Background The prevalence of acute lower gastrointestinal bleeding has been increased including colonic diverticulitis and angioplasty. However, appendiceal bleeding is extremely rare. Case presentation We present a case of lower gastrointestinal bleeding from the appendix in an elderly male who presented with melena. Appendiceal bleeding was diagnosed using lower gastrointestinal endoscopy, and laparoscopic appendectomy was performed. The patient did not have melena postoperatively, and was discharged 6 days after the surgery. Conclusion It is important to distinguish appendiceal bleeding from lower gastrointestinal bleeding and to treat it as soon as possible with less invasiveness.
The results of the present study suggested that pretreatment screening with total colonoscopy is meaningful for patients with esophageal cancer, because the frequency of synchronous colorectal cancer was not negligible. Particularly, in patients >70 years and with history of heavy smoking, pretreatment colonoscopy might be necessary.
Trastuzumab in combination with cisplatin and capecitabine could be a new standard treatment for patients with HER2-positive advanced gastric cancer. We herein report a case of advanced gastric cancer with peritoneal dissemination that was successfully treated with trastuzumab combined with cisplatin and capecitabine followed by gastrectomy. A 49-year-old man complained of epigastric pain and was diagnosed with advanced gastric cancer. A staging laparoscopy revealed peritoneal dissemination that was overexpressing HER2 protein. After five courses of chemotherapy comprising trastuzumab, cisplatin and capecitabine, laparoscopic restaging was performed. The disseminated nodules had disappeared, and biopsy of the scar of peritoneal seeding and cytology of the peritoneal lavage fluid both found no malignant cells. Therefore, total gastrectomy with D2 lymph node dissection was performed. Pathologically, there were no residual tumor cells in the resected stomach or peritoneal wall. Trastuzumab in combination with chemotherapy may have curative potential for peritoneal dissemination from HER2positive gastric cancer.
The solubilities of palladium(II) -diketonates (PdL 2 , L = acetylacetonate (acac), trifluoroacetylacetonate (tfa), and thenoyltrifluoroacetonate (tta)) in supercritical carbon dioxide (SC-CO 2 ) from 318 -338 K and 8 -25 MPa were investigated by UV-vis spectrophotometer equipped with a high-pressure optical cell. The molar absorptivities for Pd(acac) 2 , Pd(tfa) 2 , and Pd(tta) 2 in SC-CO 2 were estimated as 1.14 10 4 M -1 cm -1 at 324 nm, 8.16 10 3 M -1 cm -1 at 336.5 nm, and 2.70 10 4 M -1 cm -1 at 322.5 nm, respectively. Solubilities in SC-CO 2 increase in order of Pd(tta) 2 < Pd(acac) 2 < Pd(tfa) 2 , i.e., 6.5 10 -6 < 5.2 10 -5 < 1.3 10 -4 M at 318 K and 11.5 MPa. The experimental solubilities were correlated using the equation proposed by Chrastil and the thermodynamic parameters for each PdL 2 were estimated.
A 62-year-old male was admitted because of lower left abdominal pain and diarrhea. The patient was diagnosed with rectal cancer and multiple liver metastases. First, the laparoscopic Hartmann operation with a D3 lymph node dissection was performed. After five cycles of folinic acid, 5-fluorouracil and oxaliplatin (FOLFOX) and bevacizumab, and one additional FOLFOX, the tumor markers dramatically decreased; with carcinoembryonic antigen levels ranging from 1096.3 to 7.6 ng/ml and carbohydrate antigen 19–9 levels ranging from 3248.0 to 42.1 U/ml. Computed tomography showed a bilateral 14 colorectal liver metastases which indicated stable disease by the Response Evaluation Criteria In Solid Tumors (RECIST) criteria and optimal morphologic response. A two-stage hepatectomy was performed to complete a curative resection because of the insufficient remnant liver volume. Five partial hepatic resections in the left liver and the right portal vein ligation were performed during the first operation. Thirty-four days later, a right hepatectomy was successfully performed. Pathologically, there was tumor necrosis in 90 percent of the area of the metastasized liver, and viable cells were detected in only a marginal part of the liver. The patient had an uneventful postoperative course and was discharged fifteen days after the second operation. Uracil-tegafur plus leucovorin was administered for 6 months as an adjuvant chemotherapy treatment. The patient is currently alive and has remained disease-free for more than 5 years. In conclusion, an ideal combination of perioperative chemotherapy and curative resection may provide a chance of long-term survival without recurrence of disease for selected patients with more than ten bilateral colorectal liver metastases.
Purpose: Gastric cancer (GC) is an aggressive cancer metastasizing with a high propensity for peritoneal dissemination and liver metastasis. Some studies have been shown that not only cancer cells but also their surrounding stroma, especially cancer-associated fibroblasts (CAFs) play an important role in tumor development. Previously, we reported that CXCL12-CXCR4 and integrin β1 signal activation by CAFs co-operates for promoting FAK phosphorylation and enhances the invasiveness of GC cells in extracellular matrix (ECM).On the other hand, a previous study presented that CXCR4 and integrin signaling co-operates in mediating adhesion and chemoresistance in small cell lung cancer cells. Therefore, we hypothesized that CXCL12-CXCR4 and integrin signal activation by CAFs enhances the chemoresistance in GC as well. The aim of current study is to elucidate the significance of CAFs mediating signal activation for chemoresistance in GCs. Experimental Design: We first performed chemo-sensitive assays using GC cells cultured with fresh medium or with CAF-conditioned-medium (CM), and these experiments were conducted on non-coated and Matrigel-coated plates. Next, we examined the CXCL12-CXCR4 and integrin related signaling by western blotting analysis. Furthermore, we investigated the critical molecule for chemoresistance using silencing CXCR4 or integrin β1 in GC cells. Results: Chemo-sensitive assays revealed that GC cells cultured with CAF-CM showed more resistant to cisplatin and reactive oxygen spices (ROS) than those cultured with fresh medium. Moreover, GC cells with CAF-CM on Matrigel-coated plates exhibited remarkable resistance in these assays. On the other hand, western blotting analysis showed that Akt activity in GC cells cultured with CAF-CM was up-regulated in concurrence with FAK phosphorylation. Finally, the chemoresitance induced by CAFs was significantly suppressed by CXCR4 or integrin β1 silencing. Conclusions: These results suggest that CXCL12/CXCR4 and integrinβ1 signal activation by CAFs promoted the chemoresistance through enhancing their interaction with ECM in GC. This mechanism underlying the chemoresistance may provide a novel therapeutic target in advanced GCs. Citation Format: Yuka Tamaoki, Takatsugu Ishimoto, Keisuke Miyake, Daisuke Izumi, Daisuke Kuroda, Tsugio Eto, Kota Arima, Hironobu Shigaki, Junji Kurashige, Masaaki Iwatsuki, Yoshifumi Baba, Yasuo Sakamoto, Naoya Yoshida, Hideo Baba. CXCL12/CXCR4 and integrin signal activation by cancer-associated fibroblasts enhances the chemoresistance in gastric cancer. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 5113.
Background: Gastric cancer (GC) is one of the most general causes of cancer related death, especially in East Asia and is divided into intestinal type and diffuse type by Lauren classification. Five-year survival rate of diffuse-type gastric cancer (DGC) is poor compared with the Intestinal-type gastric cancer (IGC). To improve the prognosis of advanced GC patients, molecularly targeted drugs against gastric cancer have been developed including trastuzumab, a recombinant monoclonal antibody against HER2. But, HER2 gene amplification rate is about 10% in DGC, though 30% in IGC. DGC-specific molecular carcinogenic mechanisms have still remained unclear. Recently, some studies revealed RHOA mutations occur specifically in DGCs. They also demonstrated that proliferation and organoid formation are related with RHOA mutations in DGC. However, there is no report in terms of the functional difference among RHOA mutational hotspots in DGCs. Aim: To investigate the functional difference among RHOA mutations and the impact on prognosis in DGCs. Method: We prepared RHOA wild type vector and three RHOA mutation vectors (G17E, Y42C, and L57V). We introduced these RHOA vectors into DGC cell lines and examined invasion assay. In invasion assay of RHOA introduced DGC cell lines, we conducted experiments with or without TGFβ1 (RHOA activator). Result: RHOA overexpression in DGC cells did not exhibit significant upregulation of invasiveness compared with empty vector introduced DGC cells. However, all RHOA mutation introduced DGC cells acquired more significant elevation of invasiveness as well as wild type after treatment with TGF-β1. (wild:p = 0.0001, G17E:p = 0.0001, Y42C:p = 0.0001, L57V: p<0.0001). Among these RHOA mutations, G17E and Y42C RHOA mutation introduced DGC cells exhibited remarkable upregulation of invasiveness compared with wild type RHOA introduced DGCs (G17E:p<0.0001 Y42C:p = 0.009).These results indicate particular RHOA mutations cause higher response to TGF-β1 compared with wild type. Conclusion: We evaluated the functional difference among RHOA mutations in DGC. These results suggest particular RHOA mutation might have possibility to cause invasion in DGCs. A large cohort study across RHOA mutations in DGCs will be required to identify the clinical significance between hotspot RHOA mutations. Citation Format: Tsugio Eto, Takatsugu Ishimoto, Daisuke Izumi, Yuka Tamaoki, Daisuke Kuroda, Kota Arima, Takayoshi kaida, Mayuko Ohuchi, Kenichi Nakamura, Ryuma Tokunaga, Hironobu Shigaki, Junji Kurashige, Masaaki Iwatsuki, Yoshifumi Baba, Yasuo Sakamoto, Naoya Yoshida, Hideo Baba. The impact of RHOA mutation related with invasion in diffuse-type gastric cancer. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 5074.
Background: Gastrointestinal stromal tumor (GIST) is, though it is as rare as its incidence is about 7 to 20 cases per million population per year, one of the most common non-epithelial malignant tumors of the gastrointestinal tract. Recently it was reported that Fluorine-18 fluorodeoxyglucose (18F-FDG) positron emission tomography-computed tomography (PET/CT) is useful in diagnosis and evaluation of malignant grade of GIST. At the same time, expression of glucose transporter 1 (GLUT1), which is a membranous protein facilitates the transport of glucose across the plasma membranes into cells, was reported to be correlated with maximum standardized uptake value (SUVmax) in PET/CT and malignant grade of various kinds of cancers. In this study, the correlation of GLUT1 expression with malignant grade in GIST was investigated. Methods: We evaluated the protein expression of GLUT1 in immunohistochemistry in the surgically resected specimens in 67 GIST cases, and analyzed the correlation of the other clinicopathological factors. Results: The number of cases in which the expression of GLUT1 judged to be confirmed in immunohistochemistry was 45 (73.7%). GLUT1 expression group had significantly higher preoperative SUVmax in PET/CT than GLUT1 non-expression group (p = 0.03), had larger tumors in diameter (p = 0.015), and was more malignant by Fletcher classification (p<0.01). Additionally, tumor rupture rate tended to be higher in GLUT1 expression group, though there is no tendency of the correlation with tumor necrosis. Eventually, relapse free survival, as not significantly, tend to be shorter in GLUT1 expression group. Conclusion: In our study, expression of GLUT1 is correlated with malignant grade in GIST. GLUT1 expression might be a phase of higher metabolic and malignant activity of GIST cells. GLUT1 might be a useful prognostic marker in GIST cases. Citation Format: Daisuke Kuroda, Junji Kurashige, Masaaki Iwatsuki, Tsugio Eto, Yuka Tamaoki, Mayuko Ohuchi, Kenichi Nakamura, Ryuma Tokunaga, Hironobu Shigaki, Hiromitsu Hayashi, Takatsugu Ishimoto, Yoshifumi Baba, Yasuo Sakamoto, Naoya Yoshida, Hideo Baba. The clinical significance of GLUT1 expression in gastrointestinal stromal tumor. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 38.
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