These findings raise the possibility that Myc - Gcn5 could also work together to
promote tumor formation.
Cancer researchers at Columbia have discovered three genes that undermine the DNA repair process and
promote tumor formation in cells with BRCA mutations.
«Why premature cell division promotes cancers: Researchers have discovered how genes responsible for cell division, when mutated, disrupt the replication process of the genome and
promote tumor formation.»
Repeated triclosan exposure and continued liver fibrosis eventually
promote tumor formation.
We have found that the initiation of pancreatic cancer does not follow the classic paradigm seen in colon cancer where loss of a tumor suppressor gene initiates tumorigenesis and then acquisition of an oncogene
promotes tumor formation.
By putting E. coli bacteria into mice that were raised under sterile conditions, the team also found that the presence of E. coli
promoted tumor formation.
Not exact matches
But when their functioning is altered, as the UCL researchers observed in
tumor cells, the mitochondria can
promote cell migration, thus leading to the
formation of metastasis.
Due to the lack of oxygen in the cancer cells, VEGF - A (Vascular Endothelial Growth Factor) is formed and this
promotes the
formation of new blood vessels to supply the
tumor.
However, when these myeloid cells migrate to
tumor sites, they can differentiate to
tumor associated macrophages (TAMs), which can in turn stimulate the
formation of blood vessels in
tumors and
promote enhanced
tumor cell invasion and motility.
«These strategies would focus on
promoting myelination in the peripheral nervous system for neuropathic disease or inhibiting Schwann cell over-proliferation that occurs during
formation of peripheral nerve sheath
tumors like neurofibromas.»
«Metastatic
tumor cells can
promote either bone
formation or bone resorption,» lead author Kyoko Hashimoto explains.
We also found that the EphB4 receptor expressed on the surface of breast cancer cells can
promote tumor xenograft growth by enhancing blood vessel
formation through interactions with its preferred ligand, ephrin - B2, present in
tumor endothelial cells.