Establishment and characterisation of a new tumorigenic cell line with a normal karyotype derived from a human breast adenocarcinoma.

A new cell line (CAL51) was isolated from a malignant pleural effusion of a woman with metastatic breast cancer. These cells grow in continuous culture and exhibit the morphological, ultrastructural and immunohistochemical features of epithelial cells of mammary origin. They are tumorigenic in nude mice and clone in soft agar. Oestrogen receptors are not detected. CAL51 consists of a homogeneous population of cells with normal chromosomes even after the use of high resolution banding. Cytogenetic analysis of the cells from the tumour induced by CAL51 in the nude mouse confirmed the normality and the stability of the karyotype. All breast cancer cell lines established to date present abnormal karyotypes; CAL51 cell line may be more informative than cell lines with aberrant karyotypes for investigating essential genetic differences between normal and malignant mammary gland cells.

Differential effects of lectins on the in vitro growth of normal mouse lung cells and low- and high-cancer-derived cell lines.

The comparative aspects of cell growth, i.e., [3H]thymidine and [14C]leucine uptake of low-cancer (P4Bis) and high-cancer (P4BisT) cell lines and of their normal counterparts, have been studied in the presence and absence of concanavalin and Robinia lectins. These lectins have similar effects on cell growth, on thymidine and leucine uptake, and on incorporation of these precursors. The growth of normal cells is stimulated by both lectins, whereas the growth of transformed cells is inhibited. In all cases the uptake of both leucine and thymidine by cells is increased by the lectins, but the percentage of incorporation of the precursors is affected in a different manner. The percentage of thymidine incorporated by normal and transformed cells increases or decreases in direct proportion to cell growth; leucine incorporation is not affected significantly. The reversibility of these lectin effects by specific inhibitors shows that cell membranes are implicated in these phenomena. Our study with normal and transformed cells suggests that cell surface may play a role in the process of malignant transformation and that P4Bis cells are "transitory" between PB1 normal cells and P4BisT high-cancer cells.

Activation of "eclipsed" lymphoid cells from advanced tumor-bearing mice through adoptive transfer to sublethally irradiated syngeneic hosts.

Immunologically inactive or "eclipsed" lymphoid cells from advanced tumor-bearing mice were investigated following their adoptive transfer to irradiated syngeneic hosts. Experiments were performed with two syngeneic tumor-host system: the T5-BALB/c tumor line chronically infected with a low-leukemogenic Rauscher virus variant and the TM1-C3H tumor line developed from a spontaneous C3H/He mouse mammary tumor. In confirmation of our previous data, peritoneal cells (PC) from advanced tumor-bearing mice (EPC) appeared to have lost any capacity to inhibit specifically the growth of corresponding tumor target cells in vitro colony inhibition (CI) tests, whereas PC from immunized mice (IPC) were perfectly active. When these EPC were adoptively transferred by intraperitoneal inoculation into sublethally irradiated (450 R) syngeneic mice in association with respective tumor extracts (TE), the PC from such recipient mice, taken 5 to 13 days later, were nearly as active in in vitro CI tests as were PC from parallel IPC-recipient mice. For this recovery of specific immunological activity following the adoptive transfer of EPC the adjunction of the TE and irradiation of the recipient animals seem important and may be necessary. On the other hand, no specific immunological activity was seen in PC from irradiated mice to which PC from normal mice had been transferred with TE. In addition to the in vitro results, an effect of adoptive transfer of EPC (retardation of tumor growth) was also observed in vivo. It is concluded that the "eclipsed" immunologically inactive state of the EPC in mice bearing advanced tumor is not irreversible and that activation of these cells can occur in vivo under certain conditions helped by the presence of tumor-specific antigenic stimulus.