Journal articles: 'Precursor T-Cell Lymphoblastic Leukemia-Lymphoma'

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Lazarchick, J. "Precursor T-Lymphoblastic Leukemia/Lymphoma." ASH Image Bank 2001, no. 1205 (December 5, 2001): 100187. http://dx.doi.org/10.1182/ashimagebank-2001-100187.

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Czuchlewski, David R., and Kathryn Foucar. "Early T-cell Precursor Acute Lymphoblastic Leukemia/Lymphoma." Surgical Pathology Clinics 6, no. 4 (December 2013): 661–76. http://dx.doi.org/10.1016/j.path.2013.08.002.

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Chang, Myung Hee, Seok Jin Kim, Won Seog Kim, Chul Won Choi, Cheolwon Suh, Sung Hyun Kim, Deok-Hwan Yang, Jong-Ho Won, and Soon Il Lee. "Treatment Outcome and Prognostic Factors in Patients with Precursor B and T Lymphoblastic Lymphoma." Blood 112, no. 11 (November 16, 2008): 3601. http://dx.doi.org/10.1182/blood.v112.11.3601.3601.

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Abstract Introduction: Lymphoblastic lymphoma is an uncommom subtype of non-Hodgkin’s lymphoma. Lymphoblastic lymphoma represents a distinctive lymphoma entity with cytological and histological features similar to those of acut lymphoblastic leukemia (ALL). Thus, World Health Organization (WHO) classification classifies this disease entity as precursor B and T lymphoblastic lymphoma/leukemia. At present, precursor B and T lymphoblastic lymphoma has been treated with intensive chemotherapy similar to acute lymphoblastic leukemia. However, there is few study about the treatment outcome and prognostic factors in precursor B and T lymphoblastic lymphoma presenting as lymphoma not leukemia. Thus. the purpose of this retrospective study was to investigate clinical features and treatment outcomes of lymphoblastic lymphoma. Patients and methods: We analyzed 62 patients newly diagnosed with precursor B and T lymhpoblastic lymphoma. All patients were histologically confirmed by pathologists between October 1996 and November 2007, who met the following criteria were included in this retrospective evaluation: age over 15 years, presence of an extramedullary primary and ≤20% blasts in bone marrow, the presence of lymphoblastic histology, the immunophenotype of the malignant cells. Results: The patients were male predominent (77%), with 77% (48) of patients having a T-cell immunophenotype. The median age at time of presentation was 28.5 years (16–69). The presenting sites of primary disease included mediastinal mass in twenty-eight cases. The bone marrow was involved in 22.6% (14) patients. Extranodal involvements were found in 40 patients. Four major chemotherapeutic regimens including vincristine, prednisone, daunorubicin, L-asparginase (VPDL), CALGB 19802, Standford/NCOG, CHOP were used to treat 25,12,9 and 5 patients, respectively. Eleven other patients were treated with five different chemotherapeutic regimens, respectively. Two patients in relapse received allogeneic stem cell transplantation, and the other two received autologous stem cell transplantation. In 19 patients with first complete response, they were treated with autologous stem cell transplantation. When we compared precursor T lymphoblastic lymphoma with precursor B lymphoblastic lymphoma, precursor T lymphoblastic lymphoma showed older age (40≤ p=0.031), more mediastinal involvement (p=0.002), and male predominenance (p=0.005). Overall response rate of patients treated with initial chemotherapy was 83.9% (50% of CR, 33.9% of PR). Event-free survival (EFS) and overall survival (OS) rate at 30 months were estimated to be 53%±6 and 59%±6, respectively, with a median follow-up of 31 months. Twenty-six of 52 relapses occurred. ALL-type chemotherapy is not superior to conventional chemotherapy used for non-Hodgkin’s lymphoma (p=0.531). The survival differences was observed between stage I to III patients and IV patients (p=0.007), and patients with and without two or more extranodal sites of disease(p=0.038). There is no difference between precursor B lymphoblastic lymphoma and precursor B lymphoblastic lymphoma. Therefore, stage IV and two or more than two of extranodal involvements were found to be as prognostic factor in precursor B and T lymphoblastic lymphoma. Conclusion: Overall prognosis of precursor B and T lymphoblastic lymphoma was poor although they showed a good response to chemotherapy because of their high relpase rate. And stage and the number of extranodal involvement are two pretreatment prognostic factors for adult lymphoblastic lymphoma. Thus, newer treatment strategy adapted on the poor prognostic factors should be warranted.

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Han, Xin, and Carlos E. Bueso-Ramos. "Precursor T-Cell Acute Lymphoblastic Leukemia/ Lymphoblastic Lymphoma and Acute Biphenotypic Leukemias." American Journal of Clinical Pathology 127, no. 4 (April 2007): 528–44. http://dx.doi.org/10.1309/2qe3a6ekq8uydyrc.

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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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Maslak, P. "Precursor T-cell Acute Lymphoblastic Leukemia." ASH Image Bank 2003, no. 1231 (December 31, 2003): 100945. http://dx.doi.org/10.1182/ashimagebank-2003-100945.

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Pervez, Hira, Salwa Pervez, Soomro Niaz, and Saima Imam. "Huge complex mediastinal mass presenting as a rare variant of lymphoblastic leukemia/lymphoma." Professional Medical Journal 27, no. 10 (October 10, 2020): 2271–78. http://dx.doi.org/10.29309/tpmj/2020.27.10.4156.

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The mediastinum is the space that separates the lungs from the rest of the chest. The most common mediastinal masses are neurogenic tumors (20% of mediastinal tumors), followed by thymoma (15-20%). Other masses include lymphoma, pheochromocytoma, germ cell tumors, including teratoma, thyroid tissue, and parathyroid lesions. Lymphoblastic leukemias/lymphomas are neoplasms of precursor T cells and B cells also known lymphoblasts. World Health Organization (WHO) classification has unified these entities as precursor B-cell and T-cell lymphoblastic leukemia/lymphoma. We present here a rare variant of non-Hodgkins lymphoma in a 12-year-old female who complained of worsening dyspnea and lower left-sided chest pain. The patient was empirically treated with anti-tuberculous drugs without relief. On admission, a CT scan chest showed an anterior mediastinal mass approximately 25x12.5 cm adherent to the mediastinal structures. Resection of the mass was done sparing the phrenic nerve. The sample was sent for histopathology which suggested small cells with hyperchromatic nuclei and positive tumor markers. Rare occurrence of this ailment can lead to mistakes with the diagnosis. Therefore the uniqueness of our case lies in the fact that a T-LBL can present with such a huge mass.

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Viardot, Andreas, Franco Locatelli, Julia Stieglmaier, Faraz Zaman, and Elias Jabbour. "Concepts in immuno-oncology: tackling B cell malignancies with CD19-directed bispecific T cell engager therapies." Annals of Hematology 99, no. 10 (August 27, 2020): 2215–29. http://dx.doi.org/10.1007/s00277-020-04221-0.

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Abstract The B cell surface antigen CD19 is a target for treating B cell malignancies, such as B cell precursor acute lymphoblastic leukemia and B cell non-Hodgkin lymphoma. The BiTE® immuno-oncology platform includes blinatumomab, which is approved for relapsed/refractory B cell precursor acute lymphoblastic leukemia and B cell precursor acute lymphoblastic leukemia with minimal residual disease. Blinatumomab is also being evaluated in combination with other agents (tyrosine kinase inhibitors, checkpoint inhibitors, and chemotherapy) in various treatment settings, including frontline protocols. An extended half-life BiTE molecule is also under investigation. Patients receiving blinatumomab may experience cytokine release syndrome and neurotoxicity; however, these events may be less frequent and severe than in patients receiving other CD19-targeted immunotherapies, such as chimeric antigen receptor T cell therapy. We review BiTE technology for treating malignancies that express CD19, analyzing the benefits and limitations of this bispecific T cell engager platform from clinical experience with blinatumomab.

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Wang, Ping, Xian’gui Peng, Xiaojuan Deng, Li Gao, Xi Zhang, and Yimei Feng. "Diagnostic challenges in T-lymphoblastic lymphoma, early T-cell precursor acute lymphoblastic leukemia or mixed phenotype acute leukemia." Medicine 97, no. 41 (October 2018): e12743. http://dx.doi.org/10.1097/md.0000000000012743.

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Li, Shiyong, and Glen Lew. "Is B-Lineage Acute Lymphoblastic Leukemia With a Mature Phenotype and L1 Morphology a Precursor B-Lymphoblastic Leukemia/Lymphoma or Burkitt Leukemia/Lymphoma?" Archives of Pathology & Laboratory Medicine 127, no. 10 (October 1, 2003): 1340–44. http://dx.doi.org/10.5858/2003-127-1340-iballw.

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Abstract Context.—B-lineage acute lymphoblastic leukemia (ALL) with a mature phenotype and L1 morphology is a rare condition that may pose a diagnostic and management challenge. Objective.—To report our experience with 2 such unusual cases of pediatric B-lineage ALL. Design.—Morphologic, immunophenotypic, and cytogenetic features of the leukemic blast cells were reviewed in conjunction with clinical and other laboratory findings. Results.—The leukemic blast cells in both cases were small to medium with scant basophilic cytoplasm and several small inconspicuous nucleoli, characteristic of L1 lymphoblasts. Immunophenotypically, they were positive for CD19, CD22, and low-density CD20, with expression of surface immunoglobulin λ light chain. They were negative for immature (CD34 and terminal deoxynucleotidyl transferase), myeloid, and T-cell–associated markers. Conventional cytogenetic and fluorescent in situ hybridization studies failed to demonstrate chromosomal translocations involving the c-myc gene. Both patients were treated with Children's Cancer Group ALL protocols and had good responses. Conclusions.—B-lineage ALL with a mature phenotype, L1 morphology, and absent chromosomal translocations involving the c-myc gene is best classified and managed as precursor B-lymphoblastic leukemia/lymphoma instead of Burkitt leukemia/lymphoma.

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Kroeze, Emma, Jan L. C. Loeffen, Vera M. Poort, and Jules P. P. Meijerink. "T-cell lymphoblastic lymphoma and leukemia: different diseases from a common premalignant progenitor?" Blood Advances 4, no. 14 (July 28, 2020): 3466–73. http://dx.doi.org/10.1182/bloodadvances.2020001822.

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Abstract T-cell lymphoblastic lymphoma (T-LBL) and lymphoblastic leukemia (T-ALL) represent malignancies that arise from the transformation of immature precursor T cells. Similarities in T-LBL and T-ALL have raised the question whether these entities represent 1 disease or reflect 2 different diseases. The genetic profiles of T-ALL have been thoroughly investigated over the last 2 decades, whereas fairly little is known about genetic driver mutations in T-LBL. Nevertheless, the comparison of clinical, immunophenotypic, and molecular observations from independent T-LBL and T-ALL studies lent strength to the theory that T-LBL and T-ALL reflect different presentations of the same disease. Alternatively, T-LBL and T-ALL may simultaneously evolve from a common malignant precursor cell, each having their own specific pathogenic requirements or cellular dependencies that differ among stroma-embedded blasts in lymphoid tissues compared with solitary leukemia cells. This review aims to cluster recent findings with regard to clinical presentation, genetic predisposition, and the acquisition of additional mutations that may give rise to differences in gene expression signatures among T-LBL and T-ALL patients. Improved insight in T-LBL in relation to T-ALL may further help to apply confirmed T-ALL therapies to T-LBL patients.

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Conde-Sterling, Daniel A., Nadine S. I. Aguilera, Meenakshi A. Nandedkar, and Susan L. Abbondanzo. "Immunoperoxidase Detection of CD10 in PrecursorT-Lymphoblastic Lymphoma/Leukemia." Archives of Pathology & Laboratory Medicine 124, no. 5 (May 1, 2000): 704–8. http://dx.doi.org/10.5858/2000-124-0704-idocip.

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Abstract Context.—CD10 was originally reported in non–T-cell lymphoblastic lymphomas/leukemias. It has since been identified, however, in a minority of cases of T-lympho-blastic lymphoma/leukemia and other hematopoietic and nonhematopoietic entities. The usual method for the detection of CD10 previously required fresh tissue. A new antibody for CD10 (56C6) in paraffin embedded tissue sections, however, has recently become available. Objective.—To study the expression of CD10 in paraffin sections of T-lymphoblastic lymphoma/leukemia using monoclonal antibody 56C6. Design.—Twenty-four cases of T-lymphoblastic lymphoma/leukemia in various anatomic sites were studied. Immunohistochemical analysis with CD10 and a panel of other hematolymphoid antibodies was performed in all 24 cases. Gene rearrangement studies for the T-cell receptor by the polymerase chain reaction were performed in 18 of 24 cases. Results.—All cases were positive with at least 2 T-cell markers. In 15 (63%) of 24 cases CD10 was positive. T-cell receptor gene rearrangement was detected in 10 of 18 cases. Conclusions.—Immunodetection of CD10 in T-lympho-blastic lymphoma/leukemia using monoclonal antibody 56C6 is common. This finding is useful in the evaluation of T-cell neoplasms.

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Teachey, David T., and David O’Connor. "How I treat newly diagnosed T-cell acute lymphoblastic leukemia and T-cell lymphoblastic lymphoma in children." Blood 135, no. 3 (January 16, 2020): 159–66. http://dx.doi.org/10.1182/blood.2019001557.

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Abstract T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy that has historically been associated with a very poor prognosis. Nevertheless, despite a lack of incorporation of novel agents, the development of intensified T-ALL–focused protocols has resulted in significant improvements in outcome in children. Through the use of several representative cases, we highlight the key changes that have driven these advances including asparaginase intensification, the use of induction dexamethasone, and the safe omission of cranial radiotherapy. We discuss the results of recent trials to explore key topics including the implementation of risk stratification with minimal residual disease measurement and how to treat high-risk subtypes such as early T-cell precursor ALL. In particular, we address current discrepancies in treatment between different cooperative groups, including the use of nelarabine, and provide rationales for current treatment protocols for both T-ALL and T-lymphoblastic lymphoma.

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Kim, Me-Ae, Gyeong-Won Lee, and Kook-Young Maeng. "An unusual presenting feature of precursor T-cell acute lymphoblastic leukemia/lymphoma." Annals of Hematology 84, no. 8 (April 21, 2005): 553–54. http://dx.doi.org/10.1007/s00277-005-1042-4.

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Goutzanis, Lampros, John Apostolidis, Chara Giatra, Evanthia Chrysomali, and Dimitrios Deskos. "A case of systemic precursor T-cell lymphoblastic lymphoma presenting with single tooth mobility." SAGE Open Medical Case Reports 8 (January 2020): 2050313X2092796. http://dx.doi.org/10.1177/2050313x20927961.

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Lymphoblastic lymphoma, seen primarily in children or young adults, is a type of non-Hodgkin lymphoma that originates from B or T lymphocyte precursors and rarely occurs in the oral cavity. A case of systemic precursor T-cell lymphoblastic lymphoma mimicking periodontitis of a lower second molar in a 20-year-old adult is currently presented. The case was initially misdiagnosed as periodontal disease and treated with tooth extraction by a dentist. Re-evaluation of the patient due to worsening of symptoms lead to cone beam computed tomography scanning that thoroughly revealed an extended osteolytic lesion of the right mandible. Afterward, a biopsy was performed, thus reaching the diagnosis of precursor T-cell lymphoblastic lymphoma. This report discusses differences in epidemiology of T-cell and B-cell lymphoblastic lymphomas, as well as their various intraoral manifestations that are mimicking a large family of oral pathology. It also focuses on conventional imaging findings that imply malignancy, which are often neglected during routine radiology interpretation.

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Lin, Yingwei, Rebecca A. Nichols, John J. Letterio, and Peter D. Aplan. "Acquired Notch1 Mutations in Murine Precursor-T Leukemia/Lymphoma Models." Blood 106, no. 11 (November 16, 2005): 2612. http://dx.doi.org/10.1182/blood.v106.11.2612.2612.

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Abstract NOTCH1 has been implicated in hematopoiesis, T-cell differentiation, and the pathogenesis of precursor T-cell lymphoblastic leukemia/lymphoma (pre-T LBL). Although rare patients with pre-T LBL have chromosomal translocations that activate NOTCH1, it has recently been shown that over 50% of human pre-T LBL samples which did not have chromosomal aberrations involving NOTCH1 had activating mutations in the NOTCH1 heterodimerization (HD) and/or the PEST domain. We examined murine pre-T LBL cell lines as well as primary thymic tumors that arose in SCL/LMO1, OLIG2, OLIG2/LMO1, LMO1, NUP98/HOXD13 transgenic mice, and [p27(− /−) /SMAD3(−/+)] mice for evidence of Notch1 mutations. We also investigated the timing of Notch1 mutation in SCL/LMO1 transgenic mice. We found that 13/19 cell lines and 29/49 primary thymic tumors had Notch1 mutations in either the HD or PEST domain, but not both. Of the thirteen cell lines with Notch1 mutations, twelve had mutations in the PEST domain. The cell lines with Notch1 mutations were sensitive to gamma-secretase inhibitor treatment, indicating that the mutations were important for the survival of these cells. Of twenty-nine tumors with Notch1 mutations, 23 were in the PEST domain and 6 in the HD. All HD mutations were single base substitutions, whereas all PEST domain mutations were insertion/deletion mutations. Intriguingly, half of the PEST domain mutations mapped to one of two mutational hot spots, suggesting that these regions may be prone to insertion/deletion mutations. Thymocytes from clinically healthy SCL/LMO1 mice aged 5 weeks showed evidence of oligoclonal T-lymphocyte expansion, but did not have Notch1 mutations and did not form tumors when injected into nude mice (pre-malignant thymocytes), whereas thymocytes from SCL/LMO1 mice aged 8–12 weeks had Notch1 mutations and formed tumors upon transplantation into nude mice. Thus, Notch1 mutations are very frequent secondary events that can cooperate with a wide range of primary events as cells progress from a pre-malignant to a fully transformed state.

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Sasaki, Eiichi, Yasushi Yatabe, Mitsuyoshi Hashimoto, Yoriko Yamashita, Yuichi Hasegawa, Hiroshi Kojima, Toshiro Nagasawa, and Naoyoshi Mori. "Development-dependent expression of cyclin D3 in precursor T-cell lymphoblastic leukemia/lymphoma." Pathology International 57, no. 2 (February 2007): 53–59. http://dx.doi.org/10.1111/j.1440-1827.2006.02058.x.

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Fielding, Adele K., Lalita Banerjee, and David I. Marks. "Recent Developments in the Management of T-Cell Precursor Acute Lymphoblastic Leukemia/Lymphoma." Current Hematologic Malignancy Reports 7, no. 2 (April 3, 2012): 160–69. http://dx.doi.org/10.1007/s11899-012-0123-4.

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Kundu, Mondira, Sheila Compton, Lisa Garrett, Terryl Stacy, Mathew Starost, Michael Eckhaus, Nancy A. Speck, and Pu Paul Liu. "Runx1 Deficiency Predisposes Mice to T-Cell Lymphoblastic Lymphoma." Blood 104, no. 11 (November 16, 2004): 3490. http://dx.doi.org/10.1182/blood.v104.11.3490.3490.

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Abstract Chromosomal rearrangements affecting RUNX1 and CBFB are common in acute leukemias. These mutations result in the expression of fusion proteins that act in a dominant negative manner to suppress the normal function of the CBF β/RUNX1 complex. In addition, loss-of-function mutations in RUNX1 have been identified in sporadic cases of acute myeloid leukemia (AML) and in association with familial platelet disorder with propensity to develop AML (FPD/AML). In order to examine the hypothesis that decreased gene dosage of RUNX1 may be a critical event in the development of leukemia, we treated chimeric mice generated from Runx1lacZ/lacZ embryonic stem (ES) cells that have homozygous disruption of the RUNX1 gene, as well as Runx1+/lacZ mice with N-ethyl-N-nitrosurea (ENU). The heterozygous Runx1+/lacZ mice did not show increased incidence of any malignancy. On the other hand, we observed an increased incidence of precursor T-lymphoblastic lymphoma in Runx1lacZ/lacZ compared to wild-type chimeras, and confirmed that the tumors were of ES cell origin. It was determined by PCR that Runx1lacZ/lacZ ES cells contributed to the T cell progenitor population in the chimeras prior to leukemia development, which may explain the tissue-specificity of the malignancy we observed. Our results suggest that deficiency of Runx1 can indeed predispose mice to hematopoietic malignancies.

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Shi, Yang, and Endi Wang. "Blastic Plasmacytoid Dendritic Cell Neoplasm: A Clinicopathologic Review." Archives of Pathology & Laboratory Medicine 138, no. 4 (April 1, 2014): 564–69. http://dx.doi.org/10.5858/arpa.2013-0101-rs.

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Blastic plasmacytoid dendritic cell neoplasm is a rare entity grouped with the acute myeloid leukemia–related precursor neoplasms in the 2008 World Health Organization classification. It was previously postulated to originate from natural killer cells, T cells, or monocytes but is now believed to arise from the plasmacytoid dendritic cell. The pathogenesis of blastic plasmacytoid dendritic cell neoplasm is not well understood, although the neoplasm demonstrates frequent deletion of tumor suppressor genes, including RB1, CDKN1B, CDKN2A, and TP53. Blastic plasmacytoid dendritic cell neoplasm is a clinically aggressive tumor that often initially presents as cutaneous lesions and subsequently progresses to bone marrow involvement and leukemic dissemination. It is characterized by enhanced expression of CD56, CD4, and CD123, which can be detected by flow cytometry/immunohistochemistry. The differential diagnoses include myeloid sarcoma/acute myeloid leukemia, T-cell lymphoblastic leukemia/lymphoma, NK-cell lymphoma/leukemia, and some mature T-cell lymphomas/leukemias. Patients usually respond to initial chemotherapy but often relapse. Stem cell transplant may improve survival.

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Onciu, Mihaela, Raymond Lai, Francisco Vega, Carlos Bueso-Ramos, and L. Jeffrey Medeiros. "Precursor T-Cell Acute Lymphoblastic Leukemia in Adults." American Journal of Clinical Pathology 117, no. 2 (February 2002): 252–58. http://dx.doi.org/10.1309/08dj-gpbh-h0vr-rc6f.

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Smith, Jenny, Albert Kheradpour, Craig Zuppan, Jun Wang, Rhett Ketterling, and Edward Rowsell. "Secondary Precursor T-Cell Lymphoblastic Lymphoma Following Precursor B-cell Acute Lymphoblastic Leukemia: A Case Report and Review of the Literature." Journal of Cancer Research Updates 3, no. 2 (May 9, 2014): 117–22. http://dx.doi.org/10.6000/1929-2279.2014.03.02.6.

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Khurana, Sharad, Manuel Beltran, Liuyan Jiang, Ernesto Ayala, and Vivek Roy. "Primary Cutaneous T-Cell Lymphoblastic Lymphoma: Case Report and Literature Review." Case Reports in Hematology 2019 (February 20, 2019): 1–6. http://dx.doi.org/10.1155/2019/3540487.

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Cutaneous involvement by precursor T-cell lymphoblastic leukemia/lymphoma (T-ALL/LBL) is rare, and almost all cases are seen in association with bone marrow, blood, and/or lymph node involvement. Presentation with isolated skin involvement is very rare. Literature review revealed only one case report of primary cutaneous T-cell LBL. We discuss here another patient diagnosed with primary cutaneous T-cell LBL at our institute. This patient was initially misdiagnosed as having peripheral T-cell lymphoma NOS. Cytogenetic analysis showed the CDKN2A deletion (−9p21×2) in addition to three intact copies of ABL1 (+9q34). Although she failed multiple lines of intensive chemotherapy, her disease remained confined to the skin. We believe that this presentation of T-LBL is underreported, and many patients are likely misdiagnosed as having high-grade cutaneous T-cell lymphomas. With this case and literature review, we would like to highlight the importance of keeping lymphoblastic lymphoma on the differential diagnosis of cutaneous T-cell lymphoma-like lesions to avoid delay in diagnosis and inappropriate treatment of this aggressive disease.

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Nahimana, Aimable, Antoine Attinger, Dominique Aubry, Peter Greaney, Christopher Ireson, Annemette V. Thougaard, Jette Tjørnelund, Keith M. Dawson, Marc Dupuis, and Michel A. Duchosal. "The NAD biosynthesis inhibitor APO866 has potent antitumor activity against hematologic malignancies." Blood 113, no. 14 (April 2, 2009): 3276–86. http://dx.doi.org/10.1182/blood-2008-08-173369.

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Abstract APO866 inhibits nicotinamide phosphoribosyltransferase (NMPRTase), a key enzyme involved in nicotinamide adenine dinucleotide (NAD) biosynthesis from the natural precursor nicotinamide. Intracellular NAD is essential for cell survival, and NAD depletion resulting from APO866 treatment elicits tumor cell death. Here, we determine the in vitro and in vivo sensitivities of hematologic cancer cells to APO866 using a panel of cell lines (n = 45) and primary cells (n = 32). Most cancer cells (acute myeloid leukemia [AML], acute lymphoblastic leukemia [ALL], mantle cell lymphoma [MCL], chronic lymphocytic leukemia [CLL], and T-cell lymphoma), but not normal hematopoietic progenitor cells, were sensitive to low concentrations of APO866 as measured in cytotoxicity and clonogenic assays. Treatment with APO866 decreased intracellular NAD and adenosine triphosphate (ATP) at 24 hours and 48 to72 hours, respectively. The NAD depletion led to cell death. At 96 hours, APO866-mediated cell death occurred in a caspase-independent mode, and was associated with mitochondrial dysfunction and autophagy. Further, in vivo administration of APO866 as a single agent prevented and abrogated tumor growth in animal models of human AML, lymphoblastic lymphoma, and leukemia without significant toxicity to the animals. The results support the potential of APO866 for treating hematologic malignancies.

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Glukhanyuk, E. V., A. V. Stepanov, A. M. Popov, and M. A. Maschan. "CD-19-directed immunotherapy resistance mechanisms of B-precursor acute lymphoblastic leukemia." Oncohematology 13, no. 4 (January 3, 2019): 27–36. http://dx.doi.org/10.17650/1818-8346-2019-13-4-27-36.

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Immunotherapy is the most rapidly evolving field in clinical malignant hematology. Targeting of the B-lineage surface antigen CD19 in B-lineage acute lymphoblastic leukemia and B-cell lymphoma is a story of great success. Recently two approaches of CD19 immunotargeting were approved for clinical application: CD3 × CD19 bi-specific T-cell engager blinatumomab and CD19 chimeric antigen receptor (CAR) Tcells. Both approaches demonstrated an unprecedented activity in a cohort of patients with relapsed and refractory B-cell leukemia and lymphoma both in the adult and pediatric population. Early clinical research has showed that tumors are able to escape the immunological control and become resistant to the immune attack. Mechanisms of the tumor immune escape are being actively studied and include diverse pathways, such as alternative splicing of CD19 and immunosuppressive tumor microenvironment. Current review briefly summarizes data regarding the mechanisms of CD19-positive leukemia resistance to CD19 immune targeting and discusses potential approaches to overcome it.

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Xu, Xinjie, Christian N. Paxton, Robert J. Hayashi, Kimberly P. Dunsmore, Stuart S. Winter, Stephen P. Hunger, Naomi J. Winick, et al. "Genomic and clinical characterization of early T-cell precursor lymphoblastic lymphoma." Blood Advances 5, no. 14 (July 23, 2021): 2890–900. http://dx.doi.org/10.1182/bloodadvances.2021004334.

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Abstract Early T-cell precursor phenotype acute lymphoblastic leukemia (ETP-ALL) is a subtype of T-ALL with a unique immunophenotype and genetic abnormalities distinct from conventional T-ALL. A subset of T lymphoblastic lymphoma (T-LLy) also demonstrates the early T-cell precursor immunophenotype and may be a counterpart of ETP-ALL. Unlike ETP-ALL, the incidence, clinical features, and genomic features of ETP-LLy are unknown. We reviewed the immunophenotyping data of 218 T-LLy patients who enrolled in the Children’s Oncology Group AALL0434 clinical trial and identified 9 cases (4%) exhibiting a definitive ETP immunophenotype. We performed single-nucleotide polymorphism array profiling on 9 ETP-LLy and 15 non-ETP T-LLy cases. Compared with non-ETP T-LLy, ETP-LLy showed less frequent deletion of 9p (CKDN2A/B), more frequent deletion of 12p (ETV6) and 1p (RPL22), and more frequent absence of biallelic T-cell receptor γ deletions. Recurrent abnormalities previously described in ETP-ALL such as deletions of 5q and 13q and gain of 6q were not observed in ETP-LLy cases. There were no failures of therapy among the ETP-LLy subtype with a 4-year event-free survival of 100%. Overall, ETP-LLy does not exhibit unifying genetic alterations but shows some distinct genomic features from non-ETP T-LLy suggesting that ETP-LLy may be a distinct entity from non-ETP T-LLy.

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Pham, Alexander, Amir Steinberg, Brian Kwok, Angela Lopez, Stephen Lim, and Michael Lill. "Precursor T-Cell acute lymphoblastic leukemia/lymphoma with rare presentation in the urinary bladder." Hematology Reports 3, no. 2 (October 20, 2011): 18. http://dx.doi.org/10.4081/hr.2011.e18.

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Flex, Elisabetta, Valentina Petrangeli, Lorenzo Stella, Sabina Chiaretti, Tekla Hornakova, Laurent Knoops, Cristina Ariola, et al. "Somatically acquired JAK1 mutations in adult acute lymphoblastic leukemia." Journal of Experimental Medicine 205, no. 4 (March 24, 2008): 751–58. http://dx.doi.org/10.1084/jem.20072182.

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Aberrant signal transduction contributes substantially to leukemogenesis. The Janus kinase 1 (JAK1) gene encodes a cytoplasmic tyrosine kinase that noncovalently associates with a variety of cytokine receptors and plays a nonredundant role in lymphoid cell precursor proliferation, survival, and differentiation. We report that somatic mutations in JAK1 occur in individuals with acute lymphoblastic leukemia (ALL). JAK1 mutations were more prevalent among adult subjects with the T cell precursor ALL, where they accounted for 18% of cases, and were associated with advanced age at diagnosis, poor response to therapy, and overall prognosis. All mutations were missense, and some were predicted to destabilize interdomain interactions controlling the activity of the kinase. Three mutations that were studied promoted JAK1 gain of function and conferred interleukin (IL)-3–independent growth in Ba/F3 cells and/or IL-9–independent resistance to dexamethasone-induced apoptosis in T cell lymphoma BW5147 cells. Such effects were associated with variably enhanced activation of multiple downstream signaling pathways. Leukemic cells with mutated JAK1 alleles shared a gene expression signature characterized by transcriptional up-regulation of genes positively controlled by JAK signaling. Our findings implicate dysregulated JAK1 function in ALL, particularly of T cell origin, and point to this kinase as a target for the development of novel antileukemic drugs.

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Drakos, Elias, George Z. Rassidakis, Wei Guo, L. Jeffrey Medeiros, and Lalitha Nagarajan. "Differential Expression of the Homeobox Gene MIXL1 in Non Hodgkin (NHL) and Hodgkin Lymphomas (HL)." Blood 106, no. 11 (November 16, 2005): 3014. http://dx.doi.org/10.1182/blood.v106.11.3014.3014.

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Abstract The gene MIXL1 (Mix1 homeobox-like) encodes a paired class homeobox transcription factor involved in early hematopoietic specification during embryogenesis. Previous studies have shown that MIXL1 gene is expressed in hematopoietic cells during adult life (Guo et al. Blood100;1;89–96, 2002). Furthermore 5′ MIXL1 sequences are a target of retroviral insertion in murine T-cell lymphoma (http:RTCGD.ncifcrf.gov), suggesting a selection advantage for aberrant expression of this gene. However, the status of MIXL1 expression in human lymphomas has not been examined. Using a highly specific antibody, we assessed for MIXL1 protein expression in 14 lymphoma cell lines (9 B-cell and 5 T-cell) by immunobloting. MIXL1 was detected predominantly in nuclear extracts of lysates of all cell lines tested, although at a variable level. We also assessed for MIXL1 protein expression in 126 B-cell and 21 T-cell NHLs of various types, as well as 14 Hodgkin lymphomas using immunohistochemical methods. The results of the immunohistochemical studies are summarized in table 1. Once again, MIXL1 immunoreactivity was primarily nuclear in the tumor cells. Based on distribution data (histogram), a 50% cutoff was selected for high versus low MIXL1 expression. Among B-cell tumors, high expression levels of MIXL1 protein were more frequently detected in high-grade NHL and HL compared with low/intermediate grade NHL (p<0.0001, chi-square test). As a continuous variable, the percentage of MIXL1-positive tumor cells was also significantly higher in high-grade B-cell NHL and HL compared with low/intermediate grade NHL (p<0.0001, Kruskal Wallis test). All Hodgkin lymphomas expressed high levels of MIXL1 with 60% to 100% of neoplastic cells being positive for MIXL1. Most T-cell NHLs also expressed high levels of MIXL1. In contrast, most low/intermediate-grade B-cell NHL and multiple myelomas expressed low levels of MIXL1. Frequent overexpression of MIXL1 gene product in most high-grade B-cell NHLs, HL and T-cell NHLs suggests that aberrant expression of MIXL1 may play a role in proliferation, block of differentiation or both. Table 1. HL (n=14) B-NHL (n =126) T-NHL (n =21) N (%) Low/intermediate grade N (%) N (%) Classical HL 12/12(100%) Chronic lymphocytic leukemia /small lymphocytic lymphoma 0/8 (0% T-precursor lymphoblastic leukemia/lymphoma 2/2 (0%) Nodular lymphocyte predominance HL 2/2 (100%) MALT-lymphoma 0/8 (0%) Mycosis fungoides/Sezary syndrome 2/2 (0%) Follicular lymphoma 9/24 (38%) Extranodal NK/T-cell lymphoma, nasal type 3/3 (100%) Mantle cell lymphoma 5/34 (15%) Peripheral T-cell lymphoma, unspecified 6/9 (66% High grade Anaplastic large cell lymphoma 5/5 (100%) B-precursor lymphoblastic leukemia/lymphoma 1/3 (33%) Burkitt lymphoma/leukemia 2/2 (100%) Diffuse large B-cell lymphoma 30/31 (97%) Plasma cell myeloma/plasmacytoma 0/16 (0%)

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Raizen, Yuval, Mark M. Udden, Hao Liu, Meng-Fen Wu, and Martha P. Mims. "Risk and Therapeutic Outcomes in a Multiethnic Group of Acute Lymphoblastic Leukemia Patients Treated at a Large Public Hospital." Blood 112, no. 11 (November 16, 2008): 3938. http://dx.doi.org/10.1182/blood.v112.11.3938.3938.

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Abstract Despite improvements in the treatment of adults with acute lymphoblastic leukemia (ALL) during the last decade, most patients will relapse and ultimately die of disease. Although some factors that affect risk of disease and treatment outcome are known, our ability to predict response and tailor treatments is far from perfect. In particular, we observed that the majority of the ALL patients treated at our large public hospital in Houston, TX were Hispanic. In order to more closely examine this trend and attempt to identify characteristics that would predict risk or therapeutic response, we performed a retrospective analysis of all patients with precursor B-cell ALL, T-cell ALL, and Burkitt lymphoma treated at our hospital over a fifteen year period. One hundred thirteen patients were identified, including sixty-one with precursor B-cell ALL, thirty-two with Burkitt lymphoma, sixteen with T-cell ALL, and four patients with additional features. All patients were treated with HyperCVAD, alternating with methoxtrexate and cytarabine, although some patients had therapeutic modifications because of disease characteristics, particularly in the first course. The median overall survival for all patients was 357 days. Patients with precursor B-cell ALL had the poorest outcome in both overall survival and progression-free survival, and a less favorable outcome than expected from the literature with a 38% two-year survival (95% CI: 54–92%). In contrast, patients with Burkitt lymphoma had an 80% 2-year survival (95% CI: 54%–92%) and those with T-cell ALL had a 63% 2-year survival (95% CI: 32%–83%). The outcomes for Burkitt lymphoma and T-cell ALL are similar to those reported in the literature. Nearly 80% of the patients with precursor B-cell ALL were Hispanic, and most were older than thirty (mean age 36.4 years) with few comorbidities. In contrast, only about 40% of the other high grade leukemia/lymphoma patients were Hispanic, reflecting more closely the racial/ethnic distribution of the population served by the hospital. While our precursor B-cell ALL patients were predominantly Hispanic, there was no statistical difference in overall survival or progression-free survival for Hispanic versus non-Hispanic patients. Hispanic patients with pre-B ALL had a 38% 2-year survival (95% CI: 20%–55%) while non- Hispanic patients had a 41% 2-year survival (95% CI: 12%–69%). Patients younger than thirty with precursor B-cell ALL had a statistically significant survival benefit compared to older patients. Fourteen patients (22.6%) with precursor B-cell ALL had a white blood cell count greater than 50,000, and these patients had significantly poorer outcomes. There was no correlation between cytogenetic abnormalities and outcome; however, very few patients were found to harbor the 9:22 translocation. There was a high incidence of CD20 positivity (55.7%) in patients with precursor B-cell ALL; however, there was no statistically significant correlation with overall survival or progression-free survival. Thus in our multiethnic patient population, patients with precursor B-cell ALL had significantly poorer outcomes than those reported in the literature, while patients with T-cell ALL or Burkitt lymphoma had outcomes to those reported in the literature using the identical chemotherapy regimen. The older age of the precursor B-cell ALL patients may have contributed to this poorer outcome. As noted above, our precursor B-cell ALL patients were predominately Hispanic as compared to the other leukemia patients we studied. Although Hispanic ethnicity did not clearly contribute to outcome, risk of developing precursor B-cell ALL appears to be greater in the Hispanic population.

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Wei, Eric X., Vasiliki Leventaki, John K. Choi, Susana C. Raimondi, Elizabeth M. Azzato, Sheila A. Shurtleff, Menchu G. Ong, Diana M. Veillon, James D. Cotelingam, and Rodney E. Shackelford. "γδ T-Cell Acute Lymphoblastic Leukemia/Lymphoma: Discussion of Two Pediatric Cases and Its Distinction from Other Mature γδ T-Cell Malignancies." Case Reports in Hematology 2017 (2017): 1–7. http://dx.doi.org/10.1155/2017/5873015.

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Gamma delta (γδ) T-cell antigen receptor (TCR) expression and its related T-cell differentiation are not commonly reported in T-cell acute lymphoblastic leukemia/lymphoma (T-ALL). Here we report two pediatric T-ALL cases and present their clinical features, histology, immunophenotypes, cytogenetics, and molecular diagnostic findings. The first patient is a two-year-old girl with leukocytosis, circulating lymphoblasts, and a cryptic insertion of a short-arm segment at 10p12 into the long-arm segment of 11q23 resulting in an MLL and AF10 fusion transcript, which may be the first reported in γδ T-ALL. She responded to the chemotherapy protocol poorly and had persistent diseases. Following an allogeneic bone marrow transplant, she went into remission. The second patient is an eleven-year-old boy with a normal white cell count, circulating blasts, and a normal karyotype, but without any immature cellular markers by flow cytometric analysis. He responded to the chemotherapy well and achieved a complete remission. These cases demonstrate the diverse phenotypic, cytogenetic, and molecular aspects of γδ T-ALL. Early T-precursor- (ETP-) ALL and their differential diagnosis from other mature γδ T-cell leukemia/lymphomas are also discussed.

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Edlefsen, Kerstin Lara, Anneclaire De Roos, and Andrea LaCroix. "Application of the InterLymph Consortium’s Proposed Classification of Lymphoid Neoplasms for Epidemiologic Research to a Large, Nationwide Health Study: Experience in the Women’s Health Initiative." Blood 112, no. 11 (November 16, 2008): 4669. http://dx.doi.org/10.1182/blood.v112.11.4669.4669.

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Abstract Large cohort studies, such as the Women’s Health Initiative, have traditionally grouped hematopoietic neoplasms (HPN) into disease categories including multiple myeloma (MM), non-Hodgkin lymphoma (NHL), Hodgkin lymphoma (HL), and leukemia, however this may not allow for optimal distinction of biologically relevant associations. The 2001 World Health Organization (WHO) classification of HPN represents the current gold standard classification scheme, and has been incorporated into the International Classification of Disease for Oncology, Third Edition (ICD-O-3). In 2007, the International Lymphoma Epidemiology Consortium (InterLymph) proposed a classification of lymphoid neoplasms for epidemiologic research that is based upon the WHO/ICD-O-3 classification (Morton LM, et al. Blood, 2007;110:695–708). Here we report on the application of this proposed classification scheme within the Women’s Health Initiative (WHI), a large, nationwide health study. All incident cases of HPN reported by women in the WHI cohort of 161,808 women were adjudicated by SEER-trained cancer coders according to SEER criteria, including assignment of histology codes based on ICD-O-3 guidelines. Cases were simultaneously assigned to one of the four traditional categories (leukemia, NHL, HL, and MM). Histologic subtypes were then grouped according to the recommendations of InterLymph. A total of 1534 women with incident HPN were identified within the WHI cohort. This included 405 within the general category of leukemia, 853 NHL, 237 MM, and 39 HL. Within the leukemia category, 221 are of lymphoid origin. See Table 1 for the InterLymph classification of the lymphoid neoplasms. These findings highlight the critical importance of appropriately classifying HPN for epidemiologic research. The traditional classification of all blood-based HPN as “leukemias” is particularly problematic, as this grouping includes neoplasms from both the myeloid and lymphoid lineages. In addition, disorders with both leukemic and solid disease phases, such as CLL/SLL, are split between those two traditional categories (leukemia and NHL). These groups also include entities with both indolent and aggressive clinical behaviors. HPN are a heterogeneous group of neoplasms that are known to have distinct phenotypes, presentations, and natural progressions, and they are increasingly recognized to be etiologically heterogeneous. The traditional grouping of these neoplasms into leukemia, NHL, HL, and MM is problematic, and may limit the interpretation of research findings. Classification of these neoplasms according to the recommendations of InterLymph should allow for improved detection of biologically relevant associations. TABLE 1. All incident lymphoid neoplasms since WHI enrollment, by ICD-0-3 histologic subtype (first column) and by traditional categorization as leukemia (leuk), non-Hodgkin lymphoma (NHL), Hodgkin lymphoma (HL), and multiple myeloma (MM). TOTAL NHL Leuk* MM HL *Leukemia category includes 405 total participants, 177 with myeloid leukemias (116 AML, 40 CML, 14 CMML, 7 other/unclassified) and 7 with leukemias of ambiguous/unspecified lineage ^Chronic lymphocytic leukemia/small lymphocytic lymphoma/pro-lymphocytic leukemia/mantle cell lymphoma Lymphoid neoplasms TOTAL 1350 853 221 237 39 Hodgkin (HL) TOTAL 39 0 0 0 39 Classical Hodgkin (HL, C) 23 23 Hodgkin, not otherwise specified (HL, NOS) 10 10 Nodular lymphocyte-predominant (HL, NLP) 6 6 Non-Hodgkin (NHL) B lineage: TOTAL B-NHL 1259 811 211 237 0 Precursor B-acute lymphoblastic leukemia/lymphoma (B-ALL) 7 7 Mature CLL/SLL/PLL/MCL^ 294 106 188 Lymphoplasmacytic lymphoma (LPL)/Waldenstrom macroglobulinemia (WM) 32 23 9 Burkitt lymphoma (BL) 7 6 1 Follicular lymphoma (FL) 208 208 Marginal zone lymphoma (MZL) 88 88 Hairy cell leukemia (HCL) 6 6 Diffuse large B cell (DLBCL) 275 275 Plasma cell neoplasm (PCN) 237 237 B-NHL, not otherwise specified (NOS) 105 105 T lineage: TOTAL T-NHL 47 41 6 0 0 Precursor T-acute lymphoblastic leukemia/lymphoma (T-ALL) 2 2 Mature Mycosis Fungoides(MF)/Sezary syndrome (SS) 7 7 Peripheral T cell lymphoma (PTCL) 30 30 Natural Killer/T cell lymphoma (NK/T) 1 1 Large granular lymphocyte leukemia (T-LGL) 5 5 T-prolymphocytic lymphoma (T-PLL) 2 1 1 Unknown lineage: TOTAL UKNOWN/UNSPECIFIED NHL 5 1 4 0 0 Precursor Acute lymphoblastic leukemia (U-ALL) 1 1 Mature NHL, not other specified (U-NHL) 4 1 3

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Krieger, David, Anja Moericke, Wolfram Klapper, Franziska Greene, Martin Zimmermann, Martin Schrappe, Alfred Reiter, and Birgit Burkhardt. "Pediatric T-Cell Lymphoblastic Leukemia and T-Cell Lymphoblastic Lymphoma: One and the Same or Two Different Diseases?." Blood 110, no. 11 (November 16, 2007): 1437. http://dx.doi.org/10.1182/blood.v110.11.1437.1437.

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Abstract Background/Objectives: Precursor T lymphoblastic neoplasms in children and adolescents are currently classified as either acute lymphoblastic T-cell leukemia (T-ALL) in case of ≥25% bone marrow involvement or lymphoblastic T-cell lymphoma (T-LBL) in case of <25% bone marrow involvement. This distinction is considered to be largely arbitrary because of overlapping biological and clinical features. However, comparative studies of smaller patient series reported differences of immunophenotypic and molecular genetic parameters, suggesting that T-ALL and T-LBL might indeed be biologically different. While deletions of certain chromosomal regions have long been identified in pediatric T-ALL, for T-LBL molecular or cytogenetic data are scarce. Design/Methods: The current study focused on the frequency, the association with clinical characteristics and the prognostic impact of selected chromosomal deletions, comparing 119 T-LBL patients (pts) with 125 T-ALL pts. T-LBL and T-ALL pts were registered in the NHL-BFM or ALL-BFM study center respectively. Both groups were treated according to ALL-BFM type treatment strategies. The molecular genetic analyses focused on chromosomal regions, harboring genes of functional relevance. Deletions were examined through loss-of-heterozygosity (LOH) analyses of 46 microsatellite markers. The following regions were analyzed: Chromosome 6q (25 markers), 7q (4 markers), 9p (5 markers), 11q (5 markers), 12p (6 markers) and p53 (1 marker). Samples of tumor and germline DNA were amplified by PCR, followed by fragment-length analysis with a genetic analyzer. Results: In 119 T-LBL pts a total of 4,780 markers and in 125 T-ALL pts a total of 5,730 markers were analyzed successfully. The frequency of LOH is depicted in table 1. Frequency of LOH in T-ALL and T-LBL patients T-LBL (n LOH + pts / n total pts) T-ALL (n LOH + pts / n total pts) p-value (Fisher) LOH at 6q 25 / 118 21% 15 / 125 12% 0.059 LOH at 7q 7 / 119 6% 2 / 124 2% 0.097 LOH at 9p 57 / 116 49% 63 / 125 50% 0.898 LOH at 11q 11 / 116 9% 3 / 125 2% 0.026 LOH at 12p 13 / 119 11% 9 / 125 7% 0.374 LOH at p53 4 / 76 5% 1 / 108 1% 0.161 Regarding clinical characteristics, LOH at 9p was associated with male gender in T-ALL and T-LBL. However, LOH at 9p was associated with elevated LDH level in T-ALL, but not in T-LBL. LOH at 12p was associated with female gender and mediastinal mass in T-ALL. In T-LBL, the 11 positive cases with LOH 12p showed an uncommon distribution of disease stages with more frequent stage II and stage IV disease. Regarding the prognostic impact, LOH at 6q was associated with an increased relapse rate in T-LBL but not in T-ALL. Interestingly, 2 of 3 T-ALL pts with LOH at 11q suffered from relapse compared to 0 out of 11 LOH 11q positive T-LBL pts. LOH at all other loci was not associated with a significant change in the risk of relapse. Conclusions: Chromosomal deletions found in pediatric T-ALL were also detected in pediatric T-LBL. However, the frequency, the association with clinical characteristics and the prognostic impact of these deletions differ between pediatric T-LBL and T-ALL. These results might be a new indicator that there are indeed differences between pediatric T-LBL and T-ALL.

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Huang, Q., D. S. Snyder, P. Chu, K. K. Gaal, K. L. Chang, and L. M. Weiss. "PDGFRA rearrangement leading to hyper-eosinophilia, T-lymphoblastic lymphoma, myeloproliferative neoplasm and precursor B-cell acute lymphoblastic leukemia." Leukemia 25, no. 2 (November 23, 2010): 371–75. http://dx.doi.org/10.1038/leu.2010.272.

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Onishi, Yasushi, Yoshihiro Matsuno, Ukihide Tateishi, Akiko Miyagi Maeshima, Masahiko Kusumoto, Takashi Terauchi, Shigeru Kusumoto, et al. "Two Entities of Precursor T-Cell Lymphoblastic Leukemia/Lymphoma Based on Radiologic and Immunophenotypic Findings." International Journal of Hematology 80, no. 1 (July 1, 2004): 43–51. http://dx.doi.org/10.1532/ijh97.04061.

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Shah, Bijal D., Uma Borate, Vamsi K. Kota, Ling Zhang, Deniz Peker, Amanda Redden Hathaway, and Julio C. Chavez. "Multi-Institution Review of Adult Early T-Cell Precursor Acute Lymphoblastic Leukemia/Lymphoma (ETP-ALL)." Blood 126, no. 23 (December 3, 2015): 3715. http://dx.doi.org/10.1182/blood.v126.23.3715.3715.

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Abstract Background: The Early T-cell precursor (ETP) variant of acute lymphoblastic lymphoma/leukemia (ALL) is a recognized high risk variant, recognized by the absence of CD1a, with aberrant myeloid antigen expression (CD13, CD33, CD117, and CD34), and frequent absence of CD4 or CD8. Treatment intensification may improve outcome in this subset. We undertook a multi-center retrospective analysis to explore clinical features, treatment exposure, and outcomes in ETP ALL as compared to non-ETP variants. Methods Adult T-ALL/T-LBL cases were compiled from 3 high volume cancer centers between the years 2003-2015. Data collected included patient demographics, tumor characteristics (white count at diagnosis, flow cytometry, FISH, cytogenetics, bone marrow involvement), treatment regimens and patient outcomes. ETP cases were defined as definite (CD1a-/CD8-/myeloid+) or probable (CD1a unk/CD8-/myeloid+, or CD1a-/myeloid+ with CD4+ and/or CD8+). All other cases were defined as non-ETP. Demographic data were compared using independent t-test assuming non-equal variance. OS and PFS were calculated from diagnosis and compared by Kaplan Meier and log-rank testing. Results Among 95 cases, 33 met criteria for definite/probable ETP (35%). OS and PFS data were indistinguishable between these groups (p=0.24, p=0.34), and were subsequently analyzed as a single group. Within the ETP group, no factors were associated with OS, including histology (CD1a+ vs unk, CD3cyt vs CD3sur, CD5dim vs CD5+, CD1a+/13+ vs CD1a+/13-, or CD13, CD33, CD117, CD34, & TdT status), marrow blast burden, peripheral blast burden, white blood cell count (wbc), hemoglobin (hgb), platelet count (plt), cytogenetics/FISH status, chemotherapy choice, or allogeneic transplant (in CR1 or at any time). With regards to PFS, only the inclusion of asparaginase with induction was associated with outcome (p=0.009), while all other covariates failed to show any significance. The ETP group was compared with the non-ETP subset (table 1). ETP were more likely to abuse marijuana, possibly reflecting unrecognized pesticide exposure, and were more likely to abnormalities of chrom 5 & 7. ETP trended towards lower response and higher rate of relapse, with lower PFS. Comparison of OS was not significant, likely related to small numbers (5y OS 37% vs 22%, figure 1). Non-ETP failed to show PFS benefit with frontline asparaginase, otherwise no treatment differences were apparent. Conclusions In this muti-center cohort we were able to identify and characterize ETP cases, confirming poor outcomes. Improvement in PFS among ETP patients treated with frontline asparaginase warrants attention and prospective confirmation. Unfortunately, OS remains poor independent of treatment or receipt of allogeneic transplant, suggesting a critical need remains for development and study novel therapies. Table 1. ETP Non-ETP p-value Median Age 37.45 34.74 0.42 Male 82% 66% 0.89 FamilyHx of Lymph/Leuk 21% 8% 0.112 FamilyHx of Ca 42% 25% 0.09 THC 24% 5% 0.021 P blasts 40% 28% 0.158 >25% M blasts 30% 55% 0.0571 WBC 78.45 76.55 0.948 wbc>100 24% 24% 0.995 Hgb 10.72 11.78 0.148 hgb<12 67% 47% 0.097 plt 151.59 138.66 0.644 Chrom 5/7 40% 7% 0.005 Remission 61% 79% 0.096 Relapse 76% 58% 0.073 OS 27.00 22.00 0.595 PFS 13.00 17.00 0.048 PFS Asp ETP (asp no vs yes) 12 59 0.009 non-ETP (asp no vs yes) 17 15 0.777 Figure 1. Figure 1. Disclosures Shah: Acetylon: Membership on an entity's Board of Directors or advisory committees; Spectrum: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau; Bayer: Honoraria; Celgene: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau; PLexus Communications: Honoraria; Pharmacyclics: Speakers Bureau; Rosetta Genomics: Research Funding; Seattle Genetics: Research Funding. Kota:Pfizer: Membership on an entity's Board of Directors or advisory committees; Leukemia Lymphoma Society: Research Funding. Hathaway:OnQ Health: Research Funding.

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Lyman, Mark D., and Thomas S. Neuhauser. "Precursor T-cell acute lymphoblastic leukemia/lymphoma involving the uterine cervix, myometrium, endometrium, and appendix." Annals of Diagnostic Pathology 6, no. 2 (April 2002): 125–28. http://dx.doi.org/10.1053/adpa.2002.32381.

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Dickson, Brendan C., Catherine T.-S. Chung, Bruce J. Patterson, Robert H. Riddell, Suzanne Kamel-Reid, Hans A. Messner, and Jeffrey H. Lipton. "Precursor Lymphoblastic Lymphoma Reoccurring as a Donor-Derived Neoplasm: A Case Report and Review of the Literature." Archives of Pathology & Laboratory Medicine 132, no. 8 (August 1, 2008): 1342–45. http://dx.doi.org/10.5858/2008-132-1342-pllraa.

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Abstract Precursor lymphoblastic lymphoma is an uncommon neoplasm. We report the case of a man who presented with precursor T lymphoblastic lymphoma and ultimately received an allogeneic bone marrow transplant from his human leukocyte antigen–identical sister. Four years later he developed recurrent disease. By means of DNA probing for the amelogenin locus and fluorescence in situ hybridization, the neoplastic cells of the recurrent lesion were found to be of donor origin. We offer the report of a patient with an unusual lymphoblastic lymphoma who, after successful bone marrow transplantation, developed the same disease of donor cell origin; further, we offer a literature review on donor cell lymphoma.

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Lin, Ying-Wei, Zanna M. Beharry, Elizabeth G. Hill, Jin H. Song, Wenxue Wang, Zuping Xia, Zhenhua Zhang, et al. "A small molecule inhibitor of Pim protein kinases blocks the growth of precursor T-cell lymphoblastic leukemia/lymphoma." Blood 115, no. 4 (January 28, 2010): 824–33. http://dx.doi.org/10.1182/blood-2009-07-233445.

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Abstract The serine/threonine Pim kinases are up-regulated in specific hematologic neoplasms, and play an important role in key signal transduction pathways, including those regulated by MYC, MYCN, FLT3-ITD, BCR-ABL, HOXA9, and EWS fusions. We demonstrate that SMI-4a, a novel benzylidene-thiazolidine-2, 4-dione small molecule inhibitor of the Pim kinases, kills a wide range of both myeloid and lymphoid cell lines with precursor T-cell lymphoblastic leukemia/lymphoma (pre–T-LBL/T-ALL) being highly sensitive. Incubation of pre–T-LBL cells with SMI-4a induced G1 phase cell-cycle arrest secondary to a dose-dependent induction of p27Kip1, apoptosis through the mitochondrial pathway, and inhibition of the mammalian target of rapamycin C1 (mTORC1) pathway based on decreases in phospho-p70 S6K and phospho-4E-BP1, 2 substrates of this enzyme. In addition, treatment of these cells with SMI-4a was found to induce phosphorylation of extracellular signal-related kinase1/2 (ERK1/2), and the combination of SMI-4a and a mitogen-activated protein kinase kinase 1/2 (MEK1/2) inhibitor was highly synergistic in killing pre–T-LBL cells. In immunodeficient mice carrying subcutaneous pre–T-LBL tumors, treatment twice daily with SMI-4a caused a significant delay in the tumor growth without any change in the weight, blood counts, or chemistries. Our data suggest that inhibition of the Pim protein kinases may be developed as a therapeutic strategy for the treatment of pre–T-LBL.

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Recine, Monica, Amilcar A. Castellano-Sanchez, Jerome Sheldon, Michael Schwartz, and Beria Cabello-Inchausti. "Precursor B-cell lymphoblastic lymphoma/leukemia presenting as osteoblastic bone lesions." Annals of Diagnostic Pathology 6, no. 4 (August 2002): 236–43. http://dx.doi.org/10.1053/adpa.2002.34733.

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Sharlai, A. S., O. I. Illarionova, Y. G. Fediukova, T. Yu Verzhbitskaya, L. G. Fechina, E. G. Boichenko, A. I. Karachunskiy, and A. M. Popov. "Immunophenotypic characteristics of early T-cell precursor acute lymphoblastic leukemia." Pediatric Hematology/Oncology and Immunopathology 18, no. 2 (June 29, 2019): 66–74. http://dx.doi.org/10.24287/1726-1708-2019-18-2-66-74.

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Early T-cell precursor acute lymphoblastic leukemia (ETP-ALL) is a recently recognized T-ymphoblastic leukemia subgroup with poor prognosis and high-risk of relapse. ETP-ALL subgroup is characterized by unique gene expression and particular cell surface markers profile. Nevertheless, this group cannot be easily detected due to its biological heterogeneity. The aim of the present study was to explore the immunophenotypic characteristics of early T-cell precursor acute lymphoblastic leukemia in ETP-ALL patient. The study group consisted of 64 patients with ETP-ALL. 380 patients with other variants of T-ALL were included to the control group. The antigen expression profile was assessed by multicolor flow cytometry. TI and TII immunological variants were detected in the group of patients with ETP-ALL. Cell markers expression level was determined in both groups. In the study group of ETP-ALL patients CD11a expression was more specific to TII-ALL, while CD33 expression – for TI-ALL. This study allowed to characterize group of patients with ETP-ALL and detected immunophenotypic heterogeneity. More interlaboratory studies are needed for understanding immunological and molecular genetic features ETP-ALL. The study was approved by the Independent Ethics Committee of the Dmitry Rogachev National Medical Research Center of Pediatric Hematology, Oncology, and Immunology.

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Kovač, Lana, Mario Bilić, Boris Bumber, and Iva Topić. "Primary laryngeal manifestation in precursor T-cell acute lymphoblastic leukemia." Otolaryngology–Head and Neck Surgery 139, no. 3 (September 2008): 474–75. http://dx.doi.org/10.1016/j.otohns.2008.04.002.

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WANG, LIN, YAN MA, BOBIN CHEN, FENG TANG, XIAOPING XU, and GUOWEI LIN. "Primary laryngeal manifestation in precursor T-cell acute lymphoblastic leukemia." Oncology Letters 9, no. 2 (December 12, 2014): 691–94. http://dx.doi.org/10.3892/ol.2014.2800.

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Esmaeli, Bita. "Orbital Mass Secondary to Precursor T-Cell Acute Lymphoblastic Leukemia." Archives of Ophthalmology 119, no. 3 (March 1, 2001): 443. http://dx.doi.org/10.1001/archopht.119.3.443.

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Lin, Chung-Wu, Ting-Yun Liu, Shee-Uan Chen, Kun-Teng Wang, L. Jeffrey Medeiros, and Su-Ming Hsu. "CD94 1A transcripts characterize lymphoblastic lymphoma/leukemia of immature natural killer cell origin with distinct clinical features." Blood 106, no. 10 (November 15, 2005): 3567–74. http://dx.doi.org/10.1182/blood-2005-02-0519.

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AbstractMost lymphoblastic lymphomas (LBLs) are regarded as neoplasms of immature T cells because they express cytoplasmic CD3 and frequently carry T-cell receptor (TCR) gene rearrangements. Immature natural killer (NK) and T cells, however, have a common bipotent T/NK-cell precursor in the thymus, and NK cells also express cytoplasmic CD3. Thus, some LBLs could arise from immature NK cells. Mature NK cells express 2 CD94 transcripts: 1A, induced by interleukin 15 (IL-15), and 1B constitutively. Because immature NK cells require IL-15 for development, CD94 1A transcripts could be a marker of NK-LBL. To test this hypothesis, we used laser capture microdissection to isolate IL-15 receptor α+ lymphoid cells from the thymus and showed that these cells contained CD94 1A transcripts. We then assessed for CD94 transcripts in 21 cases of LBL that were cytoplasmic CD3+, nuclear terminal deoxynucleotidyl transferase positive (TdT+), and CD56-, consistent with either the T-cell or NK-cell lineage. We found that 7 LBLs expressed CD94 1A transcripts without TCR gene rearrangements, suggesting NK-cell lineage. Patients with NK-LBL were younger than patients with T-LBL (15 years versus 33 years; P = .11) and had a better 2-year survival (100% versus 27%; P < .01). These results improve the current classification of LBL and contribute to our understanding of NK-cell differentiation.

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46

Li, Shiyong, Jonathan Juco, Karen P. Mann, and Jeannine T. Holden. "Flow Cytometry in the Differential Diagnosis of Lymphocyte-Rich Thymoma From Precursor T-Cell Acute Lymphoblastic Leukemia/Lymphoblastic Lymphoma." American Journal of Clinical Pathology 121, no. 2 (February 2004): 268–74. http://dx.doi.org/10.1309/k2fy1ted8gegflng.

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47

Onozawa, Masahiro, Hyunkyung Kim, Sheryl M. Gough, Yingwei Lin, Yongzhi Cui, Sarah H. Beachy, Crystal L. Mackall, and Peter Aplan. "Illegitimate V(D)J Recombination Involving Notch1 and Bcl11b in Precursor T-Cell Lymphoblastic Leukemia/Lymphoma." Blood 120, no. 21 (November 16, 2012): 1323. http://dx.doi.org/10.1182/blood.v120.21.1323.1323.

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Abstract Abstract 1323 V(D)J recombination of antigen receptor loci confers diversity to the mammalian immune system. However, off-target, illegitimate V(D)J recombination between non-antigen receptor loci, leading to site-specific interstitial deletion has been reported in humans and mice with lymphoid malignancies. These recurrent, site-specific interstitial deletions are thought to be oncogenic, leading to activation of proto-oncogenes or deletion of tumor suppressor genes. Notch1 and Bcl11b are known targets for illegitimate V(D)J recombination in murine precursor T-cell leukemia/lymphoma (pre-T-LBL). The Notch1 5'-deletions remove exon1 and 2; as a consequence Notch1 transcription initiates from a cryptic promoter immediately 5' of exon 25. These alternative transcripts are translated from exon 28, and lack the N-term ligand binding domain, resulting in a Notch1 protein that is independent of ligand binding. The known Bcl11b deletions excise exon2 and 3, and result in loss of function of the Bcl11b tumor suppressor gene. The frequency with which Notch1 and Bcl11b deletions occur in concert is unknown. Here we examined both Notch1 and Bcl11b deletion mutations, as well as Notch1 mutations involving the PEST, HD, and TM domains in primary murine pre-T LBL samples (N=44), and murine pre-T LBL cell lines (N=21), that arose in specific genetically engineered mouse strains (Scl-Lmo1, NUP98-PHF23, HoxA9, Lin28B, Survivin-TCR). Analysis of 44 primary tumor samples identified 17 Notch1 5'-interstitial deletions (38.6%) and 8 Bcl11b deletions (18.1%), while analysis of 21 cell lines revealed 10 Notch1 5' deletions (47.6%) and 5 Bcl11b deletions (24%). The percent of Notch1 PEST, HD, and TM mutations were 84.1%, 13.6%, and 4.5%, respectively, in the primary tumors and 95%, 5%, and 0% in the cell lines. Two primary tumor samples showed several different 5' deletion mutations, representing multiple independent leukemic clones. Of the 13 primary tumor/cell line pairs we analyzed, 5 pairs showed identical Notch1 and Bcl11b mutations. However, for 7 pairs, the primary tumor was oligoclonal with respect to Notch1 and Bcl11b mutations, with one clone being biologically selected for growth in vitro. In 3 cases, Bcl11b deletion was not detected in primary tumor but was detected in the cell line, suggesting that the Bcl11b deletion was a secondary event in these cell lines. Notch1 PEST mutations were present in almost all cell lines, and were often accompanied by an additional Notch1 mutation (5'deletion, HD, or TM). Conversely, 5' deletion, HD, and TM mutations were mutually exclusive. These findings support the hypothesis that the 5'deletion, HD, and TM mutations lead to ligand independent activation, while the PEST domain mutations prevent proteasomal degradation leading to persistence of the transcriptionally active intracellular Notch1. In several cases, samples had an identical PEST mutation, but distinct 5' deletion or HD mutations, indicating the PEST mutation preceded the 5' deletion or HD mutation. Three of 21 cell lines had both a 5' deletion and Bcl11b deletion, however there was no statistically significant correlation between these events. One 5'-recombination recognition sequence (RSS) and 2 3'-RSSs have been reported for Notch1 5' deletions. H3K4me3 ChIP-sequence data clearly demonstrated alternative transcript initiation from exon 25 in cell lines with a 5' Notch1 deletion. Curiously, one cell line (106A) which was negative for the 5' deletion showed a marked increase of H3K4Me3 at Notch1 exon25, suggesting transcription initiation at this alternative site, and leading to the hypothesis that this cell line may have a variant form of Notch1 5' deletion which was undetectable by conventional assays. We were able to identify an alternative RSS for this cell line, leading to a novel 5' Notch1 deletion. We then reanalyzed our samples and found an additional example of this alternate 5' deletion, and a third sample which displayed yet another form of Notch1 5' deletion. Of note, this deletion did not have a cryptic RSS, and had developed in a RAG1 deficient mouse. In summary, we have identified three novel forms of Notch1 5' deletions, shown that Notch1 mutations are very common in murine pre-T LBL, shown that PEST mutations generally precede 5'deletion mutations, and shown that 5' Notch1 deletions are not consistently associated with other illegitimate VDJ recombinase-mediated events (such as Bcl11b deletions). Disclosures: No relevant conflicts of interest to declare.

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Kohla, Samah, Feryal Ibrahim, Ilham Bilal, Einas Al Kuwari, and Ahmad Al-Sabbagh. "A Challenging Case of Gamma Delta T-Cell Lymphoma with Precursor T-Cells and Marked Eosinophilia: A Case Report." Case Reports in Oncology 13, no. 3 (December 18, 2020): 1520–29. http://dx.doi.org/10.1159/000512188.

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Gamma-delta (γδ) T-cell lymphomas are very rare and aggressive neoplasms. We describe here a challenging case of γδ T-cell neoplasm composed of γδ mature T-cells and γδ precursor T-cells with marked eosinophilia that is inapplicable to the current 2016 World Health Organization (WHO) classification. A 3-year-old female child who was presented with fever and marked leukocytosis. Peripheral blood smear showed marked lymphocytosis, marked eosinophilia, neutrophilia, monocytosis, and 5% circulating blasts. CT scan showed anterior mediastinal mass, lymphadenopathy, and hepatosplenomegaly. The patient underwent a bone marrow examination and a biopsy taken from the mediastinal mass. Peripheral blood and bone marrow findings were consistent with a γδ T-cell neoplasm with increased blasts and eosinophilia. The patient was sequentially treated with imatinib (tyrosine kinase inhibitor), acute lymphoblastic leukemia protocol (BFM 2009) then shifted to lymphoma protocol (LMP 96). In conclusion, we report a unique rare case of γδ T-cell neoplasm with a combination of mature and immature γδ T-cells and eosinophilia that is inapplicable to the current 2016 WHO classifications. This case raises a challenging concept of a mature T-cell lymphoma arising in an immature T-cell neoplasm. It also highlights the need to target all neoplastic components to eradicate the disease.

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Tillman, Heather, Laura J. Janke, Amy Funk, Peter Vogel, and Jerold E. Rehg. "Morphologic and Immunohistochemical Characterization of Spontaneous Lymphoma/Leukemia in NSG Mice." Veterinary Pathology 57, no. 1 (November 18, 2019): 160–71. http://dx.doi.org/10.1177/0300985819882631.

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The NOD.Cg- Prkdcscid Il2rgtm1Wjl/SzJ strain (NOD scid gamma, NSG) is a severely immunodeficient inbred laboratory mouse used for preclinical studies because it is amenable to engraftment with human cells. Combining scid and Il2rgnull mutations results in severe immunodeficiency by impairing the maturation, survival, and functionality of interleukin 2–dependent immune cells, including T, B, and natural killer lymphocytes. While NSG mice are reportedly resistant to developing spontaneous lymphomas/leukemias, there are reports of hematopoietic cancers developing. In this study, we characterized the immunophenotype of spontaneous lymphoma/leukemia in 12 NSG mice (20 to 38 weeks old). The mice had a combination of grossly enlarged thymus, spleen, or lymph nodes and variable histologic involvement of the bone marrow and other tissues. All 12 lymphomas were diffusely CD3, TDT, and CD4 positive, and 11 of 12 were also positive for CD8, which together was consistent with precursor T-cell lymphoblastic lymphoma/leukemia (pre-T-LBL). A subset of NSG tissues from all mice and neoplastic lymphocytes from 8 of 12 cases had strong immunoreactivity for retroviral p30 core protein, suggesting an association with a viral infection. These data highlight that NSG mice may develop T-cell lymphoma at low frequency, necessitating the recognition of this spontaneously arising disease when interpreting studies.

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Fry, Terry J., and Crystal L. Mackall. "T-cell adoptive immunotherapy for acute lymphoblastic leukemia." Hematology 2013, no. 1 (December 6, 2013): 348–53. http://dx.doi.org/10.1182/asheducation-2013.1.348.

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Abstract Substantial progress has been made in the treatment of precursor B-cell acute lymphoblastic leukemia (B-ALL), but recurrent disease remains a leading cause of death in children due to cancer and outcomes for adults with B-ALL remain poor. Recently, complete clinical responses have been observed in small numbers of patients with B-ALL treated with adoptive immunotherapy using T cells genetically engineered to express chimeric antigen receptors (CARs) targeting CD19, a cell surface molecule present in essentially all cases of B-ALL. Preclinical data suggest that CARs targeting CD22, another antigen present in the majority of B-ALL cases, are similarly potent. Several clinical studies already under way will soon more clearly define the rate of response to this novel therapy in B-ALL. Further work is needed to identify optimal platforms for CAR-based adoptive immunotherapy for leukemia, to establish guidelines for managing toxicity, and to determine whether the remissions induced by this approach can be rendered durable.

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Journal articles on the topic 'Precursor T-Cell Lymphoblastic Leukemia-Lymphoma'

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