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Although the present study is relatively small, tumour marker response does not appear helpful in determining chemotherapy response.
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Thus, the combined tumor marker response did not independently predict progression-free survival upon multivariate analysis.
However, identification of genetic markers associated with drug response does not always equate to clinically useful predictors of adverse outcomes, and independent replication of genotype-phenotype association is always required before pursuing clinical implementation.
Ninety per cent of patients who achieved a marker response had done so by 8 weeks.
What response did you get?
Additionally, they did find a relation between marker response and OS.
The association of tumour marker response alone with the patient response classification was modest and did not add significantly to F-FES-PET/CT.
Tumor marker response evaluation was performed when complete remission is observed after consecutive session of TACE in most of subjects, but tumor marker response also analyzed within subject who did not get complete remission.
Tumour response and marker expression did not predict disease-free or overall survival.
Immunohistochemistry of the cerebellum with antibodies against multiple inflammation marker proteins, such as CD4 (a helper T-cell marker), CD8 (a cytotoxic T-cell marker), CD11c (a dendritic cell marker) and microglial response factor-1 (a microglial marker), did not reveal any inflammation response in HMGB1-Tg mice (Supplementary Fig S2A).
To focus on modulation of inflammation by diclofenac, and not acute phase response, only markers that did not show significant correlation to CRP response (across all subjects) were selected.
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