Peritoneal cecal cancer metastasis to a mesh-plug prosthesis : A case report

We report the case of a 77-year-old man who presented to our hospital with cecal cancer, lung metastasis, and liver metastasis in January 2013. After four courses of modified infusional intravenous fluorouracil and levofolinate with oxaliplatin (mFOLFOX 6) + bevacizumab, there was no new metastatic lesion and lung metastasis reduction was observed. Ileocecal resection was performed in May, left lower lung lobectomy in August, and extended right posterior segmentectomy + S8 partial liver resection was performed in December. The tumor marker declined initially ; thereafter, it gradually increased. Computed tomography (CT) performed in April 2014 revealed right inguinal mass around the mesh-plug prosthesis. A positron emission tomography-CT (PET-CT) also revealed a high 2-fluoro-2-deoxy-D-glucose (FDG) uptake at the same site. Right inguinal tumor resection was performed in July. Cancer tissues were confirmed by performing intraoperative rapid pathological diagnosis, and R0 resection could be achieved. Previous studies have reported malignant tumor metastases to the mesh-plug prosthesis, and this was believed to one of the sites that cancer cells can easily engraft. In particular, in patients with a history of advanced malignant tumors, if mass formation around the artifact insertion site is observed, the possibility of peritoneal metastasis should be considered

Combined resection of re-recurrent lateral lymph nodes and external iliac vein : Case Report and Literature

Herein, we describe the operative procedure for combined resection of re-recurrent lateral lymph nodes and the external iliac vein. There is no consensus on the clinical implications of resection of locally re-recurrent colorectal tumors, as the operative procedure is extremely difficult. We present the case of a 52- year-old woman who underwent abdominoperineal resection. About one year later, we excised a recurrent lymph node in the left lateral obturator area through an extraperitoneal approach. About 18 months later, lymph node re-recurrence in the left external iliac area was observed. Re-recurrent lymph nodes directly invade the left external iliac vein.We removed the re-recurrent lymph node with combined, radical segmental resection of the left external iliac vein, left obturator artery and vein, and left obturator nerve

CBP-93872 enhances oxaliplatin-, cisplatin- and gemcitabine-induced apoptosis in HT29 cells or Panc-1 cells.

<p>(A, B) HT29 cells were treated with oxaliplatin (30 μM) (A) or cisplatin (30 μM) (B) in the presence or absence of CBP-93872 (50 μM). Cells were harvested at 72 hrs, fixed and subjected to FACS analysis (left panels). The percentages of cells in sub-G1 phase are shown in the panels on the right. Data are presented as means ± SD (n = 3). Statistical significance was calculated using Student’s <i>t-</i>test (*, p < 0.01). (C) Panc-1 cells were treated with gemcitabine (0.1 μM) in the presence or absence of CBP-93872 (200 μM). (D-F) HT29 cells or Panc-1 cells, were collected at the times indicated. Total cell extracts were subjected to immunoblotting, using the indicated antibodies.</p

The G2 checkpoint inhibitor CBP-93872 increases the sensitivity of colorectal and pancreatic cancer cells to chemotherapy

<div><p>CBP-93872 suppresses maintenance of DNA double-stranded break-induced G2 checkpoint, by inhibiting the pathway between ataxia-telangiectasia mutated (ATM) and ATM- and Rad3-related (ATR) activation. To examine the potential use of CBP-93872 for clinical applications, we analyzed the synergistic effects of platinum-containing drugs, oxaliplatin and cisplatin, pyrimidine antimetabolites, gemcitabine and 5-fluorouracil (5-FU), in combination with CBP-93872, on cell lethality in colorectal and pancreatic cancer cell lines. Treatment with CBP-93872 significantly increased cancer cell sensitivities to various chemotherapeutic agents tested through suppression of checkpoint activation. Our results thus reveal that combination treatment of CBP-93872 with known chemotherapeutic agents inhibits phosphorylation of ATR and Chk1, and induces cell death.</p></div

CBP-93872 inhibits maintenance of G2 and S-phase checkpoints.

<p>(A, B) HT29 cells were treated with oxaliplatin (30 μM) (A), or cisplatin (30 μM) (B) in the presence or absence of CBP-93872 (50 μM). Nocodazole (500 nM) was added to inhibit the exit of cells from mitosis. Cells were harvested at 48 hrs, fixed, and stained with anti-H3-pS10 antibodies to determine the mitotic index. Mitotic indices (left) and typical examples (right) are shown. Data are presented as means ± SD (n = 3). Statistical significance was calculated using Student’s <i>t-</i>test (*, p < 0.01). ((C) Panc-1 cells were treated with gemcitabine (0.1 μM) in the presence or absence of CBP-93872 (200 μM) with nocodazole (500 nM).</p

CBP-93872 enhances oxaliplatin-, cisplatin- and gemcitabine-induced apoptosis in HT29 cells or Panc-1 cells.

<p>(A, B) HT29 cells were treated with oxaliplatin (30 μM) (A) or cisplatin (30 μM) (B) in the presence or absence of CBP-93872 (50 μM). Cells were harvested at 72 hrs, fixed and subjected to FACS analysis (left panels). The percentages of cells in sub-G1 phase are shown in the panels on the right. Data are presented as means ± SD (n = 3). Statistical significance was calculated using Student’s <i>t-</i>test (*, p < 0.01). (C) Panc-1 cells were treated with gemcitabine (0.1 μM) in the presence or absence of CBP-93872 (200 μM). (D-F) HT29 cells or Panc-1 cells, were collected at the times indicated. Total cell extracts were subjected to immunoblotting, using the indicated antibodies.</p

Combined treatments of CBP-93872 with oxaliplatin, cisplatin, 5-FU, or gemcitabine effectively suppresses cell growth.

<p>(A) HT29 cells were treated with the indicated concentrations of CBP-93872 for 72 hrs, followed by WST-1 assay. Data are presented as means ± SD (n = 3). (B) Panc-1 cells were treated with the indicated concentrations of CBP-93872 for 72 hrs, followed by WST-1 assay. Data are presented as means ± SD (n = 3). (C) HT29 cells were treated with CBP-93872 (50 μM) in combination with indicated concentrations of oxaliplatin, cisplatin or 5-FU for 72 hrs, followed by WST-1 assay. (D) Panc-1 cells were treated with CBP-93872 (200 μM) in combination with indicated concentrations of oxaliplatin, cisplatin or gemcitabine for 72 hrs, followed by WST-1 assay. The black bars show individual treatments; while the white bars show combined treatment with CBP-93872. Data are presented as means ± SD (n = 3). Statistical significance was calculated using Student’s <i>t-</i>test (*, p < 0.01) (C, D).</p

CBP-93872 reduces the levels of oxaliplatin-, cisplatin- and gemcitabine-induced phosphorylations of ATR and Chk1.

<p>(A, B) HT29 cells were treated with oxaliplatin (30 μM) (A), or cisplatin (30 μM) (B) in the presence of absence of CBP-93872 (50 μM). Cells were harvested at the times indicated, and total cell extracts were subjected to immmunoblotting using indicated antibodies. (C) Panc-1 cells were treated with gemcitabine (0.1 μM), in the presence or absence of CBP-93872 (200 μM).</p