Discussion In this study, data from microarray, qRT-PCR, selleck chemicals and IHC revealed differences in CDO1 expression in a cohort of liposarcoma specimens. There was a strong correlation among results from all assays used to assess CDO1 levels. We found CDO1 expression was higher in WDLS than in DDLS. This difference in CDO1 expression was retained in the well-differentiated component of DDLS. However, CDO1 expression or protein levels were not associated with clinicopathological features assessed including time to recurrence or histology upon recurrence. Results from in vitro differentiation of hMSCs suggest that CDO1 is a marker of adipogenic differentiation. WDLS is a locally aggressive tumor that does not have the potential to metastasize. Hence, it has a favorable prognosis compared to other liposarcoma subtypes.

However, some WDLS transitions into DDLS.30 Evidence suggests that this phenomenon results from the accumulation of genetic aberrations that ultimately affect tumor behavior and prognosis.31,32 The primary phenotypic alteration is a transition from entirely lipogenic components in WDLS to the presence of non-lipogenic components in DDLS. Our data demonstrate that abundant CDO1 is a feature observed in WDLS tumors while low levels are found in the DDLS tumors. We hypothesize that adipogenic cells retain the ability to synthesize CDO1, whereas the non-lipogenic cells lack that ability. PLSs are diagnosed histologically based on the presence of lipoblasts, progenitor cells for the adipogenic lineage. However, there is a wide variation in the number of lipoblasts among PLS tumors.

In our cohort of PLS assessed by qRT-PCR, we observed a biphasic distribution of CDO1 mRNA levels in which some tumors had low CDO1 mRNA levels similar to that observed in WDLS whereas other tumors had high levels of CDO1 mRNA levels similar to that observed in DDLS. Because our data suggest that CDO1 is a marker of adipogenic differentiation, it is possible that CDO1 expression in PLS reflects the number of lipoblasts present in the tumor. Thus, in those tumors with few lipoblasts, CDO1 expression would be high, whereas in those tumors with greater numbers of lipoblasts CDO1 expression would be low. This biphasic distribution of CDO1 expression would confound the ability to define a distinction between PLS and other complex karyotype liposarcomas.

To our knowledge, there is no previous work that characterizes CDO1 expression during adipogenesis. The results presented Dacomitinib here suggest that CDO1 is a marker of differentiation in the adipogenic lineage. Consistent with this, the highest level of CDO1 expression was observed in mature HAd, while the expression was much lower in less-differentiated cells in the lineage. Developmentally, HAd arise from mesenchymal stem cells that commit to the adipogenic lineage through orchestrated expression of functional genes and transcription factors.