Leukokinetic Studies. X. Blood Granulocyte Kinetics in Chronic Myelocytic Leukemia*

Leukokinetic Studies. XI. Blood Granulocyte Kinetics in Polycythemia Vera, Infection, and Myelofibrosis*

“…The prolonged tj values and the increased number of immature cell forms present in their blood are similar to the findings in patients with chronic myelocytic leukemia in relapse (3). The possible explanations for the markedly prolonged tj in such patients have been discussed (3). Some factor in addition to enlarged TBGP size must be invoked to explain the marked divergence of these four studies (Figure 4) from the findings in other patients studied.…”

“…The "extrapolated" TBGP was calculated from the blood granulocyte radioactivity at to obtained by extrapolating the blood granulocyte disappearance curve back to the ordinate. Since the determined TBGP appears to be the more accurate value (3), only these values are given in the tables. The sizes of the CGP and the MGP were determined as previously described (1).…”

“…t Leukemia Society Scholar. subject of a separate report (3). We sought to determine whether there is a characteristic granulocyte kinetic pattern in any of these diseases and whether the observed granulocytosis reflects an absolute increase in TBGP size, an intravascular redistribution of cells, or some combination thereof.…”

Leukokinetic studies

“…In regard to the first assumption, previous evidence has demonstrated a good correlation between blood granulocyte concentration and TBGP size in all clinical situations, except perhaps in patients with myelofibrosis or polycythemia who have high granulocyte counts (12,13). Admittedly, the letter data were collected in steady-state situations, while the present studies were done during a non-steady state.…”

The Bcr-Abl tyrosine kinase activates mitogenic signaling pathways and stimulates G1-to-S phase transition in hematopoietic cells

“…During the chronic phase of CML, an expansion of the leukemic cells occurs which leads to an approximately 5 ± 10-fold increase in total hematopoietic cell mass (Clarkson and Strife, 1993). While these cells do not have an increased proliferative rate, they do undergo extra cell divisions and have longer survival times than normal myeloid progenitors (Athens et al, 1965;Chervenick and Boggs, 1968;Clarkson and Strife, 1993;Galbraith and Abu-Zahra, 1972;Goto et al, 1982;Ogawa et al, 1970;Scott et al, 1971;Strife and Clarkson, 1988;Stryokmans et al, 1977). Mitogenic signals from Bcr-Abl may serve to inhibit cell cycle exit that would normally occur during the dierentiation process.…”