Osteoblastomas are primary bone tumors with an affinity for the spine. They typically involve the posterior elements, although extension through the pedicles into the vertebral body is not uncommon. Histologically, they are usually indistinguishable from osteoid osteomas. However, there are different variants of osteoblastomas, with the more aggressive type causing more pronounced bone destruction, soft-tissue infiltration, and epidural extension. A bone scan is the most sensitive radiographic examination used to evaluate osteoblastomas. These osseous neoplasms usually present in the 2nd decade of life with dull aching pain, which is difficult to localize. At times, they can present with a painful scoliosis, which usually resolves if the osteoblastoma is resected in a timely fashion. Neurological manifestations such as radiculopathy or myelopathy do occur as well, most commonly when there is mass effect on nerve roots or the spinal cord itself. The mainstay of treatment involves surgical intervention. Curettage has been a surgical option, although marginal excision or wide en bloc resection are preferred options. Adjuvant radiotherapy and chemotherapy are generally not undertaken, although some have advocated their use after less aggressive surgical maneuvers or with residual tumor. In this manuscript, the authors have aimed to systematically review the literature and to put forth an extensive, comprehensive overview of this rare osseous tumor.

Liposarcoma (LPS) is the most common soft tissue sarcoma and accounts for approximately 20 % of all adult sarcomas. Current treatment modalities (surgery, chemotherapy, and radiotherapy) all have limitations; therefore, molecularly driven studies are needed to improve the identification and increased understanding of genetic and epigenetic deregulations in LPS if we are to successfully target specific tumorigenic drivers. It can be anticipated that such biology-driven therapeutics will improve treatments by selectively deleting cancer cells while sparing normal tissues. This review will focus on several therapeutically actionable molecular markers identified in well-differentiated LPS and dedifferentiated LPS, highlighting their potential clinical applicability.

Oral cancer kills about 1 person every hour, each day in the United States and is the 6th most prevalent cancer worldwide. The pro-inflammatory cytokine ‘macrophage migration inhibitory factor’ (MIF) has been shown to be expressed in oral cancer patients, yet its precise role in oral carcinogenesis is not clear. In this study, we examined the impact of global Mif deletion on the cellular and molecular process occurring during oral carcinogenesis using a well-established mouse model of oral cancer with the carcinogen 4-nitroquinoline-1-oxide (4NQO). C57BL/6 Wild-type (WT) and Mif knock-out mice were administered with 4NQO in drinking water for 16 weeks, then regular drinking water for 8 weeks. Mif knock-out mice displayed fewer oral tumor incidence and multiplicity, accompanied by a significant reduction in the expression of pro-inflammatory cytokines Il-1β, Tnf-α, chemokines Cxcl1, Cxcl6 and Ccl3 and other molecular biomarkers of oral carcinogenesis Mmp1 and Ptgs2. Further, systemic accumulation of myeloid-derived tumor promoting immune cells was inhibited in Mif knock-out mice. Our results demonstrate that genetic Mif deletion reduces the incidence and severity of oral carcinogenesis, by inhibiting the expression of chronic pro-inflammatory immune mediators. Thus, targeting MIF is a promising strategy for the prevention or therapy of oral cancer.