The LHFP was found in a t(12;13) translocation in lipoma, where a subsequent fusion of the HMGIC gene with the HMGIC/LHFP fusion led in the generation of an HMGIC/LHFP fusion transcript. LHFP is found at much higher quantities in bone and in osteoblasts. As shown by the capacity of osteoblast lineage stem cells from LHFP-deficient mice to differentiate into the osteoblast lineage (measured by the number of daughter cells forming an osteoblast colony [CFU-U] and mineralization [assessed by alizarin red staining] in vitro, and as well as bone mineral density [measured by cortical thickness] in the mice, these mice have greater mineralization and bone mineral density. One nucleotide variation in the gene for LHFP, rs9576787, was shown to be linked with bone mineral density in the heel. The joint study on LHFP and osteoblast development found that the hormone works in control of osteoblast differentiation and bone mineral density. While studying gliosarcoma, a study of glial and mesenchymal portions of 13 tumors discovered variations in copy number at 13q13.3-q14.1, a region that includes the LHFP gene; the changes in copy number were found only in mesenchymal portions of the tumor. As opposed to the majority of gliosarcomas in the mesenchymal regions, which had increased expression of LHFP, mRNA expression investigations in a broader sample of gliosarcomas found that the mRNA for LHFP was amplified in 11% (7/64) of gliosarcomas in the mesenchymal regions. According to a separate study, it was concluded that the fusion of LHFP to HMGIC was not an inherent feature of mesenchymal tumors with chromosome structure changes at 12q13, as no transcripts for LHFP-HMGIC fusion were present in pulmonary chondroid hamartomas containing a 12q13~q15 and a t(12;13)(q14~15;q13) structural change. Because of this, it has been demonstrated that LHFP is involved in regulating bone mineral density, and in determining the differentiation potential of osteoblasts. The LHFP locus is fused to the HMGIC gene in human lipoma, resulting in a fusion transcript, and gliosarcomas are capable of bearing copy number changes in the LHFP gene, specifically in mesenchymal components of the tumor. Because our analysis mined gene expression data found in independent studies, we found that the gene encoding the HMGIC lipoma fusion partner, LHFP, was one of the most differentially expressed genes in human breast cancer, both in lymph node metastases when compared to primary tumours of the breast and in primary tumours of the breast when compared to adjacent benign breast tissue. The expression of the LHFP tumor was strongly linked with overall patient survival. From invasively-invasive breast cancer, it appears that LHFP expression seems to be graded. The significance of this may be relevant to processes associated with the transition from transformation to metastasis of invasive breast cancer and spread of invasively-invasive breast cancer to the lymph nodes.