ABSTRACT
Two human cellular lines of cancerous small lung cells obtained from biopsies specimens from two patients were characterized in vitro according to cellular morphology, growth modality, caryotype and antigenic profile. In vivo studies were carried out by inoculating the cells into nude mice of both sexes and various ages by different routes in order to study tumorigenicity and metastatic capacity and to identify a biological marker of the malignancy. Results obtained to date suggest that the two cellular lines have different biological properties similar to the classic and the variant form found in literature. A biological marker of the malignancy seems to be the antigenic profile of the cells.
Subject(s)
Carcinoma, Small Cell/pathology , Lung Neoplasms/pathology , Tumor Cells, Cultured , Age Factors , Animals , Animals, Newborn , Antigens, Neoplasm/analysis , Biomarkers, Tumor/analysis , Carcinoma, Small Cell/genetics , Carcinoma, Small Cell/immunology , Chromosome Aberrations , Female , Humans , Karyotyping , Lung Neoplasms/genetics , Lung Neoplasms/immunology , Lymphatic Metastasis/pathology , Male , Mice , Mice, Nude , Neoplasm Transplantation , Tumor Cells, Cultured/immunology , Tumor Cells, Cultured/pathology , Tumor Stem Cell AssayABSTRACT
Breast cancer development is associated with several genetic abnormalities. Loss of heterozygosity in the short arm of chromosome 11 has been observed in 30% of tumors. We found homozygosity at five chromosome 11 polymorphic loci in genomic DNA of the MCF-7 breast carcinoma cell line, suggesting a possible loss of one chromosome 11. We have studied the transformed and tumorigenic phenotypes of MCF-7 cells following introduction of a normal human chromosome 11 via microcell fusion. MCF-7/H11 cell hybrids, containing chromosome 11, showed in vitro characteristics similar to the parental cell line. However, tumorigenicity in athymic mice was completely suppressed. Since tumor formation by MCF-7 cells is estrogen dependent, we have analysed the expression of the estrogen receptor and of the estrogen-activated gene pS2. No difference was detected between the parental MCF-7 cells and the derived chromosome 11 cell hybrids, indicating that the mechanism of MCF-7 tumor suppression by chromosome 11-associated functions does not directly involve the estrogen/estrogen receptor molecular pathway.
Subject(s)
Breast Neoplasms/genetics , Chromosome Aberrations , Chromosomes, Human, Pair 11 , Mammary Neoplasms, Experimental/prevention & control , Transfection , Animals , Cell Line , Female , Genes, Tumor Suppressor , Humans , Hybrid Cells , Mice , Neoplasm Transplantation , Phenotype , Receptors, Estrogen/analysis , Transplantation, Heterologous , Tumor Cells, CulturedABSTRACT
The "in vitro" cell growth of 14 ovarian carcinomas was evaluated and related with the clinical-pathologic stage (FIGO) and grade of histologic differentiation of disease, with the patients' immunological pattern and with the relapse and survival rates. We identified 4 different patterns of "in vitro" cell growth (P1, P2, P3 and P4). Their correlation with the clinical-pathologic stages of disease as well as with the recurrence and survival rates was strong: 75% of recurrences in pattern P3 and 100% in pattern P4, while tumours with patterns P1 and P2 did not relapse. Similar results were obtained for survival, in fact 2 of the 3 patients who died from disease had cell growth pattern P4, and the other a P3. A significant correlation was found with basal natural killer cell activity of peripheral blood lymphocytes too: in patients with P1 neoplasia the basal NK cell activity was significantly higher (p < 0.05) while it was significantly lower (p < 0.05) in patients with P4 neoplasia in comparison with the others. We conclude that the "in vitro" biological behaviour of ovarian neoplasia can be regarded as prognostic factors even if patients' basal NK activity represents the most significant prognostic element, directly related to the recurrence rate (p = 0.002).
