Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 46-year-old female with chronic myelogenous leukemia (CML) in blast crisis was monitored for terminal deoxynucleotidyltransferase (TdT) activity of marrow and peripheral blood throughout the course of her illness. TdT was elevated at the time of diagnosis of blastic transformation, and the patient easily obtained remission after therapy with hydroxyurea, 6-mercaptopurine and prednisone. The patient enjoyed a remission of eight months duration, and at time of relapse, marrow TdT was again elevated. The patient again obtained complete remission with the same regimen, with the addition of vincristine, given weekly. This second remission was shortlived, however, and at relapse marrow TdT activity was undetectable. Subsequently, the patient failed to achieve remission, despite the use of a wide variety of chemotherapeutic agents. This case suggests that loss of TdT activity in blastic CML cells marks the emergence of cells resistant to existing chemotherapeutic agents.
Cancer 1979 Nov
PMID:Loss of terminal deoxynucleotidyl transferase (TdT) activity as a predictor of emergence of resistance to chemotherapy in a case of chronic myelogenous leukemia in blast crisis. 29 71

Sixteen chronic myeloid leukaemia (CML) patients in remission were tested with solubilized membrane antigens from CML leukaemic cells, CML blasts, AML blasts and ALL blasts for cellular immunity in vitro by lymphocyte transformation (LT) and leucocyte migration inhibition (LMI) assays. Twelve CML patients in remission were tested with allogeneic PHA-transformed normal lymphoblasts. As controls, peripheral-blood leucocytes from 9 healthy persons were tested with the same antigen preparations. It was seen that 8/16 (50%) CML patients responded to CML antigens by both LT and LMI assays, while 5/16 (31%) patients reacted to CML blasts and 44% (7/16) patients reacted to AML blast antigens. It was interesting to note that 5/11 (45%) CML patients reacted to ALL blast antigens by both assays. One out of 12 patients reacted to PHA-transformed lymphoblasts. None of the healthy controls reacted to leukaemia-associated antigens. The results suggest the sharing of antigens between myeloid leukaemic cells, myeloid blasts and lymphoid blasts.
Br J Cancer 1979 Sep
PMID:Cellular sensitization in chronic myeloid leukaemia patients to leukaemic blast antigens. 29 50

Vindesine was administered to 18 patients with acute leukemia who had failed conventional chemotherapy. Each course of therapy consisted of an iv bolus infusion at a dose of 1-2 mg/m2 given daily x 5-10 days. Of 13 patients with acute lymphoblastic leukemia, two had partial remissions which lasted 2 and 3 months and five had minor responses. One of three patients with acute nonlymphoblastic leukemia and one of two patients with blastic crisis of chronic myelogenous leukemia each had a minor response. The data suggest that vindesine has activity in the treatment of acute leukemia.
Cancer Treat Rep
PMID:Phase II trial of vindesine in patients with acute leukemia. 29 7

Eleven patients with myeloid blast cell crisis and two patients with lymphoid blast cell crisis of chronic myeloid leukemia were treated with ICRF-159. Two of the patients with myeloid blast cell crisis achieved partial bone marrow remission and survived for 8+ and 18 months. One of the patients with lymphoid blast cell crisis reverted to the chronic phase of chronic myeloid leukemia after therapy with ICRF-159 in combination with prednisolone. The only significant toxic effect was myelosuppression.
Cancer Treat Rep
PMID:Treatment of blast cell crisis of chronic myeloid leukemia with ICRF-159 (razoxane). 29 8

Despite the incomparability in the reporting of leukemia and lymphoma incidence among populations and the relative rarity of these diseases, real differences in rates are discernible from available data. In general, the incidence of each of the leukemias and lymphomas is lower in Japan than in other Pacific rim populations whose rates are known. Particularly striking is the low incidence of CLL in Japan. Among Japanese in Hawaii, rates of some of these cancers (lymphosarcoma, CML) approach those of whites, whereas rates of other cancers (Hodgkin's disease, multiple myeloma, ALL, CLL, and AML) more closely resemble those of native Japanese. The number of Chinese living in countries served by population-based cancer reporting systems is too small for any firm conclusions to be made about leukemia and lymphoma incidence in this group. The incidence of these diseases in certain other nonwhite Pacific rim residents (i.e., Mexican Americans, blacks, and Maoris) is, by and large, similar to that of whites.
Natl Cancer Inst Monogr 1979 Nov
PMID:Geographical variation in the incidence of the leukemias and lymphomas. 29 90

The sister chromatid exchange (SCE) frequency in bone-marrow cells of 12 untreated patients with chronic myelocytic leukemia (CML) was analysed and compared with the SCE frequency in bone-marrow cells of nine healthy persons. In normal persons the SCE ranged from 3.64 to 5.15 per cell. In CML patients the SCE was significantly lower, ranging from 2.32 to 3.44 per cell. The differences found were unrelated to patients' age and contraction state of the chromosomes. It is suggested that the leukemic process could account for the low SCE rate.
Int J Cancer 1979 Dec 15
PMID:Sister chromatid exchange in Ph1-positive chronic myelocytic leukemia. 29 42

The chromosomes of a cell line (NALM-1) derived from the leukocytes of a patient with chronic myelocytic leukemia (CML) were examined with several banding techniques. The modal chromosome number was 46 and the cells contained a Philadelphia chromosome (Ph1), due to the standard translocation of the missing segment of the long arm of chromosome No. 22 onto the distal end of the long arm of chromosome No. 9, i.e., t(9;22) (q34;q11). The Ph1-positive modal cells of the NALM-1 line also had two common marker chromosomes, an extra X-chromosome, and missing chromosomes in groups No. 7, 9, and 15. Immunologic examination of the NALM-1 cells revealed them to have non-T-non-B (null) surface characteristics. An antigen specific for cells of acute leukemia and a human la-like antigen were detected. These facts suggested that the NALM-1 cell line originated from CML cells and maintained the cytogenetic and Immunologic characteristics of such cells.
J Natl Cancer Inst 1977 Sep
PMID:Cytogenetic study of a new Ph1-positive cell line (NALM-1). 30 41

Antisera were raised in New Zealand White rabbits against non-B, non-T acute lymphocytic leukemia (ALL) cells coated with antilymphocyte serum. Following minimal absorption with chronic lymphocytic leukemia (CLL) cells, the antiserum reacted mainly with non-B, non-T ALL cells. The following numbers of patients had leukemia cells that reacted with the ALL antisera: 13 of 18 with ALL, 3 of 27 with acute myelocytic leukemia, 1 of 8 with chronic myelocytic leukemia (CML), and 0 of 12 with CLL. The positive CML was a patient in CML blast crisis. Normal peripheral blood B- and T-lymphocytes and normal bone marrow were negative. Reactions of the anti-ALL serum (136K) were compared with the reactions of a rabbit anti-B-cell antiserum (63K) that reacted with approximately 70% of leukemia cells. Cultured lymphoblastoid cell lines from normal donors were negative by both cytotoxicity and immunofluorescence tests. However, by immunofluorescence testing, 8 of 17 known malignant lines from a variety of lymphoproliferative disorders were positive; 4 of these lines were of T-cell origin. By immunoprecipitation and polyacrylamide gel electrophoresis, the ALL antigen appeared to consist of a single polypeptide chain of approximately 98,000 daltons. The anti-ALL antiserum was not cytotoxic for normal myeloid stem cells (colony-forming units).
J Natl Cancer Inst 1978 Aug
PMID:Acute lymphocytic leukemia-associated cell membrane antigen. 30 2

Antisera have been raised in rabbits to the lymphoblastoid cell line NALM 1 precoated with anti-lymphocyte serum (ALS). Following absorption with chronic lymphocytic leukemia cells (CLL) the antisera reacted mainly with acute lymphocytic leukemia (ALL) cells, and were very similar in specificity to antisera raised to ALL cells precoated with ALS. Leukemia cells from the following numbers of patients were positive for the anti-NALM 1 sera in a complement-dependent cytotoxicity test; 11/14 ALL, 3/15 acute myelocytic leukemia (AML), 1/5 chronic myelocytic leukemia (CML) and 0/8 CLL. Normal B and T peripheral blood lymphocytes were negative. The titer of the anti-NALM 1 sera against positive cells was 1:64 to 1:256 whereas the undiluted sera did not react with negative cells. Ten out of 11 of the positive ALL cells were of the non-B non-T type. However, cells from 1/4 T ALL patients and a cultured T ALL line 8402 were also positive. Six of 12 cultured lymphoblastoid cell lines were positive, all of which were of malignant origin. The molecular weight of the ALL antigen detected by anti-NALM-1 serum was determined by immunoprecipitation and sodium dodecyl sulfate (SDS) polyacrylamide gel electrophoresis (PAGE) to be approximately 98,000 daltons.
Int J Cancer 1978 Dec
PMID:Heteroantiserum against acute lymphocytic leukemia raised to the lymphoblastoid cell line NALM-1. 30 68

Three generations of a family were affected by hematologic malignancies: the proband had hairy cell leukemia, his brother chronic lymphocytic leukemia, his nephew cutaneous and central nervous system lymphoma, and his father chronic granulocytic leukemia. There was no clinical evidence for immune deficiency in 17 unaffected family members. Most family members had normal serum immunoglobulins and peripheral B-cells, but some had decreased T cells. Lymphocyte responses to phytohemagglutinin and concanavalin A were markedly reduced, while pokeweed mitogen responses were essentially normal. Delayed hypersensitivity responses determined by response to a 23-antigen skin test panel were markedly diminished, as were viral antibody titers. The decreased immune function in these family members suggests a role for the immune system in the emergence of hairy cell leukemia and other lymphoid malignancies, though further follow-up will be needed to see if other family members develop malignancies.
 ...
PMID:Hairy cell leukemia-associated familial lymphoproliferative disorder: immunologic abnormalities in unaffected family members. 31 14


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