Abstract
The genomic alteration at chromosome 15 has been widely recognized as the
utmost significant and prevalent alteration in several cancers, including non-small-cell
lung cancer, breast cancer, ovarian cancer, prostate cancer, gastrointestinal cancer,
acute lymphoblastic leukemia, colorectal carcinoma, hepatocellular carcinoma,
myeloma, pituitary adenomas, etc. Emerging reports suggest that the abnormalities of
prime genes in chromosome 15 have drastic effects on tumor development and
progression, and can be candidate biomarkers of disease prognosis, disease
progression, and response to treatment. The translocations involving chromosome 15
and other chromosomes have been found in tumors, including mucoepidermoid
carcinomas, mixed-lineage leukemia, colorectal cancer, pancreatic cancer, sarcoma,
lung adenocarcinoma, melanoma, brain cancer, cholangiocarcinoma, spitz tumor,
congenital mesoblastic nephroma, papillary thyroid cancer, pontine glioma tumors, and
acute promyelocytic leukemia. The tumor suppressor genes such as C15orf65, CSK,
CRABP1, DAPK2, FES, GREM1, KNSTRN, NEDD4-1, NTRK3, PML, SPRED1,
TPM1, and TCF12 under chromosome 15 play a crucial role by enhancing cellular
growth, proliferation, migration, invasion, metastasis, cellular differentiation, and
development in various cancer, including colorectal cancer, acute promyelocytic
leukemia, myeloid leukemia, breast cancer, thyroid carcinoma, glioblastoma,
intrahepatic cholangiocarcinoma, chondrosarcoma, cartilaginous cancer, Squamous cell
carcinoma, non- small-cell lung carcinomas, mucosal melanoma, and oral squamous
cell carcinoma. Chapter 15 discusses the significance of each important gene under
chromosome 15 in mediating oncogenesis. The elevated or attenuated expression levels
of these cardinal genes can either act as an oncogene or a tumor suppressor. Thus,
shedding light on these genes would be a game changer in the field of cancer genetics
and theragnostic.