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In females with breast cancer, a possible metastasis in the stomach should be taken into account. Maspin and VSIG1 are not involved in breast cancer histogenesis. The Wnt/β-catenin signaling is not involved in the lobular carcinoma progression. The CD44/HER2 positivity in ductal carcinoma cells might indicate high risk of distant metastasis and low response to chemotherapy.

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The ability of protaglandins E1 and E2 to stimulate the proliferation of haemopoietic stem cells (CFUs) was studied in vivo. PGE2, in a dose range of 10‐4 to 10‐1μg/g body weight and PGE1 in a dose range of 10‐5 to 10‐1μg/g body weight, produced a rapid cycling wave of CFUs. The increase in the number of CFUs in S phase was not followed by a rise in the femoral CFUs content, and except for a transient increase in femoral CFUc level, no increase in differentiation was found either. Therefore, it is proposed that haemopoiesis after PG‐induced CFU stimulation is ineffective. PGE2 did not stimulate regeneration of CFUs in a perturbed state (after sublethal irradiation). All these findings support the idea that PGEs might represent potent stimulators of the haemopoietic stem cells acting in physiological doses. However, if acting concurrently with physiological control systems PGs lead to ineffective haemopoiesis (under normal conditions) or do not exert any measurable effect (after sublethal irradiation).

The effect of mouse serum interferon (IF) in vitro and an inducer in vivo on the proliferation of a pluripotent stem cell population with high turnover rate was studied. Proliferation rate was characterized by the number of CFUs in the S phase of the cell cycle. Increased proliferation of bone marrow stem cell populations was produced either by irradiating the donor mice with 3·36 Gy (336 rad) 60Co‐gamma rays 7 days before the experiment or by incubating normal bone marrow cells with 10–11 M concentration of isoproterenol. IF considerably reduced the number of CFUs in S phase in both cases without reducing the CFUs content of the samples. Injection of IF inducer (4 mg/kg poly I:C) into regenerating mice also inhibited the proliferation of CFUs without decreasing the femoral CFUs level. Regeneration kinetics of CFUs from irradiated poly I:C‐treated mice ran parallel with that of irradiated untreated animals but showed a characteristic delay corresponding to approximately one CFUs doubling. A transient, non‐cytotoxic proliferation inhibitory effect of IF or IF inducer is, therefore, proposed.

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Summary:In P-388 bearing BDF 1 mice stem cell mobilisation was tested on the survival of lethally irradiated isologous recipients. Contamination of the graft with lymphoma cells was evaluated by the number of clonogenic lymphoma cells (CFU-L) and the ability of the graft to induce lymphoma in non-irradiated recipients. A mobilisation protocol (200 mg/kg cyclophosphamide (CY) i.p. or 200 mg/kg CY followed by 125 g/kg G-CSF administered every 12 h for 3 consecutive days, starting 14 days after lymphoma initiation) that resulted in a substantial stem cell mobilisation in normal mice, mobilised too few CFU-L to induce lymphoma in the recipients: 50 l of blood obtained after mobilisation protected lethally irradiated mice but did not induce lymphoma in normal recipients. A minimum graft of bone marrow (2 × 10 5 cells, with 5580 CFU-L) from untreated P-388 bearing donors killed irradiated recipients presumably by lymphoma and not bone marrow failure. The mobilisation protocol reduced CFU-L so much that no lymphoma-associated death occurred even after the transplantation of 10 × 10 5 bone marrow cells. These data suggest that, although the PBSC mobilisation protocol may also mobilise some clonogenic lymphoma cells, with the minimum graft size no lymphoma transfer can be observed.

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