Various types of cancers metastasize to the bone, including breast, prostate, lung, thyroid, kidney, multiple myeloma, melanoma, and neuroblastoma.
It is also amplified and/or overexpressed in non-small-cell lung cancer, colorectal carcinoma, nasopharyngeal carcinoma, medulloblastoma, lymphoma, multiple myeloma and primary neuroblastoma [9], [13], [19] [22].
This phenomenon was reported previously in B-cell lymphomas [ 13], multiple myeloma [ 14], and neuroblastoma [ 15].
Immunomediated destruction of the transformed cells overexpressing survivin by cytotoxic T cells has been described in patients with multiple myeloma [ 24] and neuroblastoma [ 25], which may provide a plausible explanation for the extracellular appearance of survivin.
Surprisingly, tumor endothelial cells can harbor the same chromosomal abnormality as tumor cells in B-cell lymphomas [ 13], multiple myeloma [ 14], and neuroblastoma [ 15], suggesting a tumor origin of at least a fraction of intratumoral endothelial cells.
The observed sensitivity is also comparable to those of multiple myeloma and MYCN-amplified neuroblastoma cell lines, reported to be potentially JQ1-sensitive types types (Delmore et al., 2011; Puissant et al., 2013), and substantially higher than those of lung adenocarcinoma and MYCN-WT neuroblastoma cell lines (Lockwood et al., 2012; Puissant et al., 2013).
Nine datasets, including three large-scale cancer datasets - breast cancer (BR) [27], multiple myeloma (MM) [28] and neuroblastoma (NB) [29] with six clinical endpoints contributed to the MAQC Consortium [24] and three datasets used in previously published prognostic modeling research [4], [25], [26], were selected and utilized in this study.
This ability of cancer stem cells to give rise to capillary endothelia has been reported for other tumours, such as lymphoma (Streubel et al, 2004), myeloma (Rigolin et al, 2006) and neuroblastoma (Pezzolo et al, 2007).
Similar to our findings on OS cells, CDK inhibitors reduced the percentage of BrdU-positive S phase cells in myeloma, neuroblastoma, and colon, lung and breast carcinoma cultures; G2/M arrest, and in some instances G0/G1 arrest, was also observed.
The effects of ATO were subsequently examined in other tumor types, including multiple myeloma, glioma, neuroblastoma, esophageal carcinoma and prostate cancer, and it has been found to be efficacious in many of these as well [ 22- 27].
