Q: In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.
Context: Activation of cyclooxygenase (COX)/prostaglandin and nuclear factor B (NFB) pathways can promote breast tumor initiation, growth, and progression to drug resistance and metastasis. Thus, anti-inflammatory drugs have been widely explored as chemopreventive and antineoplastic agents. Aspirin (ASA), in particular, is associated with reduced breast cancer incidence but gastrointestinal toxicity has limited its usefulness. To improve potency and minimize toxicity, ASA ester prodrugs have been developed, in which the carboxylic acid of ASA is masked and ancillary pharmacophores can be incorporated. To date, the effects of ASA and ASA prodrugs have been largely attributed to COX inhibition and reduced prostaglandin production. However, ASA has also been reported to inhibit the NFB pathway at very high doses. Whether ASA prodrugs can inhibit NFB signaling remains relatively unexplored.', 'A library of ASA prodrugs was synthesized and screened for inhibition of NFB activity and cancer stem-like cell (CSC) properties, an important PGE2-and NFB-dependent phenotype of aggressive breast cancers. Inhibition of NFB activity was determined by dual luciferase assay, RT-QPCR, p65 DNA binding activity and Western blots. Inhibition of CSC properties was determined by mammosphere growth, CD44(+)CD24(-)immunophenotype and tumorigenicity at limiting dilution.', 'While we identified multiple ASA prodrugs that are capable of inhibiting the NFB pathway, several were associated with cytotoxicity. Of particular interest was GTCpFE, an ASA prodrug with fumarate as the ancillary pharmacophore. This prodrug potently inhibits NFB activity without innate cytotoxicity. In addition, GTCpFE exhibited selective anti-CSC activity by reducing mammosphere growth and the CD44(+)CD24(-)immunophenotype. Moreover, GTCpFE pre-treated cells were less tumorigenic and, when tumors did form, latency was increased and growth rate was reduced. Structure-activity relationships for GTCpFE indicate that fumarate, within the context of an ASA prodrug, is essential for anti-NFB activity, whereas both the ASA and fumarate moieties contributed to attenuated mammosphere growth.\Question: Does a novel aspirin prodrug inhibit NFB activity and breast cancer stem cell properties?
A:
These results establish GTCpFE as a prototype for novel ASA-and fumarate-based anti-inflammatory drugs that: (i) are capable of targeting CSCs, and (ii) may be developed as chemopreventive or therapeutic agents in breast cancer.