Laparoscopic versus open liver resection for metastatic colorectal cancer.

BACKGROUND: Application of minimally invasive surgery for oncologic liver resection is still limited to expert centers. We describe our experience in laparoscopic liver resection (LLR) for colorectal liver metastases (CLM). PATIENTS AND METHODS: Between February 2010 and February 2015, 174 patients underwent resection of CLM. LLR was chosen according to surgeon's preferences. Data was retrieved from the institutes' electronic charts and retrospectively analyzed. RESULTS: LLR was performed in 42 patients (24.5%) and OLR in 132. Increased number of metastases were found in OLR (2.82 ± 2.81 versus 1.78 ± 1.16, P = 0.02), with no difference in maximal lesion size (33.1 ± 22 versus 34.9 ± 27.5 cm, P = 0.7). Altogether 55 patients underwent major hepatectomy, and 50 of the OLR group (37.8%, 37 right hepatectomy and 7 left hepatectomy) (P = 0.02). In 5 patients (11.6%) a conversion to open surgery was indicated. Operative time was longer in LLR. Estimated blood loss was decreased in laparoscopic minor resections. One OLR patient died during the postoperative period (0.7%). Eight patients in the OLR group had major complications, versus 1 in the LLR group (P = 0.0016). Reoperation within 30 days was performed in 4 OLR patients and none in the LLR group. Patients in the LLR group had shorter length of stay (LOS) (6.78 ± 2.75 versus 8.39 ± 5.64 days, P = 0.038). R0 resection was 88% in both groups. CONCLUSIONS: In selected patients with CLM, LLR is feasible, safe and may achieve shorter LOS without inferior oncologic outcome.

Gonadotropin stimulation in mice leads to ovarian accumulation of immature myeloid cells and altered expression of proangiogenic genes.

OBJECTIVE: Ovarian hyperstimulation syndrome is associated with increased angiogenesis and vascular leakage. Immature myeloid cells (IMCs) and dendritic cells have been shown to be actively involved in angiogenesis in several disease models in mice and humans. Nevertheless, little is known about the role of these cells in the ovary. As such, this study sought to determine whether alterations in these ovarian myeloid cell populations are associated with gonadotropin stimulation in a mouse model. STUDY DESIGN: Four-week-old pre-pubertal C57Bl/6 female mice were allocated into three groups: high-dose stimulation (n=4; pregnant mare serum gonadotropins (PMSG) 20U for 2 days), low-dose stimulation (n=5; PMSG 5U for 1 day) and sham-treated controls (n=4). Human chorionic gonadotropin 5U was injected on Day 3, and the mice were killed on Day 5. Ovaries were analysed by flow cytometry, confocal microscopy and quantitative polymerase chain reaction. RESULTS: Gonadotropin stimulation increased the proportion of CD11b(+)Gr1(+) IMCs among the ovarian myeloid cells: 22.6±8.1% (high dose), 7.2±1.6% (low dose) and 4.1±0.3% (control) (p=0.02). Conversely, gonadotropin stimulation decreased the proportion of ovarian CD11c(+)MHCII(+) dendritic cells: 15.1±1.9% (high dose), 20.7±4.8% (low dose) and 27.3±8.2% (control) (p=0.02). IMCs, unlike dendritic cells, were localized adjacent to PECAM1(+) endothelial cells. Finally, gonadotropin stimulation was associated with increased expression of S100A8, S100A9, Vcan and Dmbt1, and decreased expression of MMP12. CONCLUSIONS: Gonadotropin stimulation is associated with proangiogenic myeloid cell alterations, reflected by a dose-dependent increase in ovarian IMCs and a parallel decrease in dendritic cells. Recruited IMCs localize strategically at sites of angiogenesis. These changes are associated with differential expression of key proangiogenic genes.

Unique expression patterns associated with preferential recruitment of immature myeloid cells into angiogenic versus dormant tumors.

Cancer progression from microscopic dormant tumors into disseminated disease involves tumor angiogenesis, and is commonly referred to as the 'angiogenic switch'. CD11b(+)Gr1(+) immature myeloid cells (IMCs) were reported to promote angiogenesis and tumor progression. Here, we studied a model of tumor dormancy, in which Lewis Lung Carcinoma tumor cells were inoculated intra-abdominally into C57Bl/6J mice. Dormancy versus expansive growth was determined by the site of tumor implantation (lower vs upper abdomen). Global gene expression of IMCs was evaluated in different stages of recruitment, starting in the bone marrow, followed by the peripheral blood and finally in the vascular versus dormant tumors. We first demonstrated a ∼3 fold enrichment of IMCs within vascular tumors as compared with dormant tumors, correlating with tumor-infiltrating CD31(+) endothelial cells. Although their migration from the PB into dormant tumors led to differential expression of a relatively small number of genes, recruitment of IMCs into the upper tumors was associated with a profound transcriptional response. Importantly, a large set of proangiogenic genes were significantly upregulated in IMCs derived from vascular tumors compared with those derived from dormant tumors. We therefore, suggest that proangiogenic versus nonangiogenic transcriptional patterns is associated with the ability of IMCs to promote tumor angiogenesis.

Malignant transformation in pediatric spinal intramedullary tumors: case-based update.

BACKGROUND: In children, intramedullary spinal cord neoplasms are rare. These are typically low-grade neuroepithelial tumors, most commonly astrocytomas, ependymomas, and gangliogliomas. Malignant transformation, while common in recurrent adult low-grade gliomas, is an unusual event in pediatric low-grade neoplasms, specifically in intramedullary spinal cord tumors. ILLUSTRATIVE CASES: We report two cases of malignant transformation in low-grade neuroepithelial tumors of the pediatric intramedullary spinal cord. Two children with intramedullary tumors, one with a WHO grade I ganglioglioma and one with a low-grade astrocytoma, were treated surgically, diagnosed histologically, and followed through the course of their disease. Both patients' tumors transformed to higher grades without prior irradiation or chemotherapy, and without a genetic predisposition to tumorigenesis. DISCUSSION: Malignant transformation can occur in low-grade intramedullary neoplasms in children. This is a novel documented event for pediatric intramedullary spinal cord tumors and a rare event for all pediatric low-grade neuroepithelial tumors without induction by irradiation. A survey of the relevant literature reveals an underwhelming number of studies focusing on malignant transformation in children's CNS tumors relative to adults. Further investigation into molecular mechanisms of pediatric low-grade neoplasms may reveal more aggressive tumor sub-variants predisposed to malignant degeneration.