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Journal articles on the topic 'Gamma -heavy chain disease'

Author: Grafiati

Published: 4 June 2021

Last updated: 14 February 2022

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1

Bieliauskas, Shannon, Raymond R. Tubbs, Chris M. Bacon, Camellia Eshoa, Kathryn Foucar, Sarah E. Gibson, Steven H. Kroft, Aliyah R. Sohani, Steven H. Swerdlow, and James R. Cook. "Gamma Heavy-chain Disease." American Journal of Surgical Pathology 36, no. 4 (April 2012): 534–43. http://dx.doi.org/10.1097/pas.0b013e318240590a.

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2

Kušnierová, Pavlína, David Zeman, Tomáš Jelínek, and Roman Hájek. "Gamma-heavy chain disease." Klinicka Onkologie 33, no. 4 (August 15, 2020): 282–85. http://dx.doi.org/10.14735/amko2020282.

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3

FERMAND, JEAN-PAUL, JEAN-CLAUDE BROUET, FRANÇOISE DANON, and MAXIME SELIGMANN. "Gamma Heavy Chain “Disease”." Medicine 68, no. 6 (November 1989): 321–35. http://dx.doi.org/10.1097/00005792-198911000-00001.

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4

Westin, Jan, Raili Eyrich, Enevold Falsen, Leif Lindholm, Per Lundin, Ivar Lönnroth, and Aleksander Weinfeld. "GAMMA HEAVY CHAIN DISEASE." Acta Medica Scandinavica 192, no. 1-6 (April 24, 2009): 281–92. http://dx.doi.org/10.1111/j.0954-6820.1972.tb04817.x.

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5

Kanoh, Tadashi, and Hideo Nakasato. "Osteolytic gamma heavy chain disease." European Journal of Haematology 39, no. 1 (April 24, 2009): 60–65. http://dx.doi.org/10.1111/j.1600-0609.1987.tb00165.x.

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6

Kanoh, T. "Cutaneous lesions in gamma heavy-chain disease." Archives of Dermatology 124, no. 10 (October 1, 1988): 1538–40. http://dx.doi.org/10.1001/archderm.124.10.1538.

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7

Dickson, John R., Manfred Harth, David A. Bell, Ronald Komar, and William B. Chodirker. "Gamma heavy chain disease and rheumatoid arthritis." Seminars in Arthritis and Rheumatism 18, no. 4 (May 1989): 247–51. http://dx.doi.org/10.1016/0049-0172(89)90045-0.

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8

Pontet, F., X. Gué, C. Dosquet, J. Caen, and F. Rousselet. "Rapid evolution in the immunochemical findings of a gamma heavy chain disease." Clinical Chemistry 34, no. 2 (February 1, 1988): 439–43. http://dx.doi.org/10.1093/clinchem/34.2.439.

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Abstract We noted the following major immunochemical changes in the final course of a gamma heavy-chain disease associated with a myelomonocytic leukemia: an important oligoclonal increase of IgG1/kappa, during sepsis development, whereas the lambda molecules decreased and IgG2 and IgG3 completely disappeared in a one-month interval. Initial concentrations of IgG4 were stable during that period, and gamma 1 heavy chains were slightly increased. This is a very unusual observation of the successive immunochemical events terminating a gamma heavy-chain disease.

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9

Lassoued, Kais, Catherine Picard, Françoise Danon, Marianne Pocidalo, Maggy Grossin, Béatrice Crickx, and Stéphane Beiaich. "Cutaneous manifestations associated with gamma heavy chain disease." Journal of the American Academy of Dermatology 23, no. 5 (November 1990): 988–91. http://dx.doi.org/10.1016/s0190-9622(08)80110-7.

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10

Castelino, Daniel, Faye Gray, Anthony D’Apice, Bill Paspaliaris, Alan Riglar, Robyn McLachlan, and Brendan Murphy. "Primary sjögren’s syndrome and gamma heavy chain disease." Pathology 26, no. 3 (1994): 337–38. http://dx.doi.org/10.1080/00313029400169791.

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11

Shibata, Sho, and Akiko Fukunaga. "Gamma heavy chain disease complicated by pulmonary hypertension, which was successfully treated with lenalidomide." BMJ Case Reports 13, no. 11 (November 2020): e236162. http://dx.doi.org/10.1136/bcr-2020-236162.

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Heavy chain disease (HCD) is a rare B-cell proliferative neoplasm that is characterised by the production of truncated monoclonal immunoglobulin heavy chains without light chains. Gamma HCD is a subgroup of HCD. A 67-year-old man was admitted to our hospital with dyspnoea and lower leg oedema. Based on the results of heart catheterisation, he was diagnosed with pulmonary hypertension. Laboratory tests revealed an elevated level of IgG, and serum immunoelectrophoresis showed that IgG was a monoclonal gamma heavy chain without light chains. Finally, he was diagnosed with gamma HCD complicated by pulmonary hypertension. Bortezomib and dexamethasone therapy was initiated, but became refractory within 8 months. Therefore, the treatment was switched to lenalidomide and dexamethasone therapy, and the disease has been stably controlled for more than 2 years. To the best of our knowledge, this is the first case of gamma HCD being successfully treated by lenalidomide and dexamethasone therapy.

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12

Singer, Sara, Yvonne Efebera, Naresh Bumma, Abdullah Khan, Srinivas Devarakonda, Maria Chaudhry, Don Benson, and Ashley E. Rosko. "Heavy Lifting: Nomenclature and Novel Therapy for Gamma Heavy Chain Disease and Other Heavy Chain Disorders." Clinical Lymphoma Myeloma and Leukemia 20, no. 8 (August 2020): 493–98. http://dx.doi.org/10.1016/j.clml.2020.02.020.

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13

Agrawal, Samir, Zaid Abboudi, Estella Matutes, and Daniel Catovsky. "First report of fludarabine in gamma-heavy chain disease." British Journal of Haematology 88, no. 3 (November 1994): 653–55. http://dx.doi.org/10.1111/j.1365-2141.1994.tb05094.x.

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14

Ellis, V. M., D. M. Cowley, K. M. Taylor, and P. Marlton. "GAMMA HEAVY CHAIN DISEASE DEVELOPING IN ASSOCIATION WITH MYELODYSPLASTIC SYNDROME." British Journal of Haematology 81, no. 1 (May 1992): 125–26. http://dx.doi.org/10.1111/j.1365-2141.1992.tb08184.x.

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15

Cooper, D. L. "Atrophie blanche in a patient with gamma-heavy-chain disease." Archives of Dermatology 127, no. 2 (February 1, 1991): 272b—273. http://dx.doi.org/10.1001/archderm.127.2.272b.

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16

Arnason, Jon E., and Lourdes M. Mendez. "Induction Therapy for Gamma-Heavy Chain Disease with Bortezomib and Dexamethasone: A Case Report." Blood 120, no. 21 (November 16, 2012): 5051. http://dx.doi.org/10.1182/blood.v120.21.5051.5051.

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Abstract Abstract 5051 Heavy chain diseases (HCD) are rare B-cell lymphoproliferative disorders characterized by production of a monoclonal immunoglobulin without a light chain. Three subtypes are known based on the type of monoclonal immunoglobulin produced ie. alpha-heavy chain, gamma-heavy chain and mu-heavy chain disease in order of decreasing frequency. Here we report a case of gamma-heavy chain disease in a previously healthy 48 year old African American man, which demonstrated clinical and pathologic response to treatment with bortezomib and dexamethasone. The patient was transferred to our institution for work-up of persistent high fever, hypotension and eosinophilia after a thorough negative infectious and rheumatologic work-up spanning two outside hospital admissions. The patient had originally presented with two months of constitutional symptoms and cough refractory to antibiotics and prednisone. His outside hospital admissions were notable for an RCA NSTEMI (an unexpectedly large thrombus was noted on cardiac catheterization), eosinophilia and persistent fevers to 105 degrees Fahrenheit. Imaging studies included a CT torso and tagged WBC scan which were unrevealing but for mild splenomegaly of 15 cm and notably did not show lymphadenopathy, masses or evidence for infection. The fevers transiently abated with an empiric course of steroids but recurred accompanied by shock, which responded to a pulse of high dose methylprednisolone. Ultimately he was felt to have primary adrenal insufficiency without evidence of infiltrative disease on dedicated CT. On presentation to our hospital, his initial labs showed WBC 5. 3 K/uL (83% neutrophils, 10% lymphocytes, 3% monocytes, 4% eosinophils), Hb 11. 2 g/dL, platelets 173 K/uL. Comprehensive chemistry profile was unremarkable. SPEP/IFE of the serum and urine revealed a monoclonal gamma-heavy chain without associated light chain. The total IgG was elevated at 2522 mg/dL, IgA was mildly depressed at 57 mg/dL and IgM was normal at 147 mg/dL; the monoclonal protein itself could not be quantitated; hence, total serum IgG was followed. The patient underwent a bone marrow biopsy and aspiration which showed trilineage hematopoiesis, marked esosinophilia, no evidence of leukemia or lymphoma, 10% CD138+ plasma cells, with the overwhelming majority staining for IgG but not for kappa or lambda. A skeletal survey was negative for lytic lesions. The findings were felt to be consistent with a plasma cell dyscrasia associated gamma-heavy chain disease. The observed eosinophilia was felt to be reactive to the gamma-heavy chain disease as has been previously described. In the literature, gamma heavy chain disease is reported to most commonly present as a lymphoplasmacytic process and the finding of a plasma cell dyscrasia appears to be an unusual presentation of what is already a rare disease. We decided to tailor the treatment to the finding of a plasma cell dyscrasia. Therefore the patient was started on bortezomib 1. 3 mg/m2 SC D1, 4, 8, 11 and dexamethasone 20 mg PO D1, 2, 4, 5, 8, 9, 11, 12 of a 21 day cycle. His treatment was complicated by paroxysmal atrial tachycardia; a cardiac MRI did not reveal evidence of infiltrative cardiomyopathy. After 4 cycles of bortezomib and dexamethasone, the patient's total IgG had normalized at 1265 mg/dL and though a monoclonal gamma heavy chain was still detected by IFE of the serum and urine, a repeat bone marrow biopsy and aspiration was without morphologic evidence of the heavy chain plasma cell dyscrasia. The patient reported feeling subjectively improved with abatement of his malaise and fatigue and without further episodes of fever. Interestingly, the parameter that most seemed to correlate with his clinical status was eosinophilia which also decreased from a peak of 61% (absolute eosinophil count of 5063/uL) to 8–19% after 4 cycles with bortezomib and dexamethasone. Secondary eosinophilia has been reported in the literature in a subset of gamma HCD patients. The patient further underwent stem-cell mobilization in preparation for auto stem cell transplant with high dose Cytoxan, after which the eosinophilia completely resolved. There are only approximately 120 cases of gamma HCD described in the literature. To our knowledge, this is the first reported case of plasma cell dyscrasia associated gamma HCD responding to treatment with bortezomib and dexamethasone. Disclosures: No relevant conflicts of interest to declare.

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17

Danevad, Sletten, Gaarder, Mellbye, and Husby. "The Amino Acid Sequence of a Monoclonal gamma3-Heavy Chain from a Patient with Articular gamma-Heavy Chain Deposition Disease." Scandinavian Journal of Immunology 51, no. 6 (June 2000): 602–6. http://dx.doi.org/10.1046/j.1365-3083.2000.00730.x.

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18

Van Keer, Jan, Björn Meijers, Michel Delforge, Gregor Verhoef, and Koen Poesen. "Two Cases of Heavy Chain MGUS." Case Reports in Oncological Medicine 2016 (2016): 1–4. http://dx.doi.org/10.1155/2016/8749153.

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Heavy chain diseases are rare variants of B-cell lymphomas that produce one of three classes of immunoglobulin heavy chains, without corresponding light chains. We describe two patients with asymptomatic heavy chain monoclonal gammopathy. The first patient is a 51-year-old woman with alpha paraprotein on serum immunofixation. The second case is a 46-year-old woman with gamma paraprotein on urine immunofixation. Neither patient had corresponding monoclonal light chains. Workup for multiple myeloma and lymphoma was negative in both patients. These two cases illustrate that heavy chain monoclonal gammopathy can exist in the absence of clinically apparent malignancy. Only a few reports of “heavy chain MGUS” have been described before. In the absence of specialized guidelines, we suggest a similar follow-up as for MGUS, while taking into account the higher probability of progression to lymphoma than to myeloma.

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19

Gunnar Husby, Per Blichfeldt, Loren. "Chronic Arthritis and gamma-Heavy Chain Disease: Coincidence or Pathogenic Link?" Scandinavian Journal of Rheumatology 27, no. 4 (January 1998): 258–64. http://dx.doi.org/10.1080/030097498442361.

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20

Thoren, Katie L., Marion Eveillard, Patrick Chan, Sital Doddi, Sun Cho, and Kazunori Murata. "Identification of gamma heavy chain disease using MALDI-TOF mass spectrometry." Clinical Biochemistry 77 (March 2020): 57–61. http://dx.doi.org/10.1016/j.clinbiochem.2019.12.010.

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21

Teleanu, Maria-Veronica, Martin Bommer, Rene Van Erp, Shaoxia Zhou, Elisabeth F. Gröne, Stefan Schönsteiner, Jan Krönke, Phyllis Schwarzwälder, Christian Langer, and Miriam Kull. "Gamma Heavy Chain Disease-two New Cases with Distinct Clinical Features." Clinical Lymphoma Myeloma and Leukemia 17, no. 1 (February 2017): e150. http://dx.doi.org/10.1016/j.clml.2017.03.270.

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22

Li, P., L. Qiu, W. Su, J. Han, J. Zhang, and D. Li. "Gamma heavy chain disease associated with T large granular lymphocytic leukemia." Clinica Chimica Acta 493 (June 2019): S203. http://dx.doi.org/10.1016/j.cca.2019.03.422.

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23

HAUKE, G., E. SCHILTZ, K. J. BROSS, A. HOLLMANN, H. H. PETER, and U. KRAWINKEL. "Unusual Sequence of Immunoglobulin L-Chain Rearrangements in a Gamma Heavy Chain Disease Patient." Scandinavian Journal of Immunology 36, no. 3 (September 1992): 463–68. http://dx.doi.org/10.1111/j.1365-3083.1992.tb02961.x.

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24

Ramasamy, I., and Z. Rudzki. "Two Cases of γ-Heavy Chain Disease and a Review of the Literature." Case Reports in Hematology 2018 (August 12, 2018): 1–8. http://dx.doi.org/10.1155/2018/4832619.

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Gamma heavy chain disease (γ-HCD) is a rare lymphoproliferative disorder characterised by the production of a truncated immunoglobulin heavy chain. Fewer than 200 cases have been reported in the literature. In some cases, γ-HCD occurs with other lymphoid neoplasms. This study reports clinical, biochemical, haematological, and histological findings in two cases of γ-HCD. We describe newer biochemical diagnostic tools (HevyLite measurement, capillary electrophoresis, and immunotyping) that can aid in the characterisation of γ-HCD. The first case is an 88-year-old woman with γ-HCD. The second case is an 81-year-old woman who developed γ-HCD during treatment for Waldenstrom’s macroglobulinemia. In the second patient, histopathology identified a separate clone responsible for the secretion of the gamma heavy chain. Studies on the clonal evolution of the disease may provide insight into therapeutic implications and the genomic complexity of the disease.

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25

Robier, Christoph, and Manfred Neubauer. "Gamma heavy chain disease evolving during the progression of chronic lymphocytic leukemia." Clinical Chemistry and Laboratory Medicine (CCLM) 56, no. 6 (May 24, 2018): e154-e156. http://dx.doi.org/10.1515/cclm-2017-0891.

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26

Lee, Maria Teresa, Anil Parwani, Richard Humphrey, Robert G. Hamilton, Donna I. Myers, and Barbara Detrick. "Gamma heavy chain disease in a patient with diabetes and chronic renal insufficiency: diagnostic assessment of the heavy chain fragment." Journal of Clinical Laboratory Analysis 22, no. 2 (January 2008): 146–50. http://dx.doi.org/10.1002/jcla.20233.

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27

Felix, CA, GH Reaman, SJ Korsmeyer, GF Hollis, PA Dinndorf, JJ Wright, and IR Kirsch. "Immunoglobulin and T cell receptor gene configuration in acute lymphoblastic leukemia of infancy." Blood 70, no. 2 (August 1, 1987): 536–41. http://dx.doi.org/10.1182/blood.v70.2.536.536.

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Abstract We examined immunoglobulin (Ig) heavy chain, K light chain, and T cell receptor (TCR) gamma and beta gene configuration in the leukemic cells from a series of infants aged less than 1 year with acute lymphoblastic leukemia (ALL). Each of these 11 cases demonstrated leukemic cell surface antigens that have been correlated with a B cell precursor phenotype. Of the 11, lymphoblasts of 4 retained the germline configuration of both Ig and TCR loci, whereas 7 had rearranged the Ig heavy chain gene. Two of these seven showed light chain gene rearrangement. TCB beta chain rearrangement had occurred in only one of the 11 patients' tumors. No TCR gamma chain rearrangements were identified. These results are in contrast to earlier studies of B cell precursor ALL in children in which Ig heavy chain gene rearrangements were evident in every case and approximately 40% showed Ig light chain rearrangement as well. In addition, 45% of cases of B cell precursor ALL of children had rearranged their gamma TCR genes, and 20% had rearranged beta. These data suggest that ALL in infancy represents an earlier stage of B cell development than is found in B cell precursor ALL of children. ALL in the infant age group has been associated with the worst prognosis of all patients with ALL. This study suggests that the disease in infants differs not only clinically, but also at the molecular genetic level, from the disease in children.

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28

Felix, CA, GH Reaman, SJ Korsmeyer, GF Hollis, PA Dinndorf, JJ Wright, and IR Kirsch. "Immunoglobulin and T cell receptor gene configuration in acute lymphoblastic leukemia of infancy." Blood 70, no. 2 (August 1, 1987): 536–41. http://dx.doi.org/10.1182/blood.v70.2.536.bloodjournal702536.

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We examined immunoglobulin (Ig) heavy chain, K light chain, and T cell receptor (TCR) gamma and beta gene configuration in the leukemic cells from a series of infants aged less than 1 year with acute lymphoblastic leukemia (ALL). Each of these 11 cases demonstrated leukemic cell surface antigens that have been correlated with a B cell precursor phenotype. Of the 11, lymphoblasts of 4 retained the germline configuration of both Ig and TCR loci, whereas 7 had rearranged the Ig heavy chain gene. Two of these seven showed light chain gene rearrangement. TCB beta chain rearrangement had occurred in only one of the 11 patients' tumors. No TCR gamma chain rearrangements were identified. These results are in contrast to earlier studies of B cell precursor ALL in children in which Ig heavy chain gene rearrangements were evident in every case and approximately 40% showed Ig light chain rearrangement as well. In addition, 45% of cases of B cell precursor ALL of children had rearranged their gamma TCR genes, and 20% had rearranged beta. These data suggest that ALL in infancy represents an earlier stage of B cell development than is found in B cell precursor ALL of children. ALL in the infant age group has been associated with the worst prognosis of all patients with ALL. This study suggests that the disease in infants differs not only clinically, but also at the molecular genetic level, from the disease in children.

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29

Hamadeh, F., S. MacNamara, C. M. Bacon, A. R. Sohani, S. H. Swerdlow, and J. R. Cook. "Gamma heavy chain disease lacks the MYD88 L265p mutation associated with lymphoplasmacytic lymphoma." Haematologica 99, no. 9 (May 23, 2014): e154-e155. http://dx.doi.org/10.3324/haematol.2014.108688.

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30

Husby, Gunnar. "Is there a pathogenic link between gamma heavy chain disease and chronic arthritis?" Current Opinion in Rheumatology 12, no. 1 (January 2000): 65–70. http://dx.doi.org/10.1097/00002281-200001000-00011.

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31

Galanti, L. M., C. Doyen, C. Vander Maelen, N. Daparé, A. Bosly, F. Pouthier, and JP Vaerman. "Biological diagnosis of a gamma-1-heavy chain disease in an asymptomatic patient." European Journal of Haematology 54, no. 3 (April 24, 2009): 202–4. http://dx.doi.org/10.1111/j.1600-0609.1995.tb00220.x.

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32

Sudo, Masanori, Takuya Wakamatsu, Tomomi Ishikawa, Masato Habuka, Michihiro Hosojima, Suguru Yamamoto, Yumi Ito, et al. "Successful treatment of gamma 1 heavy chain deposition disease with bortezomib and dexamethasone." Human Pathology: Case Reports 15 (March 2019): 99–104. http://dx.doi.org/10.1016/j.ehpc.2019.01.001.

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33

Naumovski, L., PJ Utz, SK Bergstrom, R. Morgan, A. Molina, JJ Toole, BE Glader, P. McFall, LM Weiss, and R. Warnke. "SUP-HD1: a new Hodgkin's disease-derived cell line with lymphoid features produces interferon-gamma [see comments]." Blood 74, no. 8 (December 1, 1989): 2733–42. http://dx.doi.org/10.1182/blood.v74.8.2733.2733.

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Abstract A new cell line, SUP-HD1, was established from the pleural effusion of a patient with nodular sclerosing Hodgkin's disease (NSHD). The SUP-HD1 cells had the characteristic morphology of Reed-Sternberg cells and contained acid phosphatase and nonspecific esterase. The cells lacked the Epstein-Barr virus (EBV) genome and reacted with monoclonal antibodies (MoAbs) against CD15 (Leu-M1), CD25 (Tac), CD71 (OKT9), Ki67, and HLA-Dr. However, the SUP-HD1 cells were nonreactive with MoAbs that specifically identify T lymphocytes, B lymphocytes, and macrophage/myeloid cells. Karyotype analysis of the cell line showed clonal abnormalities involving 1p13, 7p15, 8q22, and 11q23, chromosomal locations, at which breakpoints have been reported in HD. Southern blot analysis demonstrated rearrangement of the immunoglobulin heavy chain and kappa light chain genes as well as the gene for the beta chain of the T-cell receptor (TCR). Transcriptional analysis showed expression of RNAs for kappa light chain, interferon-gamma (IFN-gamma), and interleukin-2 receptor (IL-2R) but not IL-2. The SUP-HD1 cells lacked cytoplasmic and surface immunoglobulin heavy chain, but a small amount of cytoplasmic kappa light chain was detected. The presence of nuclear factor kappa B (NF kappa B), a B-lymphocyte-associated transcription factor, was demonstrated in stimulated and unstimulated cells. In addition, the SUP-HD1 cell line, produced IFN-gamma, a T-lymphocyte- associated lymphokine. Based on these data, the SUP-HD1 cells appear to be aberrant lymphocytes with characteristics of both activated B and T lymphocytes. Elaboration of lymphokines such as IFN-gamma by the malignant cells may represent one explanation for the unique clinical and pathologic features of HD.

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34

Naumovski, L., PJ Utz, SK Bergstrom, R. Morgan, A. Molina, JJ Toole, BE Glader, P. McFall, LM Weiss, and R. Warnke. "SUP-HD1: a new Hodgkin's disease-derived cell line with lymphoid features produces interferon-gamma [see comments]." Blood 74, no. 8 (December 1, 1989): 2733–42. http://dx.doi.org/10.1182/blood.v74.8.2733.bloodjournal7482733.

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A new cell line, SUP-HD1, was established from the pleural effusion of a patient with nodular sclerosing Hodgkin's disease (NSHD). The SUP-HD1 cells had the characteristic morphology of Reed-Sternberg cells and contained acid phosphatase and nonspecific esterase. The cells lacked the Epstein-Barr virus (EBV) genome and reacted with monoclonal antibodies (MoAbs) against CD15 (Leu-M1), CD25 (Tac), CD71 (OKT9), Ki67, and HLA-Dr. However, the SUP-HD1 cells were nonreactive with MoAbs that specifically identify T lymphocytes, B lymphocytes, and macrophage/myeloid cells. Karyotype analysis of the cell line showed clonal abnormalities involving 1p13, 7p15, 8q22, and 11q23, chromosomal locations, at which breakpoints have been reported in HD. Southern blot analysis demonstrated rearrangement of the immunoglobulin heavy chain and kappa light chain genes as well as the gene for the beta chain of the T-cell receptor (TCR). Transcriptional analysis showed expression of RNAs for kappa light chain, interferon-gamma (IFN-gamma), and interleukin-2 receptor (IL-2R) but not IL-2. The SUP-HD1 cells lacked cytoplasmic and surface immunoglobulin heavy chain, but a small amount of cytoplasmic kappa light chain was detected. The presence of nuclear factor kappa B (NF kappa B), a B-lymphocyte-associated transcription factor, was demonstrated in stimulated and unstimulated cells. In addition, the SUP-HD1 cell line, produced IFN-gamma, a T-lymphocyte- associated lymphokine. Based on these data, the SUP-HD1 cells appear to be aberrant lymphocytes with characteristics of both activated B and T lymphocytes. Elaboration of lymphokines such as IFN-gamma by the malignant cells may represent one explanation for the unique clinical and pathologic features of HD.

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35

Yin, Guang, Yan Wu, Cai-Hong Zeng, Hui-Ping Chen, and Zhi-Hong Liu. "A Unique Case of ^|^gamma;-heavy Chain Deposition Disease Characterized by Concomitant Deposition of ^|^gamma;2 and ^|^gamma;4 Subclasses." Internal Medicine 53, no. 22 (2014): 2615–18. http://dx.doi.org/10.2169/internalmedicine.53.2835.

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36

Xie, Ming, and Ralph Zade. "Gamma Heavy Chain Disease Associated With Intracytoplasmic Lambda Light Chain Expression and Loss of the CCND1 Gene." American Journal of Clinical Pathology 140, suppl 1 (September 1, 2013): A060. http://dx.doi.org/10.1093/ajcp/140.suppl1.060.

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37

Benedetto, Giorgio Di, Angelo Cataldi, Antimo Verde, Annunziata Gloghini, Guido Nicolò, and Vito Pistoia. "Gamma heavy chain disease associated with Hodgkin' disease. Clinical, pathologic, and immunologic features of one case." Cancer 63, no. 9 (May 1, 1990): 1804–9. http://dx.doi.org/10.1002/1097-0142(19900501)63:9<1804::aid-cncr2820630924>3.0.co;2-8.

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38

Ria, Roberto, Franco Dammacco, and Angelo Vacca. "HEAVY-CHAIN DISEASES AND MYELOMA-ASSOCIATED FANCONI SYNDROME: AN UPDATE." Mediterranean Journal of Hematology and Infectious Diseases 10, no. 1 (January 1, 2018): 2018011. http://dx.doi.org/10.4084/mjhid.2018.011.

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The heavy chain diseases (HCDs) are rare B-cell malignancies characterized by the production of a monoclonal immunoglobulin heavy chain without an associated light chain. There are three types of HCD, defined by the class of immunoglobulin heavy chain produced: IgA (α-HCD), IgG (γ-HCD), and IgM (μ-HCD). Alpha-HCD is the most common and usually occurs as intestinal malabsorption in a young adult from a country of the Mediterranean area. Gamma- and μ-HCDs are more rare and associated to a B-cell non-Hodgkin lymphoma that produces an abnormal Ig heavy chain. These patients may occasionally be diagnosed with a monoclonal gammopathy of undetermined significance (MGUS). Fanconi syndrome, on the other hand, can be primary (inherited) or secondary (acquired). The only exception to this rule is the idiopathic form. Adult acquired Fanconi syndrome can be a rare complication of a monoclonal gammopathy. At diagnosis, most patients have a MGUS or smoldering multiple myeloma, with renal failure and evidence of osteomalacia. During follow-up, patients can develop end-stage renal disease. Chemotherapy provides little benefit on renal function.

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39

Thomas O'Conor, G., Herman E. Wyandt, Donald J. Innes, David E. Normansell, and Charles E. Hess. "Gamma heavy chain disease: Report of a case associated with trisomy of chromosome 7." Cancer Genetics and Cytogenetics 15, no. 1-2 (February 1985): 1–5. http://dx.doi.org/10.1016/0165-4608(85)90125-6.

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40

Takano, Hina, Kaoru Nagata, Michiaki Mikoshiba, Minoru Nakane, Atsushi Kato, and Hiroyuki Hamaguchi. "Combination of rituximab and chemotherapy showing anti-tumor effect in gamma heavy chain disease expressing CD20." American Journal of Hematology 83, no. 12 (December 2008): 938–39. http://dx.doi.org/10.1002/ajh.21284.

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41

Alexander, A., I. Anicito, and J. Buxbaum. "Gamma heavy chain disease in man. Genomic sequence reveals two noncontiguous deletions in a single gene." Journal of Clinical Investigation 82, no. 4 (October 1, 1988): 1244–52. http://dx.doi.org/10.1172/jci113722.

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42

Kaneko, Keiichi, Koichi Seta, Jun Soma, Takashi Kuwahara, Mitsuteru Koizumi, Yuko Kikuchi, Akira Sugawara, and Kensei Yahata. "Gamma 1-heavy chain deposition disease accompanied by IgG kappa in serum, urine, and bone marrow." CEN Case Reports 3, no. 1 (July 10, 2013): 44–48. http://dx.doi.org/10.1007/s13730-013-0083-0.

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43

Shimohata, Homare, Kentaro Ohgi, Hiroshi Maruyama, Yasunori Miyamoto, Mamiko Takayashu, Kouichi Hirayama, and Masaki Kobayashi. "A Case of Proliferative Glomerulonephritis with Monoclonal IgG Deposits That Showed Predominantly Membranous Features." Case Reports in Nephrology 2017 (2017): 1–5. http://dx.doi.org/10.1155/2017/1027376.

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Abstract:

In 2004, the novel category of monoclonal IgG deposition disease has been proposed and termed “proliferative glomerulonephritis with monoclonal IgG deposits” (PGNMID). This disease is characterized by membranoproliferative glomerulonephritis and staining for a single light-chain isotype and gamma heavy-chain subclass. A 76-year-old male who had monoclonal gammopathy was referred to our hospital because of proteinuria. The renal biopsy showed diffuse thickening of the glomerular capillary walls with focal mesangial proliferation. On immunofluorescence study, only IgG1 among the four subclasses and lambda light chains were detected mainly in the glomerular capillary walls. From these results, we diagnosed our case as PGNMID showing predominantly membranous features. Almost all pathological findings on light microscopy of PGNMID are membranoproliferative GN or endocapillary proliferative GN, while membranous GN cases are rare. Here, we present the case of PGNMID that showed predominantly membranous features on light microscopy.

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44

Zhang, Ling, Eduardo M. Sotomayor, Peter R. Papenhausen, Haipeng Shao, Lynn C. Moscinski, Ramon L. Sandin, Gisela Caceres, et al. "Unusual concurrence of T-cell large granular lymphocytic leukemia with Franklin disease (gamma heavy chain disease) manifested with massive splenomegaly." Leukemia & Lymphoma 54, no. 1 (July 9, 2012): 205–8. http://dx.doi.org/10.3109/10428194.2012.697561.

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45

Dyer, MJ, JM Heward, VJ Zani, V. Buccheri, and D. Catovsky. "Unusual deletions within the immunoglobulin heavy-chain locus in acute leukemias." Blood 82, no. 3 (August 1, 1993): 865–71. http://dx.doi.org/10.1182/blood.v82.3.865.865.

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Abstract We have investigated the structure of the Ig heavy (IGH) chain locus in 309 cases of acute leukemia. Seventy-one cases of B-cell precursor (BCP) acute lymphoblastic leukemia (ALL) were analyzed: in six cases deletion of joining (JH) segments in the presence of cytogenetically normal chromosome 14 was observed. Similar deletions were seen in 1 out of 8 cases of biphenotypic acute leukemia analyzed: this case exhibited t(9:22)(q34;q11) and coexpressed both myeloid and B cell differentiation antigens. Five of the 7 cases analyzed had deleted the JH segments from both chromosomes. Because these deletions may have contributed to the pathogenesis of the disease we have attempted to define their boundaries. Using probes that map both 5′ and 3′ of JH, the 3′ (centromeric) boundary of the deletions was mapped to an approximately 30-kb central region of the 60 kb between C delta and C gamma 3 in 10 of the 12 deleted chromosomes. In the remaining two chromosomes, the 3′ boundary mapped to S mu. The 5′ (telomeric) boundary could not be defined. However, three cases with biallelic deletion of JH showed biallelic deletion of the most proximal variable (VH) (VH6 and VH5-B2) genes, indicating that the deletions spanned over 500 kb. VH5-B1 and VH5-B3 were retained in germline configuration and no gross deletions were observed using a VH3 subgroup-specific probe, indicating that the 5′ boundary mapped within the VH locus. Unusual deletions of the portion of the IgH locus including JH segments and the C mu and C delta genes may occur in acute leukemias with immunophenotypic evidence of commitment to the B cell differentiation pathway. The possible consequences of the deletions remain to be determined. However, the clustering of the centromeric boundary of the deletions to S mu and to a region between the C delta-C gamma 3 genes, a known “hot spot” for recombination, may indicate the operation of a distinct pathogenic mechanism.

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46

Dyer, MJ, JM Heward, VJ Zani, V. Buccheri, and D. Catovsky. "Unusual deletions within the immunoglobulin heavy-chain locus in acute leukemias." Blood 82, no. 3 (August 1, 1993): 865–71. http://dx.doi.org/10.1182/blood.v82.3.865.bloodjournal823865.

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Abstract:

We have investigated the structure of the Ig heavy (IGH) chain locus in 309 cases of acute leukemia. Seventy-one cases of B-cell precursor (BCP) acute lymphoblastic leukemia (ALL) were analyzed: in six cases deletion of joining (JH) segments in the presence of cytogenetically normal chromosome 14 was observed. Similar deletions were seen in 1 out of 8 cases of biphenotypic acute leukemia analyzed: this case exhibited t(9:22)(q34;q11) and coexpressed both myeloid and B cell differentiation antigens. Five of the 7 cases analyzed had deleted the JH segments from both chromosomes. Because these deletions may have contributed to the pathogenesis of the disease we have attempted to define their boundaries. Using probes that map both 5′ and 3′ of JH, the 3′ (centromeric) boundary of the deletions was mapped to an approximately 30-kb central region of the 60 kb between C delta and C gamma 3 in 10 of the 12 deleted chromosomes. In the remaining two chromosomes, the 3′ boundary mapped to S mu. The 5′ (telomeric) boundary could not be defined. However, three cases with biallelic deletion of JH showed biallelic deletion of the most proximal variable (VH) (VH6 and VH5-B2) genes, indicating that the deletions spanned over 500 kb. VH5-B1 and VH5-B3 were retained in germline configuration and no gross deletions were observed using a VH3 subgroup-specific probe, indicating that the 5′ boundary mapped within the VH locus. Unusual deletions of the portion of the IgH locus including JH segments and the C mu and C delta genes may occur in acute leukemias with immunophenotypic evidence of commitment to the B cell differentiation pathway. The possible consequences of the deletions remain to be determined. However, the clustering of the centromeric boundary of the deletions to S mu and to a region between the C delta-C gamma 3 genes, a known “hot spot” for recombination, may indicate the operation of a distinct pathogenic mechanism.

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47

Tycko, B., J. Ritz, S. Sallan, and J. Sklar. "Changing antigen receptor gene rearrangements in a case of early pre-B cell leukemia: evidence for a tumor progenitor cell with stem cell features and implications for monitoring residual disease." Blood 79, no. 2 (January 15, 1992): 481–88. http://dx.doi.org/10.1182/blood.v79.2.481.481.

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Abstract A case of acute lymphoblastic leukemia (ALL) was encountered in which the two clonal gamma T-cell receptor gene (TCR gamma) rearrangements found in bone marrow (BM) samples at relapse both differed from the single clonal TCR gamma rearrangement present in BM obtained at diagnosis 5 years previously. In contrast, two clonal Ig heavy chain gene (IgH) rearrangements present at relapse were identical to those present at diagnosis. Comparison of the DNA sequences of the relapse TCR gamma rearrangements with that of the diagnostic TCR gamma rearrangement indicated that they must have been generated de novo from TCR gamma loci in germline configuration. By polymerase chain reaction using clonotypic N-region oligonucleotide primers (N-PCR), cells bearing the diagnosis or relapse TCR gamma rearrangements were undetectable in the sample from the opposite time point. Two BM samples obtained at different times in clinical remission were both devoid of detectable residual tumor when analyzed by N-PCR, indicating a depth of remission of less than 1 tumor cell per 4 x 10(5) BM mononuclear cells. The tumor cells showed a primitive phenotype: T-cell antigen-negative, CALLA/CD10-negative, CD20-negative, CD19-positive, and positive for the myeloid marker My9. This case, which appears to represent a tumor arising from a progenitor cell with both early B-lineage and certain stem cell features, has implications for monitoring residual ALL and possibly also for treatment of the disease.

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48

Tycko, B., J. Ritz, S. Sallan, and J. Sklar. "Changing antigen receptor gene rearrangements in a case of early pre-B cell leukemia: evidence for a tumor progenitor cell with stem cell features and implications for monitoring residual disease." Blood 79, no. 2 (January 15, 1992): 481–88. http://dx.doi.org/10.1182/blood.v79.2.481.bloodjournal792481.

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Abstract:

A case of acute lymphoblastic leukemia (ALL) was encountered in which the two clonal gamma T-cell receptor gene (TCR gamma) rearrangements found in bone marrow (BM) samples at relapse both differed from the single clonal TCR gamma rearrangement present in BM obtained at diagnosis 5 years previously. In contrast, two clonal Ig heavy chain gene (IgH) rearrangements present at relapse were identical to those present at diagnosis. Comparison of the DNA sequences of the relapse TCR gamma rearrangements with that of the diagnostic TCR gamma rearrangement indicated that they must have been generated de novo from TCR gamma loci in germline configuration. By polymerase chain reaction using clonotypic N-region oligonucleotide primers (N-PCR), cells bearing the diagnosis or relapse TCR gamma rearrangements were undetectable in the sample from the opposite time point. Two BM samples obtained at different times in clinical remission were both devoid of detectable residual tumor when analyzed by N-PCR, indicating a depth of remission of less than 1 tumor cell per 4 x 10(5) BM mononuclear cells. The tumor cells showed a primitive phenotype: T-cell antigen-negative, CALLA/CD10-negative, CD20-negative, CD19-positive, and positive for the myeloid marker My9. This case, which appears to represent a tumor arising from a progenitor cell with both early B-lineage and certain stem cell features, has implications for monitoring residual ALL and possibly also for treatment of the disease.

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49

Humeau, Camille, Hélène Monjanel, and François Schellenberg. "Discovery of a gamma heavy chain disease in a patient followed-up for a lymphoplasma cell proliferative disorder." Annales de biologie clinique 74, no. 3 (May 2016): 338–40. http://dx.doi.org/10.1684/abc.2016.1149.

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50

Shirakura, T., Y. Kobayashi, Y. Murai, T. Inoue, and Y. Imamura. "A Case of Gamma Heavy Chain Disease Associated with Autoimmune Haemolytic Anaemia: Clinical, Haematological, Immunological and Pathological Details." Scandinavian Journal of Haematology 16, no. 5 (April 24, 2009): 387–93. http://dx.doi.org/10.1111/j.1600-0609.1976.tb00332.x.

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