Hematology: An Annotated Bibliography of Recent Literature
Authors: HEMATOLOGY COMMITTEE
Journal: Annals of Internal Medicine (1982)

The Literature of Medicine1 September 1982Hematology: An Annotated Bibliography of Recent LiteratureReferences to Journal Articles and Other PapersHEMATOLOGY COMMITTEEHEMATOLOGY COMMITTEESearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-97-3-459 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThis bibliography includes references to 100 recently published journal papers and similar sources that represent important developments in the concept and practice of internal medicine. It has been compiled by the Hematology Committee* as part of the Medical Knowledge Self-Assessment Program VI Syllabus.In preparing this bibliography, the committee reviewed MEDLINE†bibliographic printouts of journal articles published since the beginning of 1978 and also drew on sources in libraries of hospitals and other clinical institutions in the United States and Canada; thus, only papers in English are listed, and most are from American journals....Hemopoiesis and Hemopoietic Stem Cell Disorders Erythropoiesis and Disturbances in Production of Erythrocytes Erythrocyte Structure, Circulation, and Function: Hemolytic Disease Hemostasis and Thrombosis Component Transfusion, Adverse Transfusion Reactions, and Hemapheresis1. ABDOUVERDIRAMEAMAREABDOU NJMN. Heterogeneity of pathogenetic mechanisms in aplastic anemia: efficacy of therapy based on in-vitro research. Ann Intern Med. 1981;95:43-50. Culture of marrow cells from 21 patients with aplastic anemia suggested that six patients had immune inhibition of marrow progenitor cells. Three patients had evidence for failure of chemical stimulators of marrow cell progenitor growth. LinkGoogle Scholar2. ADAMSONFIALKOW JP. The pathogenesis of myeloproliferative syndromes. Br J Haematol. 1978;38:299-303. Clonal origin of chronic myelogenous leukemia, polycythemia vera, and agnogenic myeloid metaplasia is suggested by studies of glucose-6-phosphate dehydrogenase isoenzyme types in blood and tissue cells. Cells derived from hemopoietic tissue had only one of the two isoenzymes in other tissues, suggesting derivation of the disorders from a single cell. CrossrefMedlineGoogle Scholar3. APPELBAUMFEFERCHEEVER FAM. Treatment of aplastic anemia by bone marrow transplantation in identical twins. Blood. 1980;55:1033-9. Marrow transplants in two sets of identical twins were successful. In two other sets transplantation failed, but succeeded when the recipients were pretreated with cyclophosphamide. Culture studies suggested that cellular inhibitors of hemopoiesis were present in the latter cases. CrossrefMedlineGoogle Scholar4. BERKGOLDBERGSILVERSTEIN PJM. Increased incidence of acute leukemia in polycythemia vera associated with chlorambucil therapy. N Engl J Med. 1981;304:441-7. Previously untreated patients were randomly assigned to treatment groups receiving either phlebotomy, phlebotomy and radioactive phosphorus, or phlebotomy and chlorambucil. There was no significant difference in survival between the three groups; the incidence of acute leukemia was markedly increased by chlorambucil. CrossrefMedlineGoogle Scholar5. BOLLUM F. Terminal deoxynucleotidyl transferase as a hematopoietic cell marker. Blood. 1979;54:1203-15. Deoxynucleotidyl transferase (TdT) is a T-cell marker present in the thymocytes of healthy persons. Most TdT-positive leukemias are common acute lymphocytic leukemia antigen (C alla) positive, non-T, non-B cell acute lymphoblastic leukemia, but about 30% of cases of blastic phase chronic myelogenous leukemia and rare cases of acute myeloblastic leukemia and acute monomyelogenous leukemia are TdT positive. CrossrefMedlineGoogle Scholar6. DEN OTTOLANDERTE VELDEBREDEROO GJP. Megakaryoblastic leukaemia (acute myelofibrosis): a report of three cases. Br J Haematol. 1979;42:9-20. Acute myelofibrosis and acute megakaryoblastic leukemia are similar, if not identical, diseases. The leukemic megakaryoblasts may lead to a profound, secondary fibroplasia in the marrow. CrossrefMedlineGoogle Scholar7. FEFERCHEEVERTHOMAS AME. Bone marrow transplantation for refractory acute leukemia in 34 patients with identical twins. Blood. 1981;57:421-30. Patients with leukemia and identical twins should be considered prime candidates for bone marrow transplantation. At the time of transplant, patients did not have a complete remission, but in these identical-twin transplants twenty-four patients (70%) had a complete remission and eight (24%) remain in remission 29 to 103 months (median, 80 months) later. CrossrefMedlineGoogle Scholar8. FEFERCHEEVERTHOMAS AME. Disappearance of Ph1-positive cells in four patients with chronic granulocytic leukemia after chemotherapy, irradiation and marrow transplantation from an identical twin. N Engl J Med. 1979;300:333-7. An approach that may significantly improve prognosis. If cytotoxic treatment is intensive, pH1-positive cells can be profoundly reduced or suppressed, paving the way for allogeneic marrow transplantation from siblings during the chronic phase. CrossrefMedlineGoogle Scholar9. FIALKOWSINGERADAMSON PJJ. Acute nonlymphocytic leukemia: heterogeneity of stem cell origin. Blood. 1981;57:1068-73. Enzyme genetic studies have shown that some cases of childhood acute myelogenous leukemia are restricted to granulocyte-monocyte precursors, whereas adult cases indicate that erythrocytes and platelets as well as granulocytes are derived from the leukemia clone. CrossrefMedlineGoogle Scholar10. GOLOMBROWLEYVARDIMANTESTABUTLER HJJJA. "Microgranular" acute promyelocytic leukemia: a distinct clinical, ultrastructural, and cytogenetic entity. Blood. 1980;55:253-9. Classic progranulocytic leukemia cells have numerous prominent peroxidase-positive azure granules in their cytoplasm. Auer rods also are often present. A patient had translocation between chromosomes 15 and 17 and intravascular coagulation in which the cells did not appear hypergranulated but small peroxidase-positive granules were seen. This microgranular acute progranulocytic leukemia carries the same risk of intravascular coagulation as more readily recognized cases exhibiting large primary granules. CrossrefMedlineGoogle Scholar11. GRALNICK H. Classification of acute leukemia. Ann Intern Med. 1977;87:740-53. A description of criteria for the subclassification of acute myelogenous leukemia into subtypes according to morphologic and histochemical characteristics and of acute lymphocytic leukemia by morphologic and immunologic markers. LinkGoogle Scholar12. KOEFFLERGOLDE HD. Chronic myelogenous leukemia—new concepts. N Engl J Med. 1981;304:1201-9, 1269-74. The pathophysiology, management, and newer forms of therapy of this thoroughly studied but still poorly understood disease are discussed. CrossrefMedlineGoogle Scholar13. KOEFFLERGOLDE HD. Human preleukemia. Ann Intern Med. 1980;93:347-53. Pathophysiology and management of an increasingly recognized condition in the middle-aged and elderly patient with unexplained cytopenias. In some patients preleukemia represents the early stage of acute myelogenous leukemia; others may have morbidity from the cytopenias without developing overt leukemia. LinkGoogle Scholar14. POLLIACKPROKOCIMERMATZNER AMY. Lymphoblastic leukemic transformation (lymphoblastic crisis) in myelofibrosis and myeloid metaplasia. Am J Hematol. 1980;9:211-20. Further evidence of the predisposition of the chronic myeloproliferative disorders to undergo a transformation in which malignant "lymphocytes" are present in marrow and blood. This occurrence implies that the fundamental lesion in these diseases may be in the pluripotent stem cell. CrossrefMedlineGoogle Scholar15. PREISLERRUSTUMHENDERSON HYE. Treatment of acute nonlymphocytic leukemia: use of anthracycline-cytosine arabinoside induction therapy and a comparison of two maintenance regimens. Blood. 1979;53:455-64. Results of intensive induction and maintenance treatment for acute myelogenous leukemia; the overall complete remission rate was 66%. Patients over 60 years old had a decreased probability of entering a remission, although, once achieved, remission duration was not influenced by age. CrossrefMedlineGoogle Scholar16. QUESENBERRYLEVITT PL. Hematopoietic stem cells. N Engl J Med. 1979;301:755-60. Review of the proliferation and differentiation of blood cell progenitors and the mechanisms for their control in health and disease. CrossrefMedlineGoogle Scholar17. ROWLEY J. Chromosome abnormalities in human leukemia. Annu Rev Genet. 1980;14:17-39. Current techniques for analyzing chromosomes in blood and marrow cells and specific chromosome abnormalities in chronic myelogenous and acute promyelocytic leukemia are discussed. The nonrandom nature of chromosome abnormalities in human acute leukemia is emphasized. CrossrefMedlineGoogle Scholar18. STEWARTKEATINGMCCREDIE DMK. Natural history of central nervous system acute leukemia in adults. Cancer. 1981;47:184-96. Analysis of central nervous system involvement in 227 adults with acute leukemia. The overall incidence was 20% of cases. CrossrefMedlineGoogle Scholar19. STORBTHOMASBUCKNER REC. Marrow transplantation in thirty "untransfused" patients with severe aplastic anemia. Ann Intern Med. 1980;92:30-6. Thirty patients with severe aplastic anemia had no transfusions of blood products until just before marrow transplantation from HLA-identical family members. They were conditioned for grafting with cyclophosphamide on each of 4 successive days. Marrow engraftment, was sustained in 27. Early transplantation should be carried out before transfusions in any patient with severe aplastic anemia who has an HLA-identical family member. LinkGoogle Scholar20. YUNISBLOOMFIELDENSRUD JCK. All patients with acute nonlymphocytic leukemia may have a chromosomal defect. N Engl J Med. 1981;305:135-9. Using new in-vitro techniques, aneuploidy or translocations were evident in all evaluable patients. Previous studies had indicated that abnormal karyotypes were identifiable in about 50% of cases. CrossrefMedlineGoogle Scholar21. BARBOUR G. Effect of parathyroidectomy on anemia in chronic renal failure. Arch Intern Med. 1979;139:889-91. Secondary hyperparathyroidism contributes to the anemia of chronic renal failure by causing marrow fibrosis, a process that can be responsive to parathyroidectomy. CrossrefMedlineGoogle Scholar22. CARMEL R. Macrocytosis, mild anemia, and delay in the diagnosis of pernicious anemia. Arch Intern Med. 1979;139:47-50. Macrocytosis often precedes the development of anemia in patients with vitamin B12 deficiency, but its significance is usually ignored until more severe manifestations of the deficiency state ensue. CrossrefMedlineGoogle Scholar23. CARMELJOHNSON RC. Racial patterns in pernicious anemia: early age at onset and increased frequency of intrinsic-factor antibody in black women. N Engl J Med. 1978;298:647-50. Black women manifest pernicious anemia at a younger age than white women and also have a much higher incidence of circulating antibody to intrinsic factor. CrossrefMedlineGoogle Scholar24. CARTWRIGHTEDWARDSSKOLNICKAMOS GCMD. Association of HLA-linked hemochromatosis with idiopathic refractory sideroblastic anemia. J Clin Invest. 1980;65:989-92. Idiopathic refractory sideroblastic anemia permits the expression of hereditary hemochromatosis in patients carrying only a single gene for this disorder. CrossrefMedlineGoogle Scholar25. COHENDONALDSON KR. Unreliability of radiodilution assays as screening tests for cobalamin (vitamin B12) deficiency. JAMA. 1980:244:1942-5. A standard commercial radiodilution assay for serum vitamin B12 was found to be unreliable in screening a general hospital population for vitamin B12 deficiency. CrossrefMedlineGoogle Scholar26. COLMANHERBERT NV. Hematologic complications of alcoholism: overview. Semin Hematol. 1980;17:164-76. A review of alcohol metabolism, the effect of alcohol ingestion on iron, porphyrin, folic acid, and vitamin B12 metabolism, and the influence of alcohol on erythrocyte, leukocyte, and platelet function. MedlineGoogle Scholar27. HALL C. The transport of vitamin B12 from food to use within the cells. J Lab Clin Med. 1979;94:811-6. A review of the mechanisms by which food vitamin B12 is extracted, absorbed, and transported to the tissues. MedlineGoogle Scholar28. KOEFFLERGOLDWASSER HE. Erythropoietin radioimmunoassay in evaluating patients with polycythemia. Ann Intern Med. 1981;94:44-7. The newly developed radioimmunoassay for erythropoietin provides an accurate method for distinguishing polycythemia vera from other causes of erythrocytosis. Serum erythropoietin levels are normal in polycythemia vera and elevated in secondary polycythemia. LinkGoogle Scholar29. NATHLINDENBAUM BJ. Persistence of neutrophil hypersegmentation during recovery from megaloblastic granulopoiesis. Ann Intern Med. 1979;90:757-60. Neutrophil hypersegmentation due to vitamin B12 or folic acid deficiency persists for up to 2 weeks after initiating replacement therapy and can be used retrospectively as a clue to the prior existence of megaloblastic hematopoiesis. LinkGoogle Scholar30. ROSEJOHNSON MI. Reinterpretation of the haematological effects of anticonvulsant treatment. Lancet. 1978;1:1349-50. Macrocytic anemia developing in patients receiving long-term anticonvulsant therapy is due to inadequate nutrition rather than drug-induced impairment of folate metabolism. CrossrefMedlineGoogle Scholar31. WHEBY M. Effect of iron therapy on serum ferritin levels in iron-deficiency anemia. Blood. 1980;56:138-40. Iron therapy in patients with iron deficiency anemia does not cause a rise in serum ferritin until the hemoglobin level is restored to normal. CrossrefMedlineGoogle Scholar32. YORKJONESMENONSPROULE ERDB. Effects of secondary polycythemia on cerebral blood flow in chronic obstructive pulmonary disease. Am Rev Respir Dis. 1980;121:813-8. Phlebotomy reduces whole blood viscosity and improves cerebral blood flow in patients with erythrocytosis secondary to chronic obstructive lung disease. MedlineGoogle Scholar33. BYRNES J. Thrombotic thrombocytopenic purpura. Adv Intern Med. 1980;26:131-57. A review of the clinical and pathologic features and new insights into the pathogenesis and treatment of this dramatic disease, with extensive bibliography. MedlineGoogle Scholar34. COOPER R. Hemolytic syndromes and red cell membrane abnormalities in liver disease. Semin Hematol. 1980;17:103-12. Lipid composition of the normal erythrocyte membrane is reviewed. Mechanisms causing formation of spherocytes, target cells, and spur cells in hepatic disease and their contribution to hemolysis are presented. MedlineGoogle Scholar35. EICHNER E. Splenic function: normal, too much and too little. Am J Med. 1979;66:311-20. Normal splenic function, hypersplenism, and hyposplenism are discussed. Medical indications for splenectomy and lethal septicemia in hyposplenic and asplenic persons are considered. CrossrefMedlineGoogle Scholar36. FORGET B. Molecular genetics of human hemoglobin synthesis. Ann Intern Med. 1979;91:605-16. A review of the organization of the human globin genes and methods used to study the molecular bases of thalassemias. Current knowledge about thalassemias (α,β, and δβ) and disorders with thalassemic expression (elongated chains, fusion genes). LinkGoogle Scholar37. HANASHRUCKNAGEL SD. Clinical implications of recent advances in hemoglobin disorders. Med Clin N Am. 1980;64:775-800. Discussion of hemoglobinopathies and thalassemias, emphasizing diagnosis and clinical manifestations. The bibliography is extensive and includes key recent citations. CrossrefMedlineGoogle Scholar38. HORWITZ C. Autoimmune hemolytic anemia. 1. Warm antibody type; 2. Drug-induced type; 3. Cold antibody type. Postgrad Med. 1979;66:167-73, 199-202, 189-200. A concise description of the three common types of immune hemolytic anemias. Pathogenesis, diagnostic procedures, clinical course, and therapeutic management are discussed. CrossrefMedlineGoogle Scholar39. KIRTLANDMOHLERHORWITZ HDD. Methyldopa inhibition of suppressor-lymphocyte function: a proposed cause of autoimmune hemolytic anemia. N Engl J Med. 1980;302:825-32. Experimental data suggest that methyldopa alters the immune system by causing a persistent increase in lymphocyte cyclic-AMP, which inhibits suppressor T cell function allowing unregulated autoantibody production by β cells in some patients. CrossrefMedlineGoogle Scholar40. LUXWOLFE SL. Inherited disorders of the red cell membrane skeleton. Pediatr Clin N Am. 1980;27:463-86. The composition and structure of the normal erythrocyte membrane is briefly discussed, followed by an extensive review of the pathophysiology, diagnostic criteria, and therapy of hereditary spherocytosis, hereditary elliptocytosis, and hereditary pyropoikilocytosis. CrossrefMedlineGoogle Scholar41. ROSSEADAMS WJ. The variability of hemolysis in the cold agglutinin syndrome. Blood. 1980;56:409-16. Lysis induced by cold agglutinins is quantitatively related to complement fixation dependent upon antibody concentration, the temperature at which binding occurs, and the efficiency of complement fixation. CrossrefMedlineGoogle Scholar42. SEARS D. The morbidity of sickle cell trait: a review of the literature. Am J Med. 1978;64:1021-36. Sickle cell trait is associated with splenic infarction at high altitude, bacteriuria in pregnancy, hyposthenuria, hematuria, and reduced mortality from Plasmodium falciparum infections. CrossrefMedlineGoogle Scholar43. VALENTINE W. Hemolytic anemia and inborn errors of metabolism. Blood. 1979;54:549-59. Hemolytic anemia due to inherited enzyme abnormalities of the glycolytic and pentose phosphate pathways and of nucleotide metabolism is discussed. The recently described common deficiency of 5′-pyrimidine nucleotidase is particularly well covered. CrossrefMedlineGoogle Scholar44. VICHINSKYLUBIN EB. Sickle cell anemia and related hemoglobinopathies. Pediatr Clin N Am. 1980;27:429-47. The pathophysiology, laboratory diagnosis, and clinical manifestations of these diseases are discussed. Recommendations for management of crises and infections and indications for blood transfusion are outlined. Granulopoiesis, Granulocyte Circulation, and Disorders of Granulocytes CrossrefMedlineGoogle Scholar45. CLINEGOLDE MD. Immune suppression of hematopoiesis. Am J Med. 1978;64:301-10. The many hematologic disorders that may result from humoral or cellular inhibition of hematopoiesis are reviewed. Many approaches to evaluation and possible therapy of immune-mediated bone marrow failure are described. CrossrefMedlineGoogle Scholar46. DALEGUERRYWEWERKABULLCHUSID DDJJM. Chronic neutropenia. Medicine. 1979;58:128-44. An extensive review of chronic neutropenia, primarily in adults. Diagnosis, clinical manifestations, and pathophysiologic abnormalities are addressed. Long-term follow-up deals with clinical courses and responses to therapy. CrossrefMedlineGoogle Scholar47. JACOBCRADDOCKHAMMERSCHMIDTMOLDOW HPDC. Complement-induced granulocyte aggregation: an unsuspected mechanism of disease. N Engl J Med. 1980;302:789-94. A previously unrecognized abnormality may be responsible for severe tissue injury secondary to leukostasis in a variety of disorders. CrossrefMedlineGoogle Scholar48. LOGUESHIMM GD. Autoimmune granulocytopenia. Annu Rev Med. 1980;31:191-200. A review of techniques for detecting granulocyte antibodies, the diseases associated with such antibodies, and approaches to their management. CrossrefMedlineGoogle Scholar49. MICHETDOYLEGINSBURG CJW. Eosinophilic fasciitis: report of 15 cases. Mayo Clin Proc. 1981;56:27-34. A report of 15 new cases and a review of the clinical manifestations of this newly described clinical entity. MedlineGoogle Scholar50. PARRILLOFAUCIWOLFF JAS. Therapy of the hypereosinophilic syndrome. Ann Intern Med. 1978;89:167-72. A comprehensive study of the natural history and prognostic signs of progressive eosinophilic disorders. Included are approaches to treatment for patients with progressive tissue infiltration and morbidity. LinkGoogle Scholar51. WARD P. The myeloid leukocytoses. Postgrad Med. 1980;67:219-29. The secondary causes for extensive neutrophilia are discussed as well as both qualitative and quantitative neutrophil abnormalities. Leukemoid reactions, their many causes, and ways to distinguish them from leukemia are discussed. CrossrefMedlineGoogle Scholar52. WEETMANBOXER RL. Childhood neutropenia. Pediatr Clin North Am. 1980;27:361-75. A well-written account of the many causes of neutropenia that is applicable to both infants and adults. Included is a tabulation of many diagnostic studies and their relevance to the disease entities. CrossrefMedlineGoogle Scholar53. YOUNGVINCENT GP. Drug-induced agranulocytosis. Clin Haematol. 1980;93:483-504. Many drugs have been implicated in agranulocytosis. Pathogenesis, clinical manifestations, and management of this increasingly frequent clinical problem are discussed. Lymphopoiesis and Disorders of Lymphocytes and Plasma Cells CrossrefGoogle Scholar54. AULT K. Detection of small numbers of monoclonal B lymphocytes in the blood of patients with lymphoma. N Engl J Med. 1979;300:1401-5. Use of the fluorescence-activated cell sorter shows that many patients with lymphoma with apparently normal blood cell counts have lymphocytes in the blood that are derived from the malignant clone. CrossrefMedlineGoogle Scholar55. BERGSAGELBAILEYLANGLEYMACDONALDWHITEMILLER DAGRDA. The chemotherapy of plasma-cell myeloma and the incidence of acute leukemia. N Engl J Med. 1979;301:743-8. Acute leukemia may develop during the course of multiple myeloma. A particularly striking finding is that for patients surviving 4 years, the risk of developing acute leukemia is 17%. CrossrefMedlineGoogle Scholar56. COHENBALOWMAGRATHPOPLACKZIEGLER LJIDJ. Acute tumor lysis syndrome: a review of 37 patients with Burkitt's lymphoma. Am J Med. 1980;68:486-91. Rapid lysis of neoplastic tissue after chemotherapy releases metabolic products that can cause profound clinical problems. Uric acid nephropathy, hyperkalemia, or hyperphosphatemia may require hemodialysis. CrossrefMedlineGoogle Scholar57. DEVITASIMONHUBBARD VRS. Curability of advanced Hodgkin's disease with chemotherapy. Long-term follow-up of MOPP-treated patients at the National Cancer Institute. Ann Intern Med. 1980;92:587-95. Long-term follow-up shows that 68% of the 80% of patients achieving remission have remained free of disease for at least 10 years. Nodular sclerosis is associated with a higher relapse rate than other types of sclerosis. LinkGoogle Scholar58. DESFORGESRUTHERFORDPIRO JCA. Hodgkin's Disease. N Engl J Med. 1979;301:1212-22. Review of data on epidemiologic basis of Hodgkin's disease, the monocyte as the "malignant" cell, and selection of appropriate therapy. Both assets and liabilities of combined treatment are emphasized. CrossrefMedlineGoogle Scholar59. GLENNER G. Amyloid deposits and amyloidosis: the β-fibrilloses. N Engl J Med. 1980;302:1283-92, 1333-43. Fibrils aggregate in β-pleated sheet configurations to give amyloid its characteristic properties. Several different proteins may assume this configuration; the most common are immunoglobulin light chains and protein "AA." CrossrefMedlineGoogle Scholar60. GOLOMBCATOVSKYGOLDE HDD. Hairy cell leukemia: a clinical review based on 71 cases. Ann Intern Med. 1978;89:677-83. Granulocytopenia is a determining factor in infection. Splenectomy improves leukocyte and platelet count. Some patients also require chemotherapy, but in others the disease is indolent and requires no treatment. LinkGoogle Scholar61. GOREVICKASSABLEVO PHY. Mixed cryoglobulinemia: clinical aspects and long-term follow-up of 40 patients. Am J Med. 1980;69:287-308. A subset of patients with cryoglobulinemia do not show evidence of underlying lymphoproliferative disease. They have a characteristic clinical picture, which is often associated with a history of hepatitis B, and involved with multiple organs. CrossrefMedlineGoogle Scholar62. GUPTAGOOD SR. Markers of human lymphocyte subpopulations in primary immunodeficiency and lymphoproliferative disorders. Semin Hematol. 1980;17:1-29. Changes occur during maturation of normal B and T lymphocytes, that correspond to characteristic malignant B and T lymphocytes in leukemia and lymphoma. These similarities suggest the level of differentiation at which the neoplasia has developed. MedlineGoogle Scholar63. HENDERSONSCHARLAUCOOPER ECM. Combined chemotherapy and radiotherapy for acute lymphocytic leukemia in adults: results of CALGB protocol 7113. Leuk Res. 1979;3:395-407. A large study shows that 20% of adult patients receiving multidrug treatment (vincristine, prednisone, asparaginase, daunorubicin) and maintenance, and central-nervous-system prophylaxis continue disease free after 5 years. CrossrefMedlineGoogle Scholar64. KAPLAN H. Hodgkin's disease: unfolding concepts concerning its nature, management and prognosis. Cancer. 1980;45:2439-74. The tendency of Hodgkin's disease to spread continuously and the accurate location of its sites of involvement have provided opportunity for cure by radiotherapy. Proper selection of cases for specific treatment is vital to success. CrossrefMedlineGoogle Scholar65. LOUIEDAOUSTSCHWARTZ SPR. Immunodeficiency and the pathogenesis of non-Hodgkin's lymphoma. Semin Oncol. 1980;7:267-84. There is an increased incidence of lymphoma and leukemia in acquired and congenital immunodeficient states. Disturbances in immunoregulations may allow proliferation of a clone of lymphocytes to develop into lymphoma. Several studies using animal models support this hypothesis. MedlineGoogle Scholar66. PURTILOPAQUINDEFLORIOVIRZISAKHUJA DLDFR. Immunodiagnosis and immunopathogenesis of the X-linked recessive lymphoproliferative syndrome. Semin Hematol. 1979;16:309-43. Inherited factors prevent normal responses to Epstein-Barr virus. Without appropriate response to the stimulus of the Epstein-Barr virus on B cells, these cells may proliferate to produce a fatal lymphoma. MedlineGoogle Scholar67. REINHERZKUNGGOLDSTEINLEVEYSCHLOSSMAN EPGRS. Discrete states of human intrathymic differentiation: analysis of normal thymocytes and leukemic lymphoblasts of T-cell lineage. Proc Natl Acad Sci USA. 1980;77:1588-92. Monoclonal antibodies developed by the hybridoma technique can show precise antigens. This technique documents changes occurring during maturation of normal T cells and provides a means of characterizing leukemic T cells. CrossrefMedlineGoogle Scholar68. ROBINSONBROWNANDIMAN JNW. Diffuse polyclonal B-cell lymphoma during primary infection with Epstein-Barr virus. N Engl J Med. 1980;302:1293-7. A remarkable case of fatal progressive lymphoproliferative disease of polyclonal origin. (An accompanying editorial points to the potential of the Epstein-Barr virus as both mitogen and oncogen.) CrossrefMedlineGoogle Scholar69. ROSS G. Identification of human lymphocyte subpopulations by surface marker analysis. Blood. 1979;53:799-811. Lymphocytes vary with respect to surface receptors, surface antigens, and formation of E-rosettes. These change with differentiation, and lymphoproliferative diseases are associated with subsets of these markers. B-cell differentiation is emphasized. CrossrefMedlineGoogle Scholar70. SAFAIGOOD BR. Lymphoproliferative disorders of the T-cell series: a review. Medicine. 1980;59:335-51. Characteristic cytologic and pathologic features of cutaneous T cell lymphoma, other T cell lymphomas, and acute and chronic T cell leukemia are described. Because T cell markers correlate with clinical signs, they may be used in differentiating T-cell disease. CrossrefMedlineGoogle Scholar71. SCHILSKYLEWISSHERINSYOUNG RBRR. Gonadal dysfunction in patients receiving chemotherapy for cancer. Ann Intern Med. 1980;93:109-14. As the results of chemotherapy improve, the problems of remote complications become greater. Gonadal dysfunction and sterility are frequent side effects of some chemotherapeutic drugs. Gonodal toxicity is influenced both by the drugs and their combinations and by the age and sex of the patient. LinkGoogle Scholar72. SIRISSHERMANBAQUIRANSCHLATTEREROSSERMANCANFIELD EWDJER. Effects of dichloromethylene diphosphonate on skeletal mobilization of calcium in multiple myeloma. N Engl J Med. 1980;302:310-5. Preliminary studies suggest that this treatment may be an effective adjunct to treatment of multiple myeloma with extensive bone involvement. (An editorial in the same issue provides a balanced discussion of the potential role of these agents.) CrossrefMedlineGoogle Scholar73. STREULIULTMANN RJ. Non-Hodgkin's lymphomas: historical perspective and future prospects. Semin Oncol. 1980;7:223-33. Lymphomas may be divided into "favorable" and "unfavorable" types based on histology and natural history. The former are often widespread but tend to be indolent; the latter require more aggressive treatment. MedlineGoogle Scholar74. TRUMPMANNPHELPSROBERTSCONLEY DRRHC. Richter's syndrome: diffuse histiocytic lymphoma in patients with chronic lymphocytic leukemia: a report of five cases and review of the literature. Am J Med. 1980;68:539-48. Analogous to the blast crisis of chronic myelocytic leukemia, chronic lymphocytic leukemia may be complicated by transformation to a more malignant and aggressive lymphoproliferative disorder, such as to a histiocytic lymphoma or to prolymphocytic leukemia. Typical cases are described. CrossrefMedlineGoogle Scholar75. ABILDGAARDSUZUKIHARRISONJEFCOATZIMMERMAN CZJKT. Serial studies in von Willebrand's disease: variability versus "variants". Blood. 1980;56:712-16. Not only can patients wi