Kyushu University Academic Staff Educational and Research Activities Database
List of Papers
Yoneshima Yasuto Last modified date:2024.04.09

Lecturer / Kyushu University Hospital


Papers
1. Okamura Koji, Inoue Hiroyuki, Tanaka Kentaro Ikematsu Yuki, Furukawa Rie Ota Keiichi, Yoneshima Yasuto, Iwama Eiji, Okamoto Isamu, Immunostimulatory oncolytic activity of coxsackievirus A11 in human malignant pleural mesothelioma, CANCER SCIENCE, 10.1111/cas.15645, 114, 3, 1095-1107, 2023.03.
2. Ritsu Ibusuki, Yasuto Yoneshima, Mikiko Hashisako, Norikazu Matsuo, Taishi Harada, Yuko Tsuchiya-Kawano, Junji Kishimoto, Keiichi Ota, Yoshimasa Shiraishi, Eiji Iwama, Kentaro Tanaka, Yoshinao Oda, Isamu Okamoto , Association of thyroid transcription factor-1 (TTF-1) expression with efficacy of PD-1/PD-L1 inhibitors plus pemetrexed and platinum chemotherapy in advanced non-squamous non-small cell lung cancer, TRANSLATIONAL LUNG CANCER RESEARCH, 10.21037/tlcr-22-393, 2022.09.
3. Kazuki Takada 1, Mototsugu Shimokawa 2 3, Shinkichi Takamori 4, Shinichiro Shimamatsu 5, Fumihiko Hirai 5, Tetsuzo Tagawa 6, Tatsuro Okamoto 7, Motoharu Hamatake 5, Yuko Tsuchiya-Kawano 8, Kohei Otsubo 8, Koji Inoue 8, Yasuto Yoneshima 9, Kentaro Tanaka 9, Isamu Okamoto 9, Yoichi Nakanishi 8, Masaki Mori 6, A propensity score-matched analysis of the impact of statin therapy on the outcomes of patients with non-small-cell lung cancer receiving anti-PD-1 monotherapy: a multicenter retrospective study, BMC Cancer, 10.1186/s12885-022-09385-8., 22, 1, 503, 2022.06.
4. Yasuto Yoneshima, Satoshi Morita, Masahiko Ando, Atsushi Nakamura, Shunichiro Iwasawa, Hiroshige Yoshioka, Yasuhiro Goto, Masafumi Takeshita, Toshiyuki Harada, Katsuya Hirano, Tetsuya Oguri, Masashi Kondo, Satoru Miura, Yukio Hosomi, Terufumi Kato, Toshio Kubo, Junji Kishimoto, Nobuyuki Yamamoto, Yoichi Nakanishi, Isamu Okamoto, Nab-Paclitaxel for Previously Treated Advanced Non-Small Cell Lung Cancer: Analysis of Safety and Efficacy for Patients With Renal Impairment, CLINICAL LUNG CANCER, 10.1016/j.cllc.2022.08.011, 23, 7, 585-592, 2022.11.
5. Hirotsugu Kenmotsu, Kazushige Wakuda, Keita Mori, Terufumi Kato, Shunichi Sugawara, Keisuke Kirita, Yasuto Yoneshima, Koichi Azuma, Kazumi Nishino, Shunsuke Teraoka, Takehito Shukuya, Ken Masuda, Hidetoshi Hayashi, Ryo Toyozawa, Satoru Miura, Daichi Fujimoto, Kazuhiko Nakagawa, Nobuyuki Yamamoto, Toshiaki Takahashi , Randomized phase II study of osimertinib plus bevacizumab versus osimertinib for untreated patients with non-squamous non-small cell lung cancer harboring EGFR mutations; WJOG9717L study, Journal of Thoracic Oncology, 10.1016/j.jtho.2022.05.006., 2022.05.
6. Yasuto Yoneshima, Satoshi Morita, Masahiko Ando, Atsushi Nakamura, Shunichiro Iwasawa, Hiroshige Yoshioka, Yasuhiro Goto, Masafumi Takeshita, Toshiyuki Harada, Katsuya Hirano, Tetsuya Oguri, Masashi Kondo, Satoru Miura, Yukio Hosomi, Terufumi Kato, Toshio Kubo, Junji Kishimoto, Nobuyuki Yamamoto, Yoichi Nakanishi, Isamu Okamoto, Phase 3 Trial Comparing Nanoparticle Albumin-Bound Paclitaxel With Docetaxel for Previously Treated Advanced NSCLC, Journal of Thoracic Oncology, 10.1016/j.jtho.2021.03.027., 16, 9, 1523-1532, 2021.09, 初回化学療法が終了し再発した進行非小細胞肺癌症例を対象として、標準治療であるドセタキセル単剤治療に対するnab-パクリタキセルの有効性・安全性を検証するランダム化比較第3相試験(J-AXEL試験)を立案し、本試験をわが国における主要な7つの臨床試験グループの協同したインターグループ試験として全国の施設にて実施した。2015年5月から2018年3月に既治療進行再発非小細胞肺癌患者503名がドセタキセル群とnab-パクリタキセル群に1:1に無作為化割り付けされ、主要評価項目である全生存期間においてnab-パクリタキセル治療群はドセタキセル治療群に対して非劣性が証明され、無増悪生存期間、奏効率においてはnab-パクリタキセル治療群はドセタキセル治療群と比べ有意に優れた結果を示した。さらにドセタキセル治療にて懸念される発熱性好中球減少の割合が22%であったのに対してnab-パクリタキセル治療群では2%と高い安全性も示された。.
7. Kazuki Takada, Mototsugu Shimokawa, Shinkichi Takamori, Shinichiro Shimamatsu, Fumihiko Hirai, Tetsuzo Tagawa, Tatsuro Okamoto, Motoharu Hamatake, Yuko Tsuchiya-Kawano, Kohei Otsubo, Koji Inoue, Yasuto Yoneshima, Kentaro Tanaka, Isamu Okamoto, Yoichi Nakanishi, Masaki Mori, Clinical impact of probiotics on the efficacy of anti-PD-1 monotherapy in patients with nonsmall cell lung cancer: A multicenter retrospective survival analysis study with inverse probability of treatment weighting, International Journal of Cancer, 10.1002/ijc.33557., 149, 2, 473-482, 2021.07.
8. Kazuki Takada, Mototsugu Shimokawa, Shinkichi Takamori, Shinichiro Shimamatsu, Fumihiko Hirai, Tetsuzo Tagawa, Tatsuro Okamoto, Motoharu Hamatake, Yuko Tsuchiya-Kawano, Kohei Otsubo, Koji Inoue, Yasuto Yoneshima, Kentaro Tanaka, Isamu Okamoto, Yoichi Nakanishi, Masaki Mori, A propensity score-matched analysis of the impact of statin therapy on the outcomes of patients with non-small-cell lung cancer receiving anti-PD-1 monotherapy: a multicenter retrospective study, BMC Cancer, 10.1186/s12885-022-09385-8., 22, 1, 503, 2022.06.
9. Yasuto Yoneshima, Eiji Iwama, Shingo Matsumoto, Taichi Matsubara, Testuzo Tagawa, Keiichi Ota, Kentaro Tanaka, Mitsuhiro Takenoyama, Tatsuro Okamoto, Koichi Goto, Masaki Mori, Isamu Okamoto, Paired analysis of tumor mutation burden for lung adenocarcinoma and associated idiopathic pulmonary fibrosis, Scientific Reports, 10.1038/s41598-021-92098-y., 11, 1, 12732, 2021.06.
10. Renpeng Liu, Keiichi Ota, Eiji Iwama, Yasuto Yoneshima, Kentaro Tanaka, Hiroyuki Inoue, Tetsuzo Tagawa, Yoshinao Oda, Masaki Mori, Yoichi Nakanishi, Isamu Okamoto , Quantification of HER family dimers by proximity ligation assay and its clinical evaluation in non-small cell lung cancer patients treated with osimertinibRenpeng Liu 1, Keiichi Ota 2, Eiji Iwama 1, Yasuto Yoneshima 1, Kentaro Tanaka 1, Hiroyuki Inoue 3, Tetsuzo Tagawa 4, Yoshinao Oda 5, Masaki Mori 4, Yoichi Nakanishi 6, Isamu Okamoto , Lung Cancer, 10.1016/j.lungcan.2021.05.023., 158, 156-161, 2022.06.
11. Rie Furukawa, Hiroyuki Inoue, Yasuto Yoneshima, Hirono Tsutsumi, Eiji Iwama, Yuki Ikematsu, Nobuhisa Ando, Yoshimasa Shiraishi, Keiichi Ota, Kentaro Tanaka, Yoichi Nakanishi, Isamu Okamoto 1, Cytotoxic chemotherapeutic agents and the EGFR-TKI osimertinib induce calreticulin exposure in non-small cell lung cancer, Lung Cancer, 10.1016/j.lungcan.2021.03.018., 155, 144-150, 2021.05.
12. Shinkichi Takamori, Kazuki Takada, Mototsugu Shimokawa, Mikako Jinnnouchi, Taichi Matsubara, Naoki Haratake, Naoko Miura, Ryo Toyozawa, Masafumi Yamaguchi, Mitsuhiro Takenoyama, Yasuto Yoneshima, Kentaro Tanaka, Isamu Okamoto, Tetsuzo Tagawa, Masaki Mori, Prognostic impact of primary cancer adjoining emphysematous bullae in non-small cell lung cancer patients treated with immune checkpoint inhibitors, Cancer Immunology, Immunotherapy, 10.1007/s00262-020-02783-6., 70, 6, 1745-1753, 2021.06.
13. Hiroyuki Inoue, Hirono Tsutsumi, Kentaro Tanaka, Eiji Iwama, Yoshimasa Shiraishi, Aiko Hirayama, Takayuki Nakanishi, Hiroyuki Ando, Maako Nakajima, Seiji Shinozaki, Hiroaki Ogata, Kazuyasu Uryu, Koji Okamura, Shinichi Kimura, Tomohiro Ogawa, Keiichi Ota, Yasuto Yoneshima, Naoki Hamada, Yoichi Nakanishi, Isamu Okamoto, Increased plasma levels of damage-associated molecular patterns during systemic anticancer therapy in patients with advanced lung cancer, TRANSLATIONAL LUNG CANCER RESEARCH, 10.21037/tlcr-21-92, 10, 6, 2475-2486, 2021.06.
14. Yasuto Yoneshima, Koji Kato, Haruna Minami, Munehiko Ikeda, Hiroyuki Watanabe, Goichi Yoshimoto, Toshihiro Miyamoto, Koichi Akashi, Yoichi Nakanishi, Isamu Okamoto, HTLV-1 seropositive patients with lung cancer treated with PD-1 inhibitors, Cancer Sci., 10.1111/cas.14536., 2020 Sep;111(9):3395-3396. , 2021.06.
15. Shinkichi Takamori, Kazuki Takada, Mototsugu Shimokawa, Taichi Matsubara, Takatoshi Fujishita, Kensaku Ito, Ryo Toyozawa, Masafumi Yamaguchi, Tatsuro Okamoto, Yasuto Yoneshima, Kentaro Tanaka, Isamu Okamoto, Tetsuzo Tagawa, Masaki Mori, Clinical utility of pretreatment Glasgow prognostic score in non-small-cell lung cancer patients treated with immune checkpoint inhibitors, Lung Cancer, 10.1016/j.lungcan.2020.11.026., 152, 27-33, 2021.02.
16. Yuichiro Koga, Daisuke Tsuchimoto, Yoshinori Hayashi, Nona Abolhassani, Yasuto Yoneshima, Kunihiko Sakumi, Hiroshi Nakanishi, Shinya Toyokuni, Yusaku Nakabeppu, Neural stem cell-specific ITPA deficiency causes neural depolarization and epilepsy, JCI Insight., 10.1172/jci.insight.140229., 2020 Nov 19;5(22):e140229., 2020.11.
17. Hirono Tsutsumi, Yasuto Yoneshima, Keiichi Ota, Kohei Otsubo, Eiji Iwama, Hiroyuki Inoue, Kentaro Tanaka, Yoichi Nakanishi, Isamu Okamoto, Multiclonality and Radiosensitivity of Granulocyte-colony Stimulating Factor-Producing Lung Adenocarcinoma Positive for an Activating EGFR Mutation, Clinical Lung Cancer, 10.1016/j.cllc.2019.09.001, 21, 1, e21-e24, 2020.01.
18. Yasuto Yoneshima, Kentaro Tanaka, Yoshimasa Shiraishi, Kojiro Hata, Hiroyuki Watanabe, Taishi Harada, Kohei Otsubo, Eiji Iwama, Hiroyuki Inoue, Satohiro Masuda, Yoichi Nakanishi, Isamu Okamoto, Safety and efficacy of PD-1 inhibitors in non–small cell lung cancer patients positive for antinuclear antibodies, Lung Cancer, 10.1016/j.lungcan.2019.01.014, 130, 5-9, 2019.04, Objectives: To examine the possible effects of antinuclear antibodies (ANA) on the safety and efficacy of programmed cell death–1 (PD-1) inhibitors in patients with advanced non–small cell lung cancer (NSCLC). Patients and methods: Clinical data including ANA status were reviewed retrospectively for patients with advanced NSCLC who received monotherapy with a PD-1 inhibitor. Results: Of the 83 patients analyzed, 18 (21.7%) were positive for ANA. The incidence of immune-related adverse events (irAEs) did not differ significantly between patients with ANA (6/18, 33.3%) and those negative for ANA (21/65, 32.3%), although it tended to increase as the ANA titer increased. Progression-free survival (2.9 versus 3.8 months, p = 0.03) and overall survival (11.6 versus 15.8 months, p = 0.03) were significantly shorter in patients positive for ANA than in those without ANA. Conclusion: PD-1 inhibitors can be administered safely in advanced NSCLC patients positive for ANA without obvious exacerbation of autoimmune disease, although patients with a high titer of such antibodies may warrant close monitoring. However, the presence of ANA might be associated with a poor outcome of such treatment..
19. Satoshi Anai, Eiji Iwama, Yasuto Yoneshima, Kohei Otsubo, Kentaro Tanaka, Yoichi Nakanishi, Isamu Okamoto, Association of nephrotoxicity during platinum-etoposide doublet therapy with UGT1A1 polymorphisms in small cell lung cancer patients, Lung Cancer, 10.1016/j.lungcan.2018.11.002, 126, 156-161, 2018.12, Objectives: Etoposide is a key agent in the treatment of small cell lung cancer (SCLC). Uridine diphosphate (UDP)–glucuronosyltransferase 1A1 (UGT1A1) is thought to be largely responsible for the glucuronidation of etoposide as well as that of irinotecan, suggesting that polymorphisms of UGT1A1 might be predictive of etoposide toxicity. We therefore examined the relation between UGT1A1 polymorphisms and toxicity profile during platinum-etoposide doublet therapy in SCLC patients. Materials and Methods: SCLC patients who underwent platinum-etoposide doublet therapy and molecular testing for UGT1A1 genotype were reviewed for the occurrence of adverse events during treatment. Results: A total of 41 SCLC patients received platinum-etoposide doublet therapy and were genotyped for UGT1A1*6 and UGT1A1*28 alleles. These alleles were detected in 15 (36.6%) patients, with the genotypes of *6/– *6/*6, *28/– *28/*28, or *6/*28 being observed in 9 (22.0%), 2 (4.9%), 2 (4.9%), 1 (2.4%), and 1 (2.4%) patients, respectively. The presence of these alleles was significantly associated with an increase in serum creatinine concentration of grade ≥2 (incidence of 66.7% for patients with the alleles versus 11.5% for those without, P
20. Yasuto Yoneshima, Kayo Ijichi, Satoshi Anai, Keiichi Ota, Kohei Otsubo, Eiji Iwama, Kentaro Tanaka, Yoshinao Oda, Yoichi Nakanishi, Isamu Okamoto, PD-L1 expression in lung adenocarcinoma harboring EGFR mutations or ALK rearrangements, Lung Cancer, 10.1016/j.lungcan.2018.01.024, 118, 36-40, 2018.04, Objectives: Expression of programmed cell death–ligand 1 (PD-L1) has been associated with clinical outcome of programmed cell death–1 (PD-1) pathway blockade in non–small cell lung cancer (NSCLC). The PD-L1 IHC 22C3 pharmDx assay, the only companion diagnostic for pembrolizumab therapy, has revealed that ∼30% of all NSCLCs express PD-L1 at a high level. The frequency of high PD-L1 expression in NSCLCs with known driver oncogenes has remained unclear, however. Materials and methods: We retrospectively evaluated PD-L1 expression with the 22C3 assay in tumor tissue of 80 lung adenocarcinoma patients including 71 with EGFR mutations and 9 with ALK rearrangements, all of whom were treated with corresponding tyrosine kinase inhibitors (TKIs). Results: Of the 80 tumors analyzed, 26 (32.5%) had a PD-L1 tumor proportion score (TPS) of 1%–49% and 9 (11.3%) had a PD-L1 TPS of ≥50%; 35 (43.8%) thus had a PD-L1 TPS of ≥1%. Of the 71 tumors with EGFR mutations, 23 (32.4%) had a PD-L1 TPS of 1%–49% and 7 (9.9%) had a PD-L1 TPS of ≥50%. A PD-L1 TPS of ≥1% was not associated with any clinical characteristic examined. Progression-free survival on initial TKI treatment was significantly poorer for patients with a PD-L1 TPS of ≥1% than for those with a PD-L1 TPS of
21. Takaki Akamine, Kazuki Takada, Gouji Toyokawa, Fumihiko Kinoshita, Taichi Matsubara, Yuka Kozuma, Naoki Haratake, Shinkichi Takamori, Fumihiko Hirai, Tetsuzo Tagawa, Tatsuro Okamoto, Yasuto Yoneshima, Isamu Okamoto, Mototsugu Shimokawa, Yoshinao Oda, Yoichi Nakanishi, Yoshihiko Maehara, Association of preoperative serum CRP with PD-L1 expression in 508 patients with non-small cell lung cancer
A comprehensive analysis of systemic inflammatory markers, Surgical Oncology, 10.1016/j.suronc.2018.01.002, 27, 1, 88-94, 2018.03, Objectives Programmed death-1 (PD-1) and programmed death-ligand 1 (PD-L1) inhibitors have been approved as a standard therapy for metastatic non-small cell lung cancer (NSCLC). Although PD-L1 expression serves as a predictive biomarker for the efficacy of immunotherapy, there are no established biomarkers to predict the expression of PD-L1. The inflammatory markers C-reactive protein (CRP) and neutrophil-lymphocyte ratio (NLR) were recently shown to predict the efficacy of nivolumab for NSCLC patients. Therefore, here we investigated the potential association of PD-L1 expression with systemic inflammatory markers, including CRP, NLR, lymphocyte-monocyte ratio and platelet-lymphocyte ratio. Methods We retrospectively examined tumor PD-L1 expression in 508 surgically resected primary NSCLC cases by immunohistochemical analysis (cut-off value: 1%). The association of PD-L1 expression with preoperative systemic inflammatory markers was assessed by univariate and multivariate analyses. We generated a PD-L1 association score (A-score) from serum CRP level (cut-off value: 0.3 mg/dl) and smoking status to predict PD-L1 expression. Results Among the total 508 patients, 188 (37.0%) patients were positive for PD-L1 expression at the 1% cut-off value and 90 (17.5%) had elevated serum CRP level. Multivariate logistic regression revealed that PD-L1 positivity was significantly associated with advanced stage, the presence of vascular invasion and high serum CRP level (P =.0336,.0106 and 0.0018, respectively). Though not significant, smoking history tended to be associated with PD-L1 protein expression (P =.0717). There was no correlation with other inflammatory markers. Smoking history with elevated CRP level (A-score: 2) was strongly associated with PD-L1 protein expression (odds ratio: 5.18, P <.0001 while it was inversely associated with egfr mutation ratio: p conclusions our results indicate that among all systemic inflammatory markers examined serum crp seems to predict pd-l1 expression in patients nsclc however the clinical applicability is limited given obtained area under receiver operating characteristic curve values.. id="gencho_ronbuns10061294" class="qir_handle_link">
22. Kohei Otsubo, K. Nakatomi, R. Furukawa, K. Ashida, Yasuto Yoneshima, Yoichi Nakanishi, Isamu Okamoto, Two cases of late-onset secondary adrenal insufficiency after discontinuation of nivolumab, Annals of Oncology, 10.1093/annonc/mdx497, 28, 12, 3106-3107, 2017.12.
23. Yuki Ikematsu, Yasuto Yoneshima, Kayo Ijichi, Kentaro Tanaka, Taishi Harada, Yoshinao Oda, Yoichi Nakanishi, Isamu Okamoto, Marked response to pembrolizumab in a patient with pulmonary pleomorphic carcinoma highly positive for PD-L1, Lung Cancer, 10.1016/j.lungcan.2017.07.020, 112, 230-231, 2017.10.
24. Yasuto Yoneshima, Satoshi Morita, Masahiko Ando, Satoru Miura, Hiroshige Yoshioka, Tetsuya Abe, Terufumi Kato, Masashi Kondo, Yukio Hosomi, Katsuyuki Hotta, Nobuyuki Yamamoto, Junji Kishimoto, Yoichi Nakanishi, Isamu Okamoto, Treatment Rationale and Design for J-AXEL
A Randomized Phase 3 Study Comparing Nab-Paclitaxel With Docetaxel in Patients With Previously Treated Advanced Non–Small-Cell Lung Cancer, Clinical Lung Cancer, 10.1016/j.cllc.2016.08.003, 18, 1, 100-103, 2017.01, Background Nanoparticle albumin-bound (nab) paclitaxel is a promising new therapeutic agent for all histologic types of non–small-cell lung cancer (NSCLC). We recently performed a phase 2 study of weekly nab-paclitaxel in patients with previously treated advanced NSCLC, finding promising activity and acceptable toxicity for this regimen. We have now designed a randomized phase 3 intergroup study (J-AXEL, UMIN000017487) to examine the clinical benefit and safety of nab-paclitaxel compared to docetaxel in patients with previously treated advanced NSCLC. Patients and Methods Patients are randomized to receive either docetaxel (60 mg/m2 on day 1 every 3 weeks, control arm) or nab-paclitaxel (100 mg/m2 on days 1, 8, and 15 every 3 weeks, experimental arm), with each drug being administered until disease progression or unacceptable toxicity. The study will evaluate the noninferiority of nab-paclitaxel relative to docetaxel for the primary end point of overall survival. Conclusion If the primary objective is achieved, this study will provide evidence for a new alternative treatment option for patients with previously treated advanced NSCLC..
25. Yasuto Yoneshima, Nona Abolhassani, Teruaki Iyama, Sakumi Kunihiko, Naoko Shiomi, Masahiko Mori, Tadahiro Shiomi, Tetsuo Noda, Daisuke Tsuchimoto, Yusaku Nakabeppu, Deoxyinosine triphosphate induces MLH1/PMS2- and p53-dependent cell growth arrest and DNA instability in mammalian cells, Scientific reports, 10.1038/srep32849, 6, 2016.09, Deoxyinosine (dI) occurs in DNA either by oxidative deamination of a previously incorporated deoxyadenosine residue or by misincorporation of deoxyinosine triphosphate (dITP) from the nucleotide pool during replication. To exclude dITP from the pool, mammals possess specific hydrolysing enzymes, such as inosine triphosphatase (ITPA). Previous studies have shown that deficiency in ITPA results in cell growth suppression and DNA instability. To explore the mechanisms of these phenotypes, we analysed ITPA-deficient human and mouse cells. We found that both growth suppression and accumulation of single-strand breaks in nuclear DNA of ITPA-deficient cells depended on MLH1/PMS2. The cell growth suppression of ITPA-deficient cells also depended on p53, but not on MPG, ENDOV or MSH2. ITPA deficiency significantly increased the levels of p53 protein and p21 mRNA/protein, a well-known target of p53, in an MLH1-dependent manner. Furthermore, MLH1 may also contribute to cell growth arrest by increasing the basal level of p53 activity..
26. Yasuto Yoneshima, Isamu Okamoto, Tomotsugu Takano, Aimi Enokizu, Eiji Iwama, Taishi Harada, Koichi Takayama, Yoichi Nakanishi, Successful treatment with alectinib after crizotinib-induced esophageal ulceration, Lung Cancer, 10.1016/j.lungcan.2015.03.012, 88, 3, 349-351, 2015.06, Crizotinib was the first clinically available inhibitor of the tyrosine kinase ALK, and next-generation ALK inhibitors, such as alectinib, are now under development. Although crizotinib is generally well tolerated, severe esophageal injury has been reported as a rare but serious adverse event of crizotinib therapy. We now describe the successful treatment with alectinib of a patient who developed crizotinib-induced esophageal ulceration..
27. Yasuto Yoneshima, Isamu Okamoto, Masako Arimura-Omori, Shinichi Kimura, Noriko Hidaka-Fujimoto, Eiji Iwama, Taishi Harada, Koichi Takayama, Yoichi Nakanishi, Infected complex renal cysts during crizotinib therapy in a patient with non-small cell lung cancer positive for ALK rearrangement, Investigational New Drugs, 10.1007/s10637-014-0195-1, 33, 2, 510-512, 2015.04, Crizotinib is the first clinically available tyrosine kinase inhibitor that targets anaplastic lymphoma kinase (ALK) and is associated with the development of complex renal cysts. We now describe a 39-year-old woman who developed infected complex renal cysts during crizotinib treatment. After 10 months of such treatment, she presented with a high fever and low back pain. Computed tomography findings were consistent with complex renal cysts and perilesional inflammation. Interventions including cyst drainage and antibiotic administration contributed to diagnosis and management of the infected cysts..
28. Naoki Kubo, Taishi Harada, Satoshi Anai, Kohei Otsubo, Yasuto Yoneshima, Kayo Ijichi, Takaomi Koga, Koichi Takayama, Yoichi Nakanishi, Carboplatin plus paclitaxel in the successful treatment of advanced inflammatory myofibroblastic tumor, Internal Medicine, 10.2169/internalmedicine.51.7599, 51, 17, 2399-2401, 2012.10, A 26-year-old man with unresectable inflammatory myofibroblastic tumor (IMT) presented with multiple metastases in the thoracic vertebra and lymph nodes as detected by positron emission tomography (PET) received chemotherapy with carboplatin plus paclitaxel. After three cycles of chemotherapy, fluorine-18-fluorodeoxyglucose (FDG)-PET/CT revealed tumor regression and significant reduction of FDG uptake in all lesions. The patient received six cycles of chemotherapy without any severe adverse event, and there was no sign of disease progression for seven months. This regimen is well tolerated and may be considered the treatment of choice for unresectable IMT..
29. Yasuto Yoneshima, Takashi Ichiyama, Hiroshi Ayukawa, Tomoyo Matsubara, Susumu Furukawa, Fosfomycin inhibits NF-κB activation in U-937 and Jurkat cells, International Journal of Antimicrobial Agents, 10.1016/S0924-8579(03)00054-2, 21, 6, 589-592, 2003.06, Fosfomycin exerts anti-inflammatory effects through inhibiting the production of proinflammatory cytokines. Transcription of the genes for these proinflammatory cytokines is regulated by NF-κB. We tested the hypothesis that fosfomycin inhibits the activation of NF-κB induced by tumor necrosis factor-α (TNF-α) in human monocytic U-937 cells, and a T cell line (Jurkat). Western blot analysis demonstrated that fosfomycin inhibits NF-κB activation in both cells. Flow cytometry revealed that fosfomycin suppresses NF-κB activation in both cells in a dose-related manner. These findings are consistent with the idea that fosfomycin suppresses the production of proinflammatory cytokines via inhibition of NF-κB activation..