Purpose: We aimed to identify the prognostic and predictive values of post-treatment prognostic nutritional index (PNI) and PNI dynamics in nasopharyngeal cancer patients (NPC) in this study.Methods: 107 non-metastatic NPC patients were included. PNI was calculated by using the following formula: [10 x serum albumin value (gr/dL)] + [0.005 x total lymphocyte count (per mm3)]. ROC analysis was used for determining prognostic PNI values and univariate and multivariate statistical analyses for prognostic characterization of PNI.Results: The statistically signi cant cut-off values for pre-and post-treatment PNI were 50.65 and 44.75, respectively. Of the pre-treatment PNI analysis, PNI≤50.65 group had shorter loco-regional recurrence-free survival (LRRFS), distant metastasis-free survival (DMFS), and overall survival (OS). Furthermore, for post-treatment PNI analysis, PNI≤44.75 group had shorter LRRFS and OS. In univariate analysis, only pretreatment PNI was associated with LRRFS and DMFS, while pre-and post-treatment PNI were both associated with OS. In multivariate analysis, both PNI were independent prognostic markers for OS. In the combined analysis, pre-and post-treatment PNI, differences between the groups were statistically signi cant, and the PNI dynamics was an independent prognostic indicator for OS.Conclusion: PNI is a useful, independent prognostic marker for non-metastatic NPC patients. It is used for either pre-or post-treatment patients. Furthermore, changes in pre-treatment PNI value after curative treatment is a signi cant indicator for OS.
Background There is no standard treatment recommended at category 1 level in international guidelines for subsequent therapy after cyclin-dependent kinase 4/6 inhibitor (CDK4/6) based therapy. We aimed to evaluate which subsequent treatment oncologists prefer in patients with disease progression under CDKi. In addition, we aimed to show the effectiveness of systemic treatments after CDKi and whether there is a survival difference between hormonal treatments (monotherapy vs. mTOR-based). Methods A total of 609 patients from 53 centers were included in the study. Progression-free-survivals (PFS) of subsequent treatments (chemotherapy (CT, n:434) or endocrine therapy (ET, n:175)) after CDKi were calculated. Patients were evaluated in three groups as those who received CDKi in first-line (group A, n:202), second-line (group B, n: 153) and ≥ 3rd-line (group C, n: 254). PFS was compared according to the use of ET and CT. In addition, ET was compared as monotherapy versus everolimus-based combination therapy. Results The median duration of CDKi in the ET arms of Group A, B, and C was 17.0, 11.0, and 8.5 months in respectively; it was 9.0, 7.0, and 5.0 months in the CT arm. Median PFS after CDKi was 9.5 (5.0–14.0) months in the ET arm of group A, and 5.3 (3.9–6.8) months in the CT arm (p = 0.073). It was 6.7 (5.8–7.7) months in the ET arm of group B, and 5.7 (4.6–6.7) months in the CT arm (p = 0.311). It was 5.3 (2.5–8.0) months in the ET arm of group C and 4.0 (3.5–4.6) months in the CT arm (p = 0.434). Patients who received ET after CDKi were compared as those who received everolimus-based combination therapy versus those who received monotherapy ET: the median PFS in group A, B, and C was 11.0 vs. 5.9 (p = 0.047), 6.7 vs. 5.0 (p = 0.164), 6.7 vs. 3.9 (p = 0.763) months. Conclusion Physicians preferred CT rather than ET in patients with early progression under CDKi. It has been shown that subsequent ET after CDKi can be as effective as CT. It was also observed that better PFS could be achieved with the subsequent everolimus-based treatments after first-line CDKi compared to monotherapy ET.
Objective: To evaluate clinical and demographic characteristics and the results of cytotoxic treatments of KRASG12C, KRASother, and next-generation sequencing (NGS) panel negative patients. Methods: NGS data of 1264 patients with non-small cell lung cancer were retrospectively evaluated. Among these patients, the mutation distributions of 1081 patients with metastatic lung adenocarcinoma were analyzed. A total of 150 patients with negative NGS panel or mutant KRAS followed up in our clinic were included. Clinical features, overall survival, first-line chemotherapy responses, and progression-free survival of NGS panel negative, KRASG12C, and KRASother groups were compared. Results: In 1081 patients who underwent NGS from tumor tissue with the diagnosis of metastatic lung adenocarcinoma, 296 (27%) NGS panel negative and 276 (26%) KRAS mutant patients were detected. Among these patients, 150 patients whose data were available were 71 (47.3%) NGS panel negative, 54 (36%) KRASother, and 25 (16.7%) KRASG12C. Clinical features, brain metastasis, and first-line chemotherapy response were similar among groups. Bone metastases were detected more often in the NGS panel negative group ( p = 0.03). The median follow-up was 8.4 months. Overall, 107 deaths had occurred at the time of analysis. There was no difference in overall survival ( p = 0.56) or progression-free survival ( p = 0.71) among NGS panel negative, KRASother, and KRASG12C patients. Conclusion: There is no difference in overall survival, first-line chemotherapy response, or progression-free survival among patients with NGS panel negative, KRASG12C, or KRASother metastatic lung adenocarcinoma. Bone metastases were observed more frequently in the NGS panel negative group.
Introduction: The case of a patient who developed recurrent delayed immune-related pneumonitis (checkpoint inhibitor pneumonitis [CIP]) after immune checkpoint inhibitor (ICI) therapy for advanced osteosarcoma treatment is presented. Case summary: A 25-year-old female patient with metastatic osteosarcoma was treated with atezolizumab. Grade 2 pneumonitis developed three times in the first two years. Treatment was discontinued after recovery from the last episode of pneumonitis, which was complicated with secondary spontaneous pneumothorax. 2 years after discontinuation of immunotherapy, the patient again developed CIP. Pneumonitis symptoms were regressed with oral steroid therapy during follow-up and a stable disease response continued. Conclusion: Immunotherapy can cause recurrent CIP at any time during the treatment period or after discontinuation of treatment.
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