk stratification, and new treatment options such as tyrosine kinase inhibitors and monoclonal antibodies. Furthermore the role of minimal residual disease (MRD) for individual treatment decisions in prospective clinical studies in adult ALL is reviewed. Drs. Ching-Hon Pui and Mary Relling discuss late treatment sequelae in childhood ALL. The relation between the risk of second cancer and treatment schedule, pharmacogenetics, and gene expression profile studies is described. Also pathogenesis, risk factors, and management of other complications such as endocrinopathy, bone demineralization, obesity, and avascular necrosis of bone is reviewed. Dr. Fred Appelbaum addresses long-term results, late sequelae and quality of life in ALL patients after stem cell transplantation. New options for reduction of relapse risk, e.g., by intensified conditioning regimens or donor lymphocyte infusions, for reduction of mortality and new approaches such as nonmyeloablative transplantation in ALL are discussed. Drs. Jacques van Dongen and Tomasz Szczepanski demonstrate the prognostic value of MRD detection via flow cytometry or PCR analysis in childhood ALL. They discuss the relation between MRD results and type of treatment protocol, timing of the follow-up samples, and the applied technique and underline the importance of standardization and quality control. They also review MRD-based risk group definition and clinical consequences.
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