PMC7425249_01
Computed tomography scan assessments of targeted lesions in different time points before immunotherapy. Coronal unenhanced images of the thorax. a-d images at the level of the largest mass, e-f posteriorly at the level where the residual pleural thickening can be best appreciated.(a) Small pleural-based nodules in the left hemithorax, suggestive of recurrent disease after metastasectomy (0 months after recurrence); (b) 3 months after recurrence, increasing size of pleural-based nodules; (c) 7 months after recurrence, the nodules gradually coalesce, causing diffuse pleural thickening, and new loculated pleural effusions; (d) 14 months after recurrence, pleural thickening increases further taking up almost the entire left hemithorax; (e) 4 months after the initiation of nivolumab, pleural thickening has significantly decreased on the first follow-up after immunotherapy; (f) 6 months after the initiation of nivolumab, pleural thickening further decreases on the next two follow-up examinations; (g) 11 months after the initiation of nivolumab, pleural thickening further decreases on the next two follow-up examinations; (h) 31 months after the initiation of nivolumab, stable appearance of mild residual pleural thickening on follow-up examinations, likely representing post-treatment fibrosis.
10.1177_1758835920946152-fig1.jpg
PMC7425249_01_10.1177_1758835920946152-fig1.jpg
fig1-1758835920946152
CT, despite treatment, 4 months after recurrence (September 2014). Contrast enhanced CT images as well as changes in tumor burden from different follow-up time points are presented in Figures 1 and 2(a) and (b), respectively.
Changes in tumor burden (a) before and (b) after treatment with nivolumab. The maximum dimension of the largest mass was measured before initiation of nivolumab. At the time of initiation of nivolumab there was homogeneous pleural thickening taking up almost the entire left hemithorax and therefore maximum pleural thickness was measured after initiation of nivolumab. Genomic locations of detected mutations in (c) MLH1 and (d) TP53 genes. Single nucleotide mutation c.1609C>T of MLH1 gene is located in exon 14 leading to stop codon. The missense mutation c.523C>T is located in exon 4 of TP53 gene. MLH1 mutation was detected in the primary renal tumor and TP53 mutation was detected in the metastatic lung lesion.. EPM2AIP1; EPM2A Interacting Protein 1, MLH1; DNA mismatch repair protein Mlh1, TP53; Tumor Protein P53, SAT2; Spermidine/Spermine N1-Acetyltransferase Family Member 2, NAA38; N(Alpha)-Acetyltransferase 38, NatC Auxiliary Subunit.
10.1177_1758835920946152-fig2.jpg
PMC7425249_01_10.1177_1758835920946152-fig2.jpg
fig2-1758835920946152
CT, despite treatment, 4 months after recurrence (September 2014). Contrast enhanced CT images as well as changes in tumor burden from different follow-up time points are presented in Figures 1 and 2(a) and (b), respectively.