A 57-year-old woman was admitted with lower abdominal pain and bloody bowel discharge. She was diagnosed with rectal tumor by colonoscopy, and a biopsy was performed. Surgery was performed, resulting in a diagnosis of rectal paraganglioma. Since recurrence was confirmed three years later, reoperation was done, and chemotherapy with cyclophosphamide, vincristine and dacarbazine (CVD) was subsequently carried out for further recurrence. After the administration of up to 15 courses of CVD, we delivered best supportive care due to disease progression. She died a year and a half after starting chemotherapy. We herein report this rare disease with a review of the relevant literature.

PolyADP-ribosylation is a post-translational modification of proteins, and poly(ADP-ribose) (PAR) polymerase (PARP) family proteins synthesize PAR using NAD as a substrate. Poly(ADP-ribose) glycohydrolase (PARG) functions as the main enzyme for the degradation of PAR. In this study, we investigated the effects of Parg deficiency on tumorigenesis and therapeutic efficacy of DNA damaging agents, using mouse ES cell-derived tumor models. To examine the effects of Parg deficiency on tumorigenesis, Parg^+/+ and Parg^−/− ES cells were subcutaneously injected into nude mice. The results showed that Parg deficiency delays early onset of tumorigenesis from ES cells. All the tumors were phenotypically similar to teratocarcinoma and microscopic findings indicated that differentiation spectrum was similar between the Parg genotypes. The augmented anti-tumor therapeutic effects of X-irradiation were observed under Parg deficiency. These results suggest that Parg deficiency suppresses early stages of tumorigenesis and that Parg inhibition, in combination with DNA damaging agents, may efficiently control tumor growth in particular types of germ cell tumors.

Background: Relationships between cancer onset, progression, and inflammation have been reported; yet, the significance of inflammatory markers before and after treatment with nanoliposomal irinotecan and fluorouracil with folic acid (NFF) is unclear. Objectives: We aimed to (1) investigate whether worsening inflammation is associated with disease progression and whether it can be used as a biomarker by comparing inflammatory markers before and after treatment with NFF and (2) verify which is a superior biomarker. Design: This was a preplanned analysis of a retrospective cohort of the NAPOLEON-2 study, a multicenter observational study. Patients from 20 institutions were enrolled. Those with unresectable pancreatic cancer who received NFF as a second-line or later-line treatment between June 1, 2020, and May 31, 2021, were included. Methods: The primary endpoint was overall survival, and the main secondary endpoint was progression-free survival. The following inflammatory markers were assessed: neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio, Prognostic Nutrition Index (PNI), C-reactive protein/albumin ratio (CAR), Glasgow prognostic score (GPS), Prognostic Index (PI), and Komori score. Results: A total of 161 patients were enrolled. The CAR, NLR, GPS (1 vs 2), PI (1 vs 2), PNI, and Komori score were useful pre-NFF biomarkers (hazard ratios (HRs): 2.59, 2.28, 2.76/3.35, 2.16/18.89, 2.13, and 3.39, respectively). The CAR, NLR, GPS (compared with a score of 1/2), and PI (compared with a score of 1/2) were useful post-NFF biomarkers (HRs: 2.63, 1.88, 2.54/3.09, 2.30/5.39, respectively). In terms of the receiver operating characteristic curve and Akaike information criterion, the CAR, GPS, and PI showed favorable trends, and overall, CAR was a useful biomarker. Conclusion: Inflammatory markers can be used as biomarkers both before and after NFF treatment, and CAR may be useful. We hope these findings will contribute to the selection of appropriate treatment options.

Introduction: Fluorouracil, leucovorin, irinotecan, and oxaliplatin (FOLFIRINOX) improve overall survival (OS) and progression-free survival (PFS) in patients with pancreatic cancer, compared with gemcitabine (GEM). However, whether PFS is a surrogate marker of OS in pancreatic cancer chemotherapy focusing on FOLFIRINOX or GEM plus nab-paclitaxel remains unknown. We aimed to verify whether PFS can be a surrogate marker of OS in prognosis prediction. Methods: This was an integrated analysis of the NAPOLEON study and retrospective cohort of the NAPOLEON-2 study – a multicenter observational study conducted in Japan, using real-world data. The primary and secondary endpoints were OS and PFS, respectively. The correlation between OS and PFS in first- and second-line treatments was assessed using Method of Moments estimation. An analysis was performed in patients with confirmed OS at the end of follow-up. The NAPOLEON-2 cohort included only patients who received 5-fluorouracil, leucovorin, and nanoliposomal irinotecan (NFF) as second-line treatment. Results: Among 479 patients, the correlation between PFS and OS from first- and second-line chemotherapies was calculated in 310 and 225 patients, respectively. The R-squared values for the correlation between PFS and OS from first- and second-line chemotherapies were 0.74 and 0.76, respectively. There was no statistically significant difference in first-line treatment between the FOLFIRINOX and GEM plus nab-paclitaxel groups (p = 0.92). Therefore, the FOLFIRINOX group may not have shown a stronger correlation than the NFF group. Conclusion: PFS can be a surrogate marker of OS in first- and second-line therapies. Appropriate prognostic estimation might contribute to proper treatment selection.

Dabigatran is a useful and widely used drug for stroke prevention in patients with atrial fibrillation. However, it has been reported to cause esophagitis. Herein, we report the case of a 77‐year‐old man with dabigatran‐induced esophagitis with blue pigmentation, which is known to be a rare adverse effect. The patient presented to our hospital with a tightness of the chest and anorexia. Computed tomography revealed a thickening of the entire esophageal wall, with an upper esophageal predominance. Esophagogastroduodenoscopy was performed, which showed that the cervical and upper thoracic esophagus had blue pigmentation with edematous changes, partial narrowing, and longitudinal sloping. We replaced dabigatran with edoxaban, a similar anticoagulation medication. The patient was closely monitored for 1 month after switching to edoxaban. The follow‐up esophagogastroduodenoscopy showed marked improvements, revealing resolution of the bluish discoloration and edematous changes, and the patient's complaints regarding the tightness of the chest and anorexia were also resolved. It is important to recognize that such side effects can occur with dabigatran, a drug that is frequently used in daily practice. Considering the fact that strong edematous changes can cause indigo carmine pigmentation associated with dabigatran stagnation, we recommend switching to another anticoagulant if esophagitis occurs during dabigatran administration.