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Although positron emission tomography–computed tomography (PET/CT) is widely used for staging, there are limited data available to describe exactly the role of PET/CT metabolic and quantitative parameters for the prediction of disease outcome. A total of 145 patients diagnosed with histology-proven lung carcinoma in the advanced stage were included. According to the exclusion criteria remaining 76 patients (41 of them were adenocarcinoma EGFR wild-type, 35 were squamous non-small cell lung cancer (NSCLC)) were analyzed. Maximum standardized uptake value (SUV(max)) of a primary lesion was only statistically significant parameter with progression-free survival (PFS) in regression analyses in the whole study population as well as for overall survival (OS). According to the tumor histology, squamous cell carcinoma group did not have any significant PET CT parameters for PFS and OS, but adenocarcinoma group had significant PET CT parameters which were primary lesion of SUV max, SUV mean, total lesion glycolysis (TLG), mediastinal TLG and whole body TLG. In adenocarcinoma group, patients with lower than median TLG values had significantly increased overall survival than patients having higher median whole body TLG values (median OS was 11 vs 6.5 months, P = 0.031, HR 2.1), also they had more PFS without statistical significance (median PFS 6.5 vs 4 months, P = 0.3 HR 1.2). The present study showed that PET/CT metabolic parameters give some prognostic information other than staging of NSCLC, but this information was only significant in EGFR-wild type adenocarcinoma. For squamous cell carcinoma, we need to find any driver targets.

Tryptophan (Trp) is one of the important essential amino acids and Kynurenine pathway (KP) is the first and rate limiting step of degrading Trp to active metabolites. Recent studies showed that KP metabolites have antimicrobial and immunosuppressive roles. The main controller enzyme of this pathway is indoleamine-2,3-dioxygenase (IDO). IDO is an intracellular monomeric, heme-containing enzyme that controls the Trp breakdown in the KP. In this review, we discuss IDO functions on cancer progression and prognosis, and possible therapeutic aspects of inhibition of IDO on cancer immunotherapy.