Kinesin family member C1 (KIFC1), a minus end-directed motor protein, is reported to play an essential role in cancer. This study aimed to analyze KIFC1 expression and examine KIFC1 involvement in cisplatin resistance in bladder cancer (BC). Immunohistochemistry showed that 37 of 78 (47.4%) BC cases were positive for KIFC1. KIFC1-positive cases were associated with high T stage and lymph node metastasis. Kaplan-Meier analysis showed that KIFC1-positive cases were associated with poor prognosis, consistent with the results from public databases. Molecular classification in several public databases indicated that KIFC1 expression was increased in basal type BC. Immunohistochemistry showed that KIFC1-positive cases were associated with basal markers 34βE12, CK5 and CD44. KIFC1 expression was increased in altered TP53 compared to that in wild-type TP53. Immunohistochemistry showed that KIFC1-positive cases were associated with p53-positive cases. P53 knockout by CRISPR-Cas9 induced KIFC1 expression in BC cell lines. Knockdown of KIFC1 by siRNA increased the sensitivity to cisplatin in BC cells. Kaplan-Meier analysis indicated that prognosis was poor among KIFC1-positive BC patients treated with cisplatin-based chemotherapy. Immunohistochemistry showed that KIFC1-positive cases were associated with PD-L1-positive cases. High KIFC1 expression was associated with a favorable prognosis in patients treated with atezolizumab from the IMvigor 210 study. These results suggest that KIFC1 might be a promising biomarker and therapeutic target in BC.

Objectives: Previous studies have reported that cases with clinical T1 renal cell cancer upstaging to pathological T3 are a risk factor to predicting postoperative recurrence after partial nephrectomy. The aim of our study was to investigate the impact of the radiological morphology of the enhanced CT scan of clinical T1 renal cell cancer on predicting upstaging to pathological T3.Methods: Three hundred sixty-seven cases with clinical T1 renal cell cancer diagnosed from enhanced CT scans were enrolled in this study. Based on the findings from the enhanced CT scan, the cases were classified into ‘round’, the margins of which were smooth and round; ‘lobular’, one or more findings of smooth dent and no spiky dent were identified on the margin of the tumor; and ‘irregular’, one or more spiky dent were identified on the margin of the tumor. The association of postoperative upstaging with these radiological morphology and other clinical characteristics of each case was analyzed.Results: Eighteen cases (4.9%) pathologically upstaged to T3a. Two round case (0.7%), 3 lobular cases (10.0%) and 13 irregular cases (22.0%) pathologically upstaged (P < 0.001, round + lobular versus irregular). Four of 17 cases (23.5%) with hilar tumors pathologically upstaged, while 14 of 350 cases (4%) with tumors pathologically upstaged in other sites (P < 0.001). Multivariate analysis revealed that irregular case was an independent factor in predicting upstaging to pathological T3a (P < 0.001).Conclusions: Evaluation of the radiological morphology of clinical T1 renal cell cancer based on enhanced CT scans is useful for predicting pathological upstaging.

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Mycoplasma hominis, Ureaplasma parvum, and Ureaplasma urealyticum are commensal bacteria that are associated with colonization and infection of the urogenital tract. However, colonization of the respiratory tract by these microorganisms in adults has not been fully investigated. Urine and respiratory tract samples (sputum, tracheal aspirates, and bronchoalveolar lavage) of patients aged 20-80 years were analyzed to detect the presence of M. hominis, U. parvum, and U. urealyticum using a conventional PCR method. The samples were submitted to the microbiological clinical laboratory of Hiroshima University Hospital from December 1, 2021 to May 31, 2022. In total, 334 urine and 238 respiratory tract samples were analyzed. The overall detection rates of M. hominis, U. parvum, and U. urealyticum were 2.9%, 1.7%, and 2.3% in male urine; 7.0%, 13.8%, and 1.9% in female urine; 2.2%, 0%, and 2.2% in male respiratory tract; and 0%, 2.0%, and 0% in female respiratory tract, respectively. In urine samples, the detection rates of M. hominis, U. parvum, and U. urealyticum were significantly higher (p < 0.001) for women (29/159; 18.2%) than for men (10/175; 5.7%); however, in respiratory tract samples, the detection rates were not significantly different (p = 0.70) between women (2/101; 2.0%) and men (5/137; 3.7%). Further, both the urine and respiratory samples of 83 patients were analyzed. Three male samples were positive for M. hominis or U. urealyticum, and M. hominis and U. urealyticum were matched in both the urine and respiratory tract samples: M. hominis (n = 1), U. urealyticum (n = 1), M. hominis + U. urealyticum (n = 1). M. hominis, U. parvum, and U. urealyticum were detected in the respiratory tract of not only the young patients, but also of patients aged 50-60 years. Further studies are required to understand the relationship of these microorganisms in urogenital and respiratory tract samples with extra-genital infections.

Tumor growth and metastasis are determined not by cancer cells alone but also by a variety of stromal cells, various populations of which overexpress platelet‐derived growth factor receptors (PDGF‐Rs). In addition, activation of PI3K‐AKT‐mammalian target of rapamycin (mTOR) signaling is frequently observed in many cancer types as well. mTOR comprises a serine/threonine kinase that increases the production of proteins that stimulate key cellular processes such as cell growth and proliferation, cell metabolism, and angiogenesis. In this study, we investigated the impact of molecular‐targeting agents including PDGF‐R and mTOR inhibitors on the tumor stroma of human kidney cancer and examined the efficacy of combination therapy with these agents against this disease. Treatment with sunitinib did not suppress tumor growth, but significantly decreased stromal reactivity, microvessel density, and pericyte coverage of tumor microvessels in an orthotopic mouse model. In contrast, treatment with everolimus decreased tumor growth and microvessel density but not stromal reactivity. However, sunitinib and everolimus in combination reduced both the growth rate and stromal reaction. These findings suggest that target molecule‐based inhibition of the cancer–stromal cell interaction appears promising as an effective antitumor therapy.