A Reappraisal of the Results of Stopping Therapy in Childhood Leukemia

George, Stephen L.; Aur, Rhomes J. A.; Mauer, Alvin M.; Simone, Joseph V.

doi:10.1056/nejm197902083000601

Cited by 176 publications

(61 citation statements)

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“…Telomeres in leukemic MNCs gained on average 2.2 kbp after induction chemotherapy, but such as RAS, p53, mdm-overexpression or bcr-abl. 1,2,45 Telomerase, the enzyme that prevents telomere shortening, decreased 1 kbp with the continuation of chemotherapy treatment (Figure 3a and b). The overall increase ranged from 0.53 has recently received much attention due to its involvement in most tumor types, including childhood leukemia and solid to 1.56 kbp (P Ͻ 0.05).…”

Section: Bone Marrow (Bm) 31mentioning

confidence: 99%

“…The CNS germ cell tumor patient was treated according to the 2nd International malignant clone in remission and to demonstrate progressive shortening of telomeres after chemotherapy treatment. These CNS Germ Cell Tumor Protocol (cyclophosphamide 4 g/m 2 , cisplatin 105 mg/m 2 , etoposide 450 mg/m 2 , bleomycin results suggest that telomerase activity and TRF length analysis may be useful for diagnostic and remission assessment in leu-15 mg/m 2 ) and the patient with the localized malignant germ cell tumor of the ovary was treated according to CCG 8891 kemia as well as for evaluating potential complications after repeated cycles of chemotherapy treatment.…”

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confidence: 99%

“…Calculation of number of cell divisions ALL patient numerical and structural chromosome abnormalities were found (46,XY,t(2p;11p) [2], del (7p) [7],−9 [7],−13 [7], An evaluation of the number of population doublings (PD) in leukemia and tumor specimens, based on differences of mean +2mar [7][cp],46,XY). The median time to achieve a complete response in acute leukemia patients was 28 days (range, 7-and peak TRF length in leukemia and tumor block specimens, and in cell controls (such as granulocyte fractions) was per-44).…”

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Telomerase activity and telomere length in pediatric patients with malignancies undergoing chemotherapy

et al. 1998

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Telomerase activity and telomere length in mononuclear cells proliferation of lymphoid or myeloid precursors with arrested (MNCs) and granulocytes from peripheral blood (PB) and bone maturation. 1 In this disorder, the leukemic clone expands in marrow (BM) specimens were studied in pediatric acute leukethe bone marrow (BM), interferes with normal hematopoiesis mia (ALL, n = 15; AML, n = 1) and pediatric solid tumor (ST) and eventually, non-hematopoietic tissues are infiltrated. patients (n = 9) at diagnosis, during and after chemotherapy. In Acute lymphocytic leukemia (ALL) was one of the first maligfour ST patients, tumor tissue was also available. For comparative analysis, MNCs from healthy donors (n = 53) were ananancies reported to respond to chemotherapy and is curable that can synthesize telomeric repeats onto chromosomes. [3][4][5][6] telomere loss in granulocytes as compared to MNCs was more Recently, borderline telomerase activity has been detected in pronounced with 1.8 vs 1 kbp, respectively (P = 0.014). Our results demonstrate that at diagnosis, telomerase was consisthuman primitive hematopoietic cells and in stimulated lymently and highly upregulated in BM and PB specimens in leukephocytes which increased significantly with cytokine-induced mia, decreased after induction therapy, and correlated with ex vivo expansion. 7-10 However, in most other normal remission. BM specimens in leukemia had higher telomerase somatic cells, telomerase has not been detected, and conseactivity, probably due to the greater leukemic burden than in quently telomere shortening may be anticipated after a limited PB. Telomeres were significantly longer in children than in number of population doublings. [11][12][13] In contrast, spon- progressive telomere length shortening in the absence of telo-

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Section: Bone Marrow (Bm) 31mentioning

confidence: 99%

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Telomerase activity and telomere length in pediatric patients with malignancies undergoing chemotherapy

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“…1) attain a second remission (P < 0-020'$ < 0-005 respectively). (Greaves et al, 1975 (Cornbleet & Chessells, 1978;George et al, 1979). From our study it can be said that marrow relapse on treatment has a uniformly fatal outcome.…”

Section: Resultsmentioning

confidence: 63%

“…However, there is less agreement about the management of the many children who relapse while on treatment. Cornbleet & Chessells (1978) (Cornbleet & Chessells, 1978;Rivera et al, 1976;Aur et al, 1972;Jacquillat et al, 1973;Leventhal et al, 1975;George et al, 1979). As (Peto et al, 1976(Peto et al, , 1977.…”

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Marrow relapse on maintenance chemotherapy in childhood acute lymphoblastic leukaemia

Kearney¹,

Baumer²,

Howlett³

1979

Br J Cancer

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Outcome of Hepatitis in Children With Acute Leukemia

Malone¹,

Novak²

1980

Arch Pediatr Adolesc Med

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\s=b\The cases of 31 children with acute leukemia and concurrent hepatitis were evaluated for the outcome of their hepatitis. Thirteen of these children had hepatitis B and 18 children had a non-B hepatitis. Chronic hepatitis developed in more than half of the children with acute hepatitis, with the majority of cases being of the chronic, active type. A majority of these children had received at least one blood transfusion in the preceding year. No relationship was seen between the development of chronicity of the liver disease and the management of the acute hepatitis or the state of underlying disease. With the potential for a cure for acute leukemia increasing, a method of reducing the sequelae of hepatitis in children with leukemia is needed.(Am J Dis Child 134: [584][585][586][587] 1980) Hepatitis is recognized as a threat to children with cancer because they frequently receive blood-replace¬ ment therapy during intensive myelosuppressive therapy. risks of acquiring hepatitis range from 1% to 20% among children with leukemia.'"' Recently, two patients cared for at St Jude Children's Research Hospital, Memphis, who had apparently been cured of leukemia later died of hepatitis and its compli¬ cations. This led us to review our experience with hepatitis in children with acute leukemia. REPORT OF CASESCase l.-This 20-year-old man was diag¬ nosed as having acute lymphocytic leuke¬ mia five years before his death. He was treated according to the "Total Therapy VIH" protocol (first with prednisone, vin¬ cristine sulfate and daunorubicin hydro¬ chloride, followed by cranial irradiation and intrathecal methotrexate sodium for CNS prophylaxis, and then maintenance therapy with mercaptopurine, methotrex¬ ate and cyclophosphamide)1 and remained in continuous, complete remission.One month before this therapy was to be completed, nausea and vomiting developed. On physical examination, he had a lowgrade fever and mild scierai icterus. Labo¬ ratory evaluation showed an SGOT level of 72 Karmen units (normal level, 6 to 40 units) and his serum contained the hepati¬ tis surface antigen (HBsAg). A diagnosis of acute hepatitis was made. The hepati¬ tis antigenemia and elevation in trans¬ aminase levels persisted for the next 21 months. With the development of marked jaundice in September 1977, a percuta¬ neous liver biopsy was performed; the spec¬ imen showed chronic active hepatitis with cirrhosis. Over the next six months, the patient's condition progressively deterio¬ rated despite prednisone therapy, salt re¬ striction, and the administration of diuret¬ ics. No autopsy was obtained.Case 2.-This 19-year-old man was first diagnosed as having acute lymphocytic leu¬ kemia 15 years before his death. He was treated according to the Total Therapy III protocol (prednisone and vincristine fol¬ lowed by craniospinal irradiation for CNS prophylaxis and then treatment with mercaptopurine, methotrexate, and cyclophosphamide for maintenance) ' for three years, at which time his therapy was stopped. He remained in continuous, complete r...

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A Reappraisal of the Results of Stopping Therapy in Childhood Leukemia

Cited by 176 publications

References 21 publications

Telomerase activity and telomere length in pediatric patients with malignancies undergoing chemotherapy

Telomerase activity and telomere length in pediatric patients with malignancies undergoing chemotherapy

Marrow relapse on maintenance chemotherapy in childhood acute lymphoblastic leukaemia

Outcome of Hepatitis in Children With Acute Leukemia

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