Evidence for a Proliferative Advantage of Human Leukemia Colony-Forming Cells In Vitro
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Broxmeyer, Hal E.; Grossbard, Elliot; Jacobsen, N; Moore, Malcolm A.S.

doi:10.1093/jnci/60.3.513

Cited by 59 publications

(20 citation statements)

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“…Moreover, the inability to inhibit colony formation of CFU-GM from other patients, an event associated with lack of detectable Ia-antigens on these CFU-GM, suggests that these CFU-GM may contain an intrinsic or recently induced defect in responsiveness. Acidic isoferritins suppressed colony and/or cluster formation of neutrophils, eosinphils, macrophages, and neutrophils plus macrophages in a similar manner (10,30) and lack of responsiveness of CFU-GM from patients with acute leukemia in remission and chronic leukemia to inhibition by acidic isoferritins was not due to the types of colonies and clusters formed (11). It is not known if the nonresponsive CFU-GM from patients with acute leukemia in remission are part of the normal or leukemia cell population, but the nonresponsive CFU-GM from nonremission patients with acute myeloid leukemia and from patients with chronic myeloid leukemia probably represent the leukemia cell population (2).…”

Section: Discussionmentioning

confidence: 72%

Section: Resultsmentioning

confidence: 91%

“…Acidic isoferritins are inactive against CFU-GM from nonremission patients with acute leukemia and from some patients with chronic leukemia and acute leukemia in remission (11)(12)(13)26). Inactivity was not related to cycle status of patient CFU-GM as CFU-GM upon removal from patients were in cycle (11). The relationship between Ia-antigens and susceptibility to the action of acidic isofer- (-6) Bone marrow cells were treated with C', a Ia + C, or 3HTdr, washed two times and plated or placed at 370C or 4°C for 6 h in the absence or presence of GCT-CM, washed two times, and treated with C', a Ia + C', or 3HTdr prior to washing two times and plating.…”

Section: Resultsmentioning

confidence: 99%

“…An example of this is a leukemia-associated inhibitory activity (10)(11)(12), which has recently been identified as acidic isoferritins (13). Acidic-isoferritin inhibitory activity can be found in normal bone marrow and blood cells but is present in much greater concentrations in such cells from patients with acute and chronic myeloid and lymphoid leukemia (10,11,13).…”

mentioning

confidence: 99%

“…This activity has also been detected in mice infected with Abelson and Friend virus (14,15). In contrast to its inhibitory action on normal CFU-GM, which is restricted to the DNA synthetic phase of the cell cycle (S-phase), acidic isoferritin inhibitory activity is not effective in suppressing the growth of CFU-GM from many patients with leukemia and from mice infected with Abelson and Friend virus and blast progenitor cells even though the CFU-GM and blast progenitor cells are in cycle (10)(11)(12)(13)(14)(15)(16). The mechanisms involved in the lack of responsiveness of "leukemia" CFU-GM to inhibition by acidic isoferritins have not been elucidated but would be of importance for a better understanding of the progression of leukemia.…”

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confidence: 99%

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Relationship of Cell-Cycle Expression of Ia-like Antigenic Determinants on Normal and Leukemia Human Granulocyte-Macrophage Progenitor Cells to Regulation In Vitro by Acidic Isoferritins

Broxmeyer

1982

J. Clin. Invest.

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A B S T R A C T An association has been established between human Ia-like (Ia) antigenic determinants, expression during DNA synthesis on granulocyte-macrophage colony forming cells (CFU-GM) and the regulatory action of acidic isoferritins in vitro. Treatment of human bone marrow cells with monoclonal-anti-lalike (Ia) plus complement inhibited colony and cluster formation by -50% but did not affect pre-CFU-GM. Reduction of colonies and clusters was similar whether bone marrow cells were exposed to anti-Ia plus complement, high specific activity tritiated thymidine (3HTdr) or acidic isoferritins. No further decrease was apparent with 3HTdr or acidic isoferritins after Ia-antigen+ CFU-GM were removed, or with anti-Ia plus complement or acidic isoferritins after DNA synthetic phase (S-phase) CFU-GM were removed. Anti-Ia, without complement, did not reduce colony or cluster formation but did block the inhibitory action of acidic isoferritins. A relationship existed between Ia antigens and the activity of acidic isoferritins in the following ways: (a) The apparent loss of Ia-antigens from CFU-GM by 5 h in culture at 37°C, but not at 270 or 4°C, was associated with nonresponsiveness to inhibition with acidic isoferritins, (b) Ia-antigen-, noncycling pre-CFU-GM that were insensitive to acidic isoferritins could generate a population of Ia-antigen+ cycling CFU-GM in vitro that were responsive to inhibition by acidic isoferritins, and (c) nondetectability of Iaantigens on CFU-GM from patients with leukemia was associated with nonresponsiveness to inhibition by acidic isoferritins. These results implicate Ia-antigen' progenitor cells in the regulation of myelopoiesis in vitro and demonstrate that absence of Ia-antigens on patient CFU-GM is associated with im-

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Section: Discussionmentioning

confidence: 72%

Section: Resultsmentioning

confidence: 91%

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Relationship of Cell-Cycle Expression of Ia-like Antigenic Determinants on Normal and Leukemia Human Granulocyte-Macrophage Progenitor Cells to Regulation In Vitro by Acidic Isoferritins

Broxmeyer

1982

J. Clin. Invest.

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Analysis of multiple cell markers in acute leukemia complicating Hodgkin's disease

Gulati

Mertelsmann

Gee

et al. 1980

Cancer

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A multidisciplinary methodology was applied to study 6 patients with acute leukemia (AL) following treatment for Hodgkin's disease. All 6 patients developed acute monocytic leukemia according to cytochemical criteria; morphologically, 3 cases were undifferentiated monoblastic leukemia; 3 cases were partially differentiated monocytic leukemia. In 3 of the 6 cases, cell suspensions from peripheral blood and/or bone marrow bore predominantly surface receptors for the Fc fragment of IgG and/or C-3 fraction of complement and exhibited variable degrees of phagocytosis. Two cases lacked any recognizable membrane markers or phagocytic activity. Terminal transferase enzymatic activity was not diagnostically elevated. Soft agar bone marrow culture studies revealed no growth or a characteristic leukemic cluster pattern. Chromosome analysis done in 1 of the 2 patients studied revealed hypodiploidy and structural rearrangement. Prospective studies, done serially, will help determine whether development of AL in patients with Hodgkin's disease results from the influence of intensive and potentially oncogenic therapy or represents progression from a preleukemic stage inherent to the original tumor.

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Acute myeloid leukemia as the first hematologic manifestation of fanconi anemia

et al. 1982

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A six-year-old girl with Fanconi anemia (FA) developed acute myeloid leukemia (AML) as the first hematologic manifestation of the syndrome. She remains in remission 18 mo after diagnosis although her management is complicated by unusual sensitivity to chemotherapeutic agents. Marrow cells studied prior to initiation of leukemia therapy showed increased chromosome breakage and an abnormal clone in which a number 7 and a number 8 chromosome were replaced by two marker chromosomes. During the present remission her cultured lymphocytes, bone marrow cells, and fibroblasts showed increased "spontaneous" chromosome breakage as well as enhanced sensitivity to the clastogenic effect of the difunctional alkylating agent diepoxybutane (DEB), features characteristic of FA. Eight months into remission 50% of her marrow cells comprised an abnormal clone, which was monosomic for the number 7 chromosome but had both copies of number 8; in addition a variable number of unique marker chromosomes were present in clonal as well as nonclonal cells. This same marrow sample, upon culture, showed an abnormal growth pattern of CFU-GM, absence of detectable CFU-GEMM and BFUe, non-responsiveness of CFU-GM to inhibition by acidic isoferritins, increased bone marrow acidic isoferritin inhibitory activity, and absence of detectable bone marrow cell-derived GM-CSF. The implications of these findings to leukemogenesis in FA are discussed.

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Evidence for a Proliferative Advantage of Human Leukemia Colony-Forming Cells In Vitro 23

Cited by 59 publications

References 0 publications

Relationship of Cell-Cycle Expression of Ia-like Antigenic Determinants on Normal and Leukemia Human Granulocyte-Macrophage Progenitor Cells to Regulation In Vitro by Acidic Isoferritins

Relationship of Cell-Cycle Expression of Ia-like Antigenic Determinants on Normal and Leukemia Human Granulocyte-Macrophage Progenitor Cells to Regulation In Vitro by Acidic Isoferritins

Analysis of multiple cell markers in acute leukemia complicating Hodgkin's disease

Acute myeloid leukemia as the first hematologic manifestation of fanconi anemia

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