Analysis of
the tumor genes affected by the two drugs revealed that cabazitaxel had a greater effect on cellular division and regulation of chromatin — a spool for DNA that helps control which genes are in use and when — whereas docetaxel has a greater impact on DNA transcription and repair.
Not exact matches
A significant finding by the team was that either the mutant KRAS
gene or another cancer
gene is amplified, depending on which
tumor suppressor
gene is
affected and to what degree its function is impaired.
Research from other scientists at Johns Hopkins, he says, had suggested that some
tumors, particularly those that
affect the nervous system, have mutations in the ATRX
gene, which produces proteins that appear to maintain the length of telomeres, repetitive segments of DNA on the ends of chromosomes that typically shorten each time a cell divides.
Moreover, approximately 30 % of follicular lymphoma patients lose also a portion of chromosome 6,
affecting multiple
genes involved in suppressing the emergence of a
tumor.
These rearrangements
affected several known and suspected oncogenes and
tumor suppressor
genes, including Notch1, Pten, Ikzf1, Jak1, Phlda1, Trat1, and Agpat9.
«We found polyploidy in liver cells did not strongly
affect the activity of some oncogenes, but it did protect against the loss of
tumor suppressor
genes.
They also learned key details about how
genes and the cells immediately surrounding a
tumor (also called the
tumor microenvironment)
affect cancer risk.
«This enabled us to study how
genes and the
tumor microenvironment — not the
tumor itself —
affect tumor growth.»
At the time, it was thought that this
gene fusion was limited to a fraction of brain
tumors,
affecting about 300 patients in the U.S. per year.
We observed an average of 14.5 «tier 1» (coding) mutations per
tumor in the 24 WGS cases; on average, ~ 3 of these
affected recurrently mutated
genes in M1
tumors, and ~ 2
affected recurrently mutated
genes in M3
tumors.
JJ Miranda, PhD, reported that certain drugs
affect genes in
tumor cells infected with the Epstein - Barr Virus.
In a study published in the journal Biochemical and Biophysical Research Communications, a team led by Miranda examined how certain drugs
affect genes in EBV - infected
tumor cells.
We are also interested in the interplay of Eph receptor mutations with mutations
affecting well - established oncogenes and
tumor suppressor
genes.
Both mutations
affect the function of CDKN2A, a
tumor suppressor
gene associated with melanoma in humans.
Interestingly, BRCA1 is not a haploid - insufficient
tumor suppressor
gene; therefore monoallelic deletion may not
affect its function or
affect tumorigenesis of those breast cancers bearing deletions.