Recently, it has been demonstrated that a defect in homologous recombination can lead to changes in drug sensitivity profile, rendering the BRCA1 deficient breast cancers sensitive to mitomycin C, cisplatin, etoposide and other drugs that produce double-stranded lesions [33].
That same burden might also make those ultramutator cancers sensitive to mutation-inducing or DNA repair-blocking therapies.
Importantly mutations in these domains render cancers sensitive to PI3K specific inhibitors pointing towards a role for this emerging class of drugs in cancers harboring these mutations [ 27].
Similarly, MMC and gemcitabine had a synergistic effect, when administered concurrently, but not sequentially, on the HT29 human colon cancer cell line (Aung et al, 2000), suggesting that gemcitabine could be beneficial in the treatment of cancers sensitive to MMC.
To select a sub-population of gastric cancers sensitive to FGFR inhibitors in the future, gene amplification may be a more suitable biomarker than positive staining using immunohistochemistry based on the results of preclinical studies.
In general, cancers sensitive to female sex steroids are associated with several risk factors, such as low parity, infertility, early age at menarche, and late age at menopause [ 4].
While most triple-negative BCs show aggressive clinical behaviour and have very limited targeted therapies, they also encompass subgroups of cancers sensitive to chemotherapy and having a good prognosis [ 4].
The adoptive transfer of donor leukocytes from SR/CR mice can confer protection against future exposures to cancer cells, as well as the elimination of established malignancies without any further manipulation in cancer-sensitive wild-type (WT) recipient mice [ 2].
When SR/CR Nos2-/ macrophages and neutrophils were transferred into cancer-sensitive WT mice, the SR/CR Nos2-/ cells proved to be less protective against an S180 challenge compared to cells from SR/CR Nos2+/+ mice.
