~5% of cases, have areas of osteoid (see Fig. 1 in the below Histopathology of liposarcomas section) or cartilaginous material. The tumors also show large variations in their cell contents. For example, up to 10% of DDL tumors have areas with ALT/WDL histopathology and rare cases of DDL have areas containing meningothelial-like whorls of flat cells. Genetics The neoplastic cells in both DDL and ALT/WDL carry similar small supernumerary marker chromosomes (sSMCs) and/or giant marker chromosomes that contain extra parts of chromosome 12's q arm at bands 13 through 15. This chromosomal area includes two genes associated with tumor development, the MDM2 and CDK4 genes. The presence of extra copies of these two genes and/or their overproduced protein products is a highly sensitive and specific indicator that a lipomatous tumor is an ALT/WDL or DDL rather than some other type of lipomatous tumor. Overexpression of the MDM2 and CDK genes, and/or other genetic material in the sSMCs or giant marker chromosomes are suspected of promoting the development and/or progression of DDL as well as ALT/WDL tumors. Other genes in the sMMC and giant marker chromosome that are also overexpressed in ALT/WDL and DDL neoplastic cells include HMGA2, CPM, YEATS4, and DDIT3. Compared to ALT/WDL neoplastic cells, however, DDL neoplastic cells: 1) express higher levels of the genes in the two abnormal chromosomes; this may contribute to the progression of ALT/WDL to DDL; and 2) higher levels of gene products on the long arm of chromosome 1 at band 32, the long arm of chromosome 6 at band 33, and, in ~25% of cases, the short arm of chromosome 1 at band 32.2 which contains the JUN gene (this gene is overexpressed in DDL but not ALT/WDL). Since the JUN gene's product, c-jun, inhibits cell death and promotes cell proliferation, its overproduction may contribute to the progression of ALT/WDL to DDL and/or the malignancy of DDL neoplastic cells. Gene expression profiling (i.e. measurement of the expression of the products of thousands of genes made by cells, tissues, or tumors) have revealed that adipocyte cell differentiation and metabolic pathways in ALT/WDL are upregulated while cell proliferation and DNA damage response pathways are upregulated in DDL. Diagnosis The histopathological of DDL is often insufficiently clear to make a firm diagnosis. However, the diagnosis of DDL is supported in individuals: whose tumors contain ALT/WDL admixed with DDL histological components; with histories of having a