Molecular cytogenetic studies of a serially transplanted primary prostatic carcinoma xenograft (CWR22) and four relapsed tumors.

Background: Established cell lines or xenografts from prostatic carcinoma have been infrequently studied cytogenetically. CWR22 and CWR22-R are xenografts that are unique in offering one strongly androgen-dependent and several relapsed strains of a human prostate cancer that can be investigated in the laboratory. We report on the cytogenetic characterization of the hormone-dependent CWR22, and the relapsed CWR22-R serially transplanted xenografts, in our laboratory.

Chromosome number and structure both are markedly stable in RER colorectal cancers and are not destabilized by mutation of p53.

Fourteen colorectal cancer cell lines, categorized according to the presence or absence of microsatellite instability, were further analysed for chromosomal stability by karyotyping. NonRER (microsatellite stable) cell lines typically displayed highly aberrant karyotypes with alterations not only of chromosome number but also of chromosome structure including chromosomal deletions, inversions, and translocations. RER (microsatellite unstable) cell lines, in contrast, displayed significantly fewer alterations of chromosome number.

A benign cultured colon adenoma bears three genetically altered colon cancer oncogenes, but progresses to tumorigenicity and transforming growth factor-beta independence without inactivating the p53 tumor suppressor gene.

We describe the spontaneous progression of a colon adenoma cell line to tumorigenicity and growth factor independence. This system allows direct comparison of biologic stages of malignant progression with alterations of colon cancer suppressor genes and oncogenes. VACO-235, a human colon adenoma cell line, is at early passages nontumorigenic in the nude mouse, unable to grow in soft agar, growth stimulated by serum and EGF, and growth inhibited by TGF-beta.

Origin of leukemic relapse after bone marrow transplantation: comparison of cytogenetic and molecular analyses.

Leukemic relapse following bone marrow transplant (BMT) is generally due to the recurrence in recipient cells, but may rarely occur as a result of donor cell transformation. Donor cell relapse is generally identified using cytogenetic markers such as the sex chromosomes. Recently, molecular techniques have been used to identify the origin of bone marrow cells by their DNA restriction fragment length polymorphisms.