scholarly journals Chronic Granulocytic Leukemia (CGL) During the Course of Chronic Lymphocytic Leukemia (CLL): Correlation of Blood, Marrow, and Spleen Morphology and Cytogenetics

Blood ◽  
1974 ◽  
Vol 43 (3) ◽  
pp. 333-339 ◽  
Author(s):  
Jacqueline Whang-Peng ◽  
Harvey R. Gralnick ◽  
Ralph E. Johnson ◽  
Elaine C. Lee ◽  
Arnold Lear

Abstract Second malignancies occur with a greater frequency in patients with chronic lymphatic leukemia than in the general population. Previously, 20 patients having CLL have been reported as developing acute leukemia, but no cases of development of chronic granulocytic leukemia have been observed. In the present report, we will describe patients with Ph1 chromosome positive CGL associated with previously described CLL. One patient received total body radiation treatment for his CLL, while the second was not treated. It is apparent that previous therapy may not necessarily be a prerequisite for the development of a second malignancy in CLL. Cytogenetics offers a useful tool to confirm morphologic criteria in establishing the diagnosis of a second neoplasm.

Blood ◽  
1957 ◽  
Vol 12 (4) ◽  
pp. 367-372 ◽  
Author(s):  
NICHOLAS L. PETRAKIS ◽  
ESTELLE LIEBERMAN ◽  
JEAN FULLERTON

Abstract The dead leukocyte content of the blood of normal and leukemic subjects was determined by the technic of the unstained-cell counts of Schrek. A small and constant number of dead leukocytes was found in the normal blood, averaging 46 per cu. mm. In patients with chronic lymphocytic leukemia and acute leukemia, higher numbers of dead leukocytes were commonly found, ranging from normal values to as high as 4,600 per cu. mm. No correlation was found between the numbers of smudge forms on blood smears from these patients and the number of dead leukocytes. The smudge forms on blood smears appear to result from the mechanical trauma produced in making the smears. The leukocytes from chronic lymphocytic leukemia and acute leukemia appear to be much more susceptible to the mechanical forces produced in the preparation of blood smears than are leukocytes from normals and patients with chronic granulocytic leukemia.


PEDIATRICS ◽  
1979 ◽  
Vol 63 (1) ◽  
pp. 44-46
Author(s):  
Jean E. Sanders ◽  
C. Dean Buckner ◽  
Patricia Stewart ◽  
E. Donnall Thomas

A 46-month-old boy with juvenile chronic granulocytic leukemia was treated intensively with hydroxyurea dimethyl myleran, cyclophosphamide, and total body irradiation. He then received a marrow transplant from an HL-A matched brother. Thirty-two months after the transplantation, he is hematologically normal and remains disease free on no-maintenance therapy. The successful outcome of this case suggests that a bone marrow transplant for any patient with a suitable histocompatible donor should be considered in the treatment of this disease.


1984 ◽  
Vol 2 (5) ◽  
pp. 379-384 ◽  
Author(s):  
G L Phillips ◽  
G P Herzig

Four patients with Philadelphia chromosome (Ph1)-positive chronic granulocytic leukemia (CGL) in blast phase received cyclophosphamide, total body irradiation, and autologous marrow transplants using cryopreserved marrow from the stable phase. Two patients fully reestablished stable-phase leukemia that lasted for 26 and six months; the first patient developed transient Ph1-negative hematopoiesis after transplantation. Three patients eventually died of recurrent blast-phase leukemia. Previous studies using autologous marrow for CGL have reported an occasional long survivor, but incomplete engraftment and especially the rapid recurrence of blast-phase leukemia have been responsible for the overall poor results. The latter problem complicates even normal marrow transplantation, indicating the inadequacy of the current therapeutic regimens used for treating blast-phase leukemia and the possibility of improving results with more effective regimens and autologous marrow transplantation. Although it is unknown whether the reestablishment of Ph1-negative hematopoiesis after transplantation contributes to improved survival, this interesting phenomenon must be investigated further.


Blood ◽  
1964 ◽  
Vol 23 (6) ◽  
pp. 795-810 ◽  
Author(s):  
RICHARD I. WALKER ◽  
J. C. HERION ◽  
W. B. HERRING ◽  
J. G. PALMER

Abstract Leukocyte physiology in the normal and in hematopoietic disease states in humans has been studied by DNA-P labeling with inorganic P32. In the normal there is a post-mitotic granulocyte reservoir in marrow about 17 times the size of the intravascular compartment. Progress through this reservoir is orderly and requires about 6 days. Some 1-2 x 1011 cells daily are released from it into the blood. In polycythemia vera there is an increased production of granulocytes. DNA-P labeling in patients with chronic lymphocytic leukemia occurs at a very low level and is compatible with a very slow rate of cell renewal. In one patient with chronic lymphocytic leukemia, no disturbances in kinetics caused by a dose of 20 µc. of P32/Kg. were detected during the time of the study. Although a progressively rising concentration of label in circulating leukocyte DNA was found in patients with chronic granulocytic leukemia, without the lag suggesting a distinct marrow phase, it is concluded that the blood and extravascular leukopoietic compartments cannot be a single compartment. An essentially normal curve is obtained after induction of a complete remission with busulfan.


Blood ◽  
1979 ◽  
Vol 53 (5) ◽  
pp. 1014-1017
Author(s):  
GP Canellos ◽  
SB Sutliffe ◽  
VT DeVita ◽  
TA Lister

Five patients in the blastic phase of chronic granulocytic leukemia with massive splenomegaly were treated by intraarterial splenic artery infusion of cytosine arabinoside. All patients had massive splenomegaly associated with pain and/or hypersplenism and were refractory to previous therapy. All 5 patients demonstrated responses to treatment, with reduction in spleen size as well as symptomatic relief. Systemic toxicity was minimal in 4 of the 5 patients.


Blood ◽  
1948 ◽  
Vol 3 (8) ◽  
pp. 911-917 ◽  
Author(s):  
EDWIN E. OSGOOD ◽  
I. T. CHU

Abstract In cultures by the marrow culture technic of human marrow and leukemic blood containing concentrations of urethane from 1:200 to 1:40,000, marked changes in the morphology of the cells of the granulocyte series were noted. These changes were not noted in the control nor in duplicate cultures containing the methyl-bis (B-chloroethyl) amine hydrochloride form of nitrogen mustard in concentrations from 1:500,000 to 1:40,000,000, nor were they noted in previous studies of cultures containing colchicine or exposed to 200 kilovolt or million volt x-rays, neutron rays or radioactive phosphorus, nor in the bloods or marrows of patients with untreated chronic granulocytic leukemia, of healthy individuals or of persons with miscellaneous diseases. The changes consisted of an early increase in number of normal mitoses in the progranulocytes; a steadily rising percentage of granulocytes and progranulocytes showing condensation of the chromatin in the nucleus into dense fragments separated by clear spaces; a progressive increase in the number of cells of the granulocyte series with double nuclei, affecting all cells from the progranulocytes to the neutrophil lobocytes but appearing to be most numerous in the granulocyte stage; and the appearance in the cultures by 4 to 5 days of cells containing separated fragments of structureless material staining like basichromatin, which probably represents a karyorrhexis of the nucleus. Note: Nothing in this article is to be construed as a recommendation of urethane for the clinical treatment of leukemias. While many years must elapse before its place in therapy can be evaluated, it does seem worthwhile to give urethane a trial for metastatic malignant tumors. Our present impression is that either radioactive phosphorus or total body irradiation with x-rays given in small regularly spaced doses is far superior to urethane in the treatment of leukemias.17 When the cells become resistant to radiation therapy, urethane may be worthy of a trial.


Blood ◽  
1972 ◽  
Vol 40 (5) ◽  
pp. 725-732 ◽  
Author(s):  
Peter Lau ◽  
Arlan J. Gottlieb ◽  
William J. Williams

Abstract Mucopolysaccharide sulfation was demonstrated in leukemic granulocytic precursors in short-term suspension culture by incorporation of 35SO4 into a compound identified chromatographically as chondroitin sulfate. The gel filtration pattern of sulfated mucopolysaccharide obtained from leukemic leukocytes was qualitatively similar to that found with normal granulocytic precursors. Sulfation of mucopolysaccharide was about 50% of the normal level in cells from chronic granulocytic leukemia, and approximately 15% of the normal level in cells from acute granulocytic leukemia or chronic granulocytic leukemia in blastic crisis. Lymphocytes from acute and chronic lymphocytic leukemia showed only traces of sulfate incorporation. Leukocyte mucopolysaccharide sulfation was studied in cultured cells from patients with acute leukemia to determine whether this reaction could aid in distinguishing acute granulocytic leukemia from acute lymphocytic leukemia. Significant levels of sulfation were obtained in cells from all leukemias judged to be acute granulocytic, while virtually no incorporation was found in cells from acute lymphocytic leukemia when a 24-hr incubation period was employed. In studies employing a 3-hr incubation, agreement as to the cell of origin of the leukemia and the degree of sulfation in the intracellular fraction was obtained in 16 of 18 determinations performed on 16 patients with acute leukemia. It is proposed that determination of 35SO4 incorporation in the intracellular fraction may help to differentiate acute granulocytic and acute lymphocytic leukemia.


Blood ◽  
1960 ◽  
Vol 16 (2) ◽  
pp. 1104-1121 ◽  
Author(s):  
EDWIN E. OSGOOD

Abstract Analyses of the threshold dose of P32 to control 201 chronic lymphocytic leukemia patients and 100 chronic granulocytic leukemia patients and of the P32 dose to maintain 133 chronic lymphocytic leukemia patients for a mean period of 50.2 months and 49 chronic granulocytic leukemia patients for a mean period of 33.6 months are analyzed. These threshold doses fit the logarithmic probability distributions given in the tables and figures. See PDF for Figure See PDF for Figure When the dose in mc. to control was plotted against the leukocyte count, a straight line was obtained on log log paper. The equation for this curve for the median dose to control chronic granulocytic leukemia is: log mc. P32 per 12 weeks = 0.33 log L - 0.633, where L is the leukocyte count on the day the first P32 was given. The equation for the log log curve relating median dose to control chronic lymphocytic leukemia to initial counts above 15,000 is: log mc. P32 per 12 weeks = 0.47 log L - 1.420. But the 40 aleukemic or subleukemic cases with leukocyte counts below 15,000 had a median P32 requirement and standard deviation that did not differ significantly from that for the entire group, suggesting that this subleukemic group includes patients resembling the entire spectrum of cases with elevated initial leukocyte counts. See PDF for Figure See PDF for Figure The median dose of P32 per year to maintain chronic granulocytic leukemia cases fits the equation: log P32 per year = 0.546 log L - 1.506, and the corresponding equation for chronic leukemic lymphocytic leukemia is: log mc. P32 per year = 0.45 log L - 1.22. The group of lymphocytic leukemias with initial counts below 15,000 again showed a median and distribution similar to that for the entire leukemic group. The remarkable fact that the dose requirement years later is related to the initial leukocyte count is discussed. Revised recommendations on dosage schedule for titrated, regularly spaced P32 therapy of the chronic leukemias are presented. For each individual patient with chronic leukemia, there is a threshold dose of intravenously administered P32 below which no effect is observed. The dose and interval which will maintain a uniform leukocyte count of about 15,000 may remain unchanged for years or may show abrupt changes at any time to either a lower or higher requirement.


Blood ◽  
1970 ◽  
Vol 36 (3) ◽  
pp. 353-360 ◽  
Author(s):  
SIMON PROPP ◽  
FRANK A. LIZZI

Abstract It is recognized that the Ph1 chromosome anomaly is characteristic of chronic granulocytic leukemia. It has been shown however, to occur rarely in other myeloproliferative diseases. We have reported a 53-year-old roentgenologist with acute lymphocytic leukemia who showed a high percentage of Ph1 chromosomes in his marrow cells. The possible role of radiation exposure in the production of the abnormal chromosome in this patient is discussed. The data presented is evidence against the specificity of the Ph1 chromosome for myeloproliferative disorders.


1970 ◽  
Vol 18 (7) ◽  
pp. 473-481 ◽  
Author(s):  
C. Y. LI ◽  
L. T. YAM ◽  
K. W. LAM

Acid phosphatase in human leukocytes was examined in a large number of patients with a variety of hematologic diseases. In chronic lymphocytic leukemia the total leukocyte acid phosphatase activity was markedly decreased. This was due to the drastic increase of enzyme-poor leukemic lymphocytes and the concomitant decrease of enzyme-rich monocytes and neutrophils. Further examination by disc gel electrophoresis revealed that the leukocytes in this disease contained only one of the five acid phosphatase isoenzymes present in a normal leukocyte preparation. Total acid phosphatase activity was not significantly altered in other hematologic disorders, yet different ratios of the isoenzymes shown by disc gel electrophoresis were observed in Hodgkin's disease, chronic granulocytic leukemia, acute granulocytic leukemia, infectious mononucleosis and leukemic reticuloendotheliosis.


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