Modified enhanced recovery after surgery protocol in octogenarians undergoing minimally invasive colorectal cancer surgery.

BACKGROUND: Colorectal cancer (CRC) is a major health issue worldwide. As the population ages, more older patients including octogenarians will require CRC treatment. However, this vulnerable group has decreased functional reserves and increased surgical risks. Enhanced recovery after surgery (ERAS) pathways aim to reduce surgical stress and complications, but concerns remain about applying ERAS protocols to older patients. We assessed whether a modified ERAS (mERAS) protocol combined would improve outcomes in octogenarian CRC patients undergoing minimally invasive surgery. METHODS: In this retrospective cohort study, we compared 360 non-octogenarians aged 50-64 years and 114 octogenarians aged 80-89 years before and after mERAS protocol implementation. Outcomes including postoperative functionary recovery, length of stay, complications, emergency department visits, and readmissions were analyzed. RESULTS: Despite comparable tumor characteristics, octogenarians had poorer nutrition, American Society of Anesthesiologists status, and more comorbidities. After mERAS, octogenarians had reduced complications, faster return of bowel function, and shorter postoperative length of stay, similar to non-octogenarians. mERAS implementation improved recovery in both groups without increasing emergency department visits or readmissions. CONCLUSION: Although less remarkable than in non-octogenarians, mERAS protocols mitigated higher complication rates and improved recovery in octogenarians after minimally invasive surgery for CRC, confirming protocol feasibility and safety in this vulnerable population.

Diode laser hemorrhoidoplasty versus conventional Milligan-Morgan and Ferguson hemorrhoidectomy for symptomatic hemorrhoids: Meta-analysis.

Conventional hemorrhoidectomy is the mainstay of treatment for symptomatic haemorrhoids, but reported postoperative complications remains the main concern. On the contrary, with its minimally invasive nature, laser hemorrhoidoplasty showed the potential to reduce postoperative complications and discomfort. Therefore, we performed a systemic review and meta-analysis to evaluate the postoperative outcome of laser hemorrhoidoplasty compared to conventional hemorrhoidectomies, including Milligan-Morgan and Ferguson techniques. Of all studies from PubMed, EMBASE, Cochrane database, and Google Scholar, we included 17 trials with 1196 patients, of whom 596 (49.8 %) underwent laser hemorrhoidoplasty and 600 (50.2 %) underwent conventional hemorrhoidectomy. The primary outcomes were operative blood loss and postoperative haemorrhage, and the secondary outcomes were the operative time, postoperative pain score, complications, and haemorrhoid recurrence. In this study, we found that laser hemorrhoidoplasty showed benefits in operative blood loss (weighted mean difference [WMD]: -16.43 ml, 95 % confidence interval [CI]: -23.82 to -9.04), postoperative hemorrhage/bleeding (odds ratio [OR]: 0.16, 95 % CI: 0.10 to 0.28), operative time (WMD: -12.42 min, 95 % CI: -14.56 to -10.28), postoperative pain score on day 1 (WMD: -2.50, 95 % CI: -3.13 to -1.88), and anal stenosis (OR: 0.14, 95 % CI: 0.03 to 0.65) in comparison with conventional hemorrhoidectomy. However, incidence of fecal/flatus incontinence, urinary retention and hemorrhoid recurrence were not significantly different between the 2 groups. Consistent results were found in 5 subgroup analyses, including studies with low risk of bias, studies using 1470 nm laser, and studies using 980 nm laser, studies conducted in Asia, and studies conducted in Europe and America.

Laryngeal Mask Airway as an Appropriate Option in Pediatric Laparoscopic Inguinal Hernia Repair: A Systematic Review and Meta-Analysis.

OBJECTIVE: To elucidate the safety and effectiveness of laryngeal mask airway (LMA) use in pediatric patients undergoing laparoscopic inguinal hernia repair. METHODS: Studies were searched on the PubMed, EMBASE, and Cochrane Library databases. Only randomized controlled trials (RCTs) were included. Primary outcomes were major perioperative respiratory adverse events (PRAEs), namely laryngospasm, bronchospasm, desaturation, and aspiration. Secondary outcomes were minor PRAEs, anesthesia time, and recovery time. A meta-analysis was performed to calculate risk ratios (RR), weighted mean difference (WMD), and 95 % confidence intervals (CI) by using random effects models. RESULTS: In total, 5 RCTs comprising 402 patients were included. Regarding major PRAEs, laryngospasm (RR: 0.43, 95 % CI: 0.12 to 1.47; p = 0.18), bronchospasm, and aspiration all demonstrated no difference between the laryngeal and endotracheal groups. Desaturation exhibited a trend, but this trend was not sufficiently supported with statistical evidence (p = 0.09). For minor PRAEs, fewer patients experienced incidence of cough after laryngeal mask use (RR: 0.27, 95 % CI: 0.11 to 0.67; p = 0.005). Other PRAE, namely hoarseness (p = 0.06), sore throat (RR: 1.88, 95 % CI: 0.76 to 4.66; p = 0.18), and stridor, did not differ between the 2 groups. Additionally, both anesthesia time (WMD: -6.88 min, 95 % CI: -11.88 to -1.89; p < 0.00001) and recovery time (WMD: -4.85 min, 95 % CI: -6.51 to -3.19; p < 0.00001) were shortened in the LMA group. CONCLUSION: LMA used in pediatric laparoscopic inguinal hernia repair demonstrated no greater safety risks than endotracheal tube intubation did. Thus, anesthesiologists may shift from conventional endotracheal tube use to LMA use. Moreover, anesthesia and recovery times were shortened in the LMA group, which resulted in more efficient use of the operating room. Because of these benefits, LMA could be an appropriate option for pediatric patients undergoing laparoscopic inguinal hernia repair. LEVEL OF EVIDENCE: Treatment Study, LEVEL III.

Preclinical Repurposing of Sitagliptin as a Drug Candidate for Colorectal Cancer by Targeting CD24/CTNNB1/SOX4-Centered Signaling Hub.

Despite significant advances in treatment modalities, colorectal cancer (CRC) remains a poorly understood and highly lethal malignancy worldwide. Cancer stem cells (CSCs) and the tumor microenvironment (TME) have been shown to play critical roles in initiating and promoting CRC progression, metastasis, and treatment resistance. Therefore, a better understanding of the underlying mechanisms contributing to the generation and maintenance of CSCs is crucial to developing CSC-specific therapeutics and improving the current standard of care for CRC patients. To this end, we used a bioinformatics approach to identify increased CD24/SOX4 expression in CRC samples associated with poor prognosis. We also discovered a novel population of tumor-infiltrating CD24+ cancer-associated fibroblasts (CAFs), suggesting that the CD24/SOX4-centered signaling hub could be a potential therapeutic target. Pathway networking analysis revealed a connection between the CD24/SOX4-centered signaling, ß-catenin, and DPP4. Emerging evidence indicates that DPP4 plays a role in CRC initiation and progression, implicating its involvement in generating CSCs. Based on these bioinformatics data, we investigated whether sitagliptin, a DPP4 inhibitor and diabetic drug, could be repurposed to inhibit colon CSCs. Using a molecular docking approach, we demonstrated that sitagliptin targeted CD24/SOX4-centered signaling molecules with high affinity. In vitro experimental data showed that sitagliptin treatment suppressed CRC tumorigenic properties and worked in synergy with 5FU and this study thus provided preclinical evidence to support the alternative use of sitagliptin for treating CRC.

Preclinical Evaluation of a Novel Small Molecule LCC-21 to Suppress Colorectal Cancer Malignancy by Inhibiting Angiogenic and Metastatic Signatures.

Colorectal cancer (CRC) is one of the most common cancers, and it frequently metastasizes to the liver and lymph nodes. Despite major advances in treatment modalities, CRC remains a poorly characterized biological malignancy, with high reported cases of deaths globally. Moreover, cancer stem cells (CSCs) and their microenvironment have been widely shown to promote colon cancer development, progression, and metastasis. Therefore, an understanding of the underlying mechanisms that contribute to the maintenance of CSCs and their markers in CRC is crucial in efforts to treat cancer metastasis and develop specific therapeutic targets for augmenting current standard treatments. Herein, we applied computational simulations using bioinformatics to identify potential theranostic markers for CRC. We identified the overexpression of vascular endothelial growth factor-α (VEGFA)/ß-catenin/matrix metalloproteinase (MMP)-7/Cluster of Differentiation 44 (CD44) in CRC to be associated with cancer progression, stemness, resistance to therapy, metastasis, and poor clinical outcomes. To further investigate, we explored in silico molecular docking, which revealed potential inhibitory activities of LCC-21 as a potential multitarget small molecule for VEGF-A/CTNNB1/MMP7/CD44 oncogenic signatures, with the highest binding affinities displayed. We validated these finding in vitro and demonstrated that LCC-21 inhibited colony and sphere formation, migration, and invasion, and these results were further confirmed by a Western blot analysis in HCT116 and DLD-1 cells. Thus, the inhibitory effects of LCC-21 on these angiogenic and onco-immunogenic signatures could be of translational relevance as potential CRC biomarkers for early diagnosis.

Multiomics Study of a Novel Naturally Derived Small Molecule, NSC772864, as a Potential Inhibitor of Proto-Oncogenes Regulating Cell Cycle Progression in Colorectal Cancer.

Colorectal cancer (CRC) is one of the most prevalent malignant tumors, and it contributes to high numbers of deaths globally. Although advances in understanding CRC molecular mechanisms have shed significant light on its pathogenicity, current treatment options, including combined chemotherapy and molecular-targeted agents, are still limited due to resistance, with almost 25% of patients developing distant metastasis. Therefore, identifying novel biomarkers for early diagnosis is crucial, as they will also influence strategies for new targeted therapies. The proto-oncogene, c-Met, a tyrosine kinase that promotes cell proliferation, motility, and invasion; c-MYC, a transcription factor associated with the modulation of the cell cycle, proliferation, apoptosis; and cyclin D1 (CCND1), an essential regulatory protein in the cell cycle, all play crucial roles in cancer progression. In the present study, we explored computational simulations through bioinformatics analysis and identified the overexpression of c-Met/GSK3ß/MYC/CCND1 oncogenic signatures that were associated with cancer progression, drug resistance, metastasis, and poor clinical outcomes in CRC. We further demonstrated the anticancer activities of our newly synthesized quinoline-derived compound, NSC772864, against panels of the National Cancer Institute's human CRC cell lines. The compound exhibited cytotoxic activities against various CRC cell lines. Using target prediction tools, we found that c-Met/GSK3ß/MYC/CCND1 were target genes for the NSC772864 compound. Subsequently, we performed in silico molecular docking to investigate protein-ligand interactions and discovered that NSC772864 exhibited higher binding affinities with these oncogenes compared to FDA-approved drugs. These findings strongly suggest that NSC772864 is a novel and potential antiCRC agent.

Comparison of robotic reduced-port and laparoscopic approaches for left-sided colorectal cancer surgery.

BACKGROUND/OBJECTIVE: The reduced-port approach can overcome the limitations of single-incision laparoscopic surgery while maintaining its advantages. Here, we compared the effects of robotic reduced-port surgery and conventional laparoscopic approaches for left-sided colorectal cancer. METHODS: Between January 2015 and December 2016, the clinicopathological characteristics and treatment outcomes of 17 patients undergoing robotic reduced-port surgery and 49 patients undergoing laparoscopic surgery for left-sided colorectal cancer were compared. RESULTS: The two groups were comparable in almost all outcome measures except for the distal resection margin, which was significantly longer in the laparoscopic group (P < 0.001). The between-group differences in reoperation, incisional hernia development, and overall and progression-free survival were nonsignificant; however, the total hospital cost was significantly higher in the robotic group than in the laparoscopic group (US$13779.6 ± US$3114.8 vs. US$8556.3 ± US$2056.7, P < 0.001). CONCLUSION: Robotic reduced-port surgery for left-sided colorectal cancer is safe and effective but more expensive with no additional benefit compared with the conventional laparoscopic approach. This observation warrants further evaluation.

Preclinical Identification of Sulfasalazine's Therapeutic Potential for Suppressing Colorectal Cancer Stemness and Metastasis through Targeting KRAS/MMP7/CD44 Signaling.

Approximately 25% of colorectal cancer (CRC) patients will develop metastatic (m)CRC despite treatment interventions. In this setting, tumor cells are attracted to the epidermal growth factor receptor (EGFR) oncogene. Kirsten rat sarcoma (RAS) 2 viral oncogene homolog (KRAS) mutations were reported to drive CRC by promoting cancer progression in activating Wnt/ß-catenin and RAS/extracellular signal-regulated kinase (ERK) pathways. In addition, KRAS is associated with almost 40% of patients who acquire resistance to EGFR inhibitors in mCRC. Multiple studies have demonstrated that cancer stem cells (CSCs) promote tumorigenesis, tumor growth, and resistance to therapy. One of the most common CSC prognostic markers widely reported in CRC is a cluster of differentiation 44 (CD44), which regulates matrix metalloproteinases 7/9 (MMP7/9) to promote tumor progression and metastasis; however, the molecular role of CD44 in CRC is still unclear. In invasive CRC, overexpression of MMP7 was reported in tumor cells compared to normal cells and plays a crucial function in CRC cetuximab and oxaliplatin resistance and distant metastasis. Here, we utilized a bioinformatics analysis and identified overexpression of KRAS/MMP7/CD44 oncogenic signatures in CRC tumor tissues compared to normal tissues. In addition, a high incidence of mutations in KRAS and CD44 were associated with some of the top tumorigenic oncogene's overexpression, which ultimately promoted a poor response to chemotherapy and resistance to some FDA-approved drugs. Based on these findings, we explored a computational approach to drug repurposing of the drug, sulfasalazine, and our in silico molecular docking revealed unique interactions of sulfasalazine with the KRAS/MMP7/CD44 oncogenes, resulting in high binding affinities compared to those of standard inhibitors. Our in vitro analysis demonstrated that sulfasalazine combined with cisplatin reduced cell viability, colony, and sphere formation in CRC cell lines. In addition, sulfasalazine alone and combined with cisplatin suppressed the expression of KRAS/MMP7/CD44 in DLD-1 and HCT116 cell lines. Thus, sulfasalazine is worthy of further investigation as an adjuvant agent for improving chemotherapeutic responses in CRC patients.

Gamma-mangostin isolated from garcinia mangostana suppresses colon carcinogenesis and stemness by downregulating the GSK3ß/ß-catenin/CDK6 cancer stem pathway.

BACKGROUND: Despite advances in chemotherapies and targeted drugs, colorectal cancer (CRC) remains challenging to treat due to drug resistance. Emerging evidence indicates that cancer-associated fibroblasts (CAFs) facilitate the generation of cancer stem-like cells (CSCs) and drug resistance. Glycogen synthase kinase-3 (GSK) associated signaling pathways have been implicated in the generation of CSCs and represent a target for therapeutics development. HYPOTHESIS: Gamma-mangostin (gMG) isolated from Garcinia mangostana was evaluated for its ability to downregulate GSK3ß-associated signaling in CRC cells and overcome CAF-induced 5-fluorouracil resistance and CSC generation. METHODS: Bioinformatics analysis, in silico molecular docking, in vitro assays, including cell viability tests, colony- and tumor sphere-formation assays, transwell migration assays, ELISA, SDS-PAGE, Western blotting, miR expression, qPCR, and flow cytometry, as well as in vivo mouse xenograft models were used to evaluate the antitumor effects of gMG. RESULTS: Bioinformatics analyses indicated that GSK3ß/CDK6/ß-catenin mRNA signature was significantly higher in colon cancer patients. Additional algorithms predicted a higher miR-26b level was associated with significantly higher survival in CRC patients and GSK3ß and CDK6 as targets of miR-26b-5p. To validate these findings in vitro, we showed that CAF-cocultured CRC cells expressed an increased expression of GSK3ß, ß-catenin, CDK6, and NF-κB. Therapeutically, we demonstrated that gMG treatment suppressed GSK3ß-associated signaling pathways while concomitantly increased the miR-26b-5p level. Using a xenograft mouse model of CAFs cocultured HCT116 tumorspheres, we showed that gMG treatment reduced tumor growth and overcame CAF-induced 5-fluorouracil resistance. CONCLUSIONS: Pharmacological intervention with gMG suppressed CRC carcinogenesis and stemness via downregulating GSK3/ß-catenin/CDK6 and upregulating the miR-26b-5p tumor suppressor. Thus, gMG represents a potential new CRC therapeutic agent and warrants further investigation.

Comprehensive Omics Analysis of a Novel Small-Molecule Inhibitor of Chemoresistant Oncogenic Signatures in Colorectal Cancer Cell with Antitumor Effects.

Tumor recurrence from cancer stem cells (CSCs) and metastasis often occur post-treatment in colorectal cancer (CRC), leading to chemoresistance and resistance to targeted therapy. MYC is a transcription factor in the nuclei that modulates cell growth and development, and regulates immune response in an antitumor direction by mediating programmed death ligand 1 (PD-L1) and promoting CRC tumor recurrence after adjuvant chemotherapy. However, the molecular mechanism through which c-MYC maintains stemness and confers treatment resistance still remains elusive in CRC. In addition, recent reports demonstrated that CRC solid colon tumors expresses C-X-C motif chemokine ligand 8 (CXCL8). Expression of CXCL8 in CRC was reported to activate the expression of PD-L1 immune checkpoint through c-MYC, this ultimately induces chemoresistance in CRC. Accumulating studies have also demonstrated increased expression of CXCL8, matrix metalloproteinase 7 (MMP7), tissue inhibitor of metalloproteinase 1 (TIMP1), and epithelial-to-mesenchymal transition (EMT) components, in CRC tumors suggesting their potential collaboration to promote EMT and CSCs. TIMP1 is MMP-independent and regulates cell development and apoptosis in various cancer cell types, including CRC. Recent studies showed that TIMP1 cleaves CXCL8 on its chemoattractant, thereby influencing its mechanistic response to therapy. This therefore suggests crosstalk among the c-MYC/CXCL8/TIMP1 oncogenic signatures. In this study, we explored computer simulations through bioinformatics to identify and validate that the MYC/CXCL8/TIMP1 oncogenic signatures are overexpressed in CRC, Moreover, our docking results exhibited putative binding affinities of the above-mentioned oncogenes, with our novel small molecule, RV59, Finally, we demonstrated the anticancer activities of RV59 against NCI human CRC cancer cell lines both as single-dose and dose-dependent treatments, and also demonstrated the MYC/CXCL8/TIMP1 signaling pathway as a potential RV59 drug target.

Preclinical investigation of ovatodiolide as a potential inhibitor of colon cancer stem cells via downregulating sphere-derived exosomal ß-catenin/STAT3/miR-1246 cargoes.

Patients with advanced-stage colon cancer often exhibit resistance against treatment and distant metastasis, both key contributors to poor prognosis. Emerging evidence indicates that cancer stem cells (CSCs), characterized by the enhanced ability to self-renew, resist therapeutics, and promote metastasis, represents a clinical challenge to target. Alternative therapeutic approaches are urgently required. Here, we explored the feasibility of disrupting the intracellular communications between CSCs and the tumor microenvironment by way of exosomes. First, we demonstrated that exosomes secreted by colon tumorspheres (Exosp) promoted 5-FU resistance, migration, and tumorsphere formation. Exosp also increased the generation of cancer-associated fibroblasts and M2 polarized macrophages in vitro. Oncogenic molecules, including IL-6, p-STAT3, TGF-ß1, and ß-catenin, were identified as the cargoes of Exosp. Furthermore, the public database revealed the high abundance of miR-1246 in serum exosomes from colon cancer patients, and we verified in the Exosp from HCT116 and HT29 cells. Therapeutically, we demonstrated the ovatodiolide treatment reduced exosomal cargoes from tumorspheres (Exosp_OV). Exosp_OV were significantly less capable of promoting 5-FU resistance, migration, and tumorsphere formation when co-cultured with HCT116 and HT29 cells. Notably, Exosp_OV was less CAF- and M2 TAM-transformative. Computational docking analysis revealed that OV could bind and significantly reduced ß-catenin activity. Finally, mouse xenograft data indicated that ovatodiolide suppressed tumor growth via down-regulating IL-6, STAT3, ß-catenin expression, and serum exosomal miR-1246. In conclusion, our findings provided preclinical supports for ovatodiolide as a colon CSC inhibitor by reducing ß-catenin/STAT3/miR-1246 signaling conveyed by CSC derived exosomes.

Preclinical Evaluation of the Novel Small-Molecule MSI-N1014 for Treating Drug-Resistant Colon Cancer via the LGR5/ß-catenin/miR-142-3p Network and Reducing Cancer-Associated Fibroblast Transformation.

Colorectal cancer represents one of the most prevalent malignancies globally, with an estimated 140,000 new cases in the United States alone in 2019. Despite advancements in interventions, drug resistance occurs in virtually all patients diagnosed with late stages of colon cancer. Amplified epidermal growth factor receptor (EGFR) signaling is one of the most prevalent oncogenic drivers in patients and induces increased Janus kinase (JAK)/signal transduction and activator of transcription (STAT) and ß-catenin functions, all of which facilitate disease progression. Equally important, cancer-associated fibroblasts (CAFs) transformed by cancer cells within the tumor microenvironment (TME) further facilitate malignancy by secreting interleukin (IL)-6 and augmenting STAT3 signaling in colon cancer cells and promoting the generation of cancer stem-like cells (CSCs). Based on these premises, single-targeted therapeutics have proven ineffective for treating malignant colon cancer, and alternative multiple-targeting agents should be explored. Herein, we synthesized a tetracyclic heterocyclic azathioxanthone, MSI-N1014, and demonstrated its therapeutic potential both in vitro and in vivo. First, we used a co-culture system to demonstrate that colon cancer cells co-cultured with CAFs resulted in heightened 5-fluorouracil (5-FU) resistance and tumor sphere-forming ability and increased side populations, accompanied by elevated expression of cluster of differentiation 44 (CD44), ß-catenin, leucine-rich repeat-containing G-protein-coupled receptor 5 (LGR5), and ATP-binding cassette super-family G member 2 (ABCG2). MSI-N1014 suppressed cell viability, colony formation, and migration in both DLD1 and HCT116 cells. MSI-N1014 treatment led to decreased expressions of oncogenic markers, including mammalian target of rapamycin (mTOR), EGFR, and IL-6 and stemness markers such as CD44, ß-catenin, and LGR5. More importantly, MSI-N1014 treatment suppressed the transformation of CAFs, and was associated with decreased secretion of IL-6 and vascular endothelial growth factor (VEGF) by CAFs. Furthermore, MSI-N1014 treatment resulted in significantly reduced oncogenic properties, namely the migratory ability, tumor-sphere generation, and resistance against 5-FU. Notably, an increased level of the tumor suppressor, miR-142-3p, whose targets include LGR5, IL-6, and ABCG2, was detected in association with MSI-N1014 treatment. Finally, we demonstrated the therapeutic potential of MSI-N1014 in vivo, where combined treatment with MSI-N1014 and 5-FU led to the lowest tumor growth, followed by MSI-N1014 only, 5-FU, and the vehicle control. Tumor samples from the MSI-N1014 group showed markedly reduced expressions of LGR5, ß-catenin, IL-6, and mTOR, but increased expression of the tumor suppressor, miR-142-3p, according to qRT-PCR analysis. Collectively, we present preclinical support for the application of MSI-N1014 in treating 5-FU-resistant colon cancer cells. Further investigation is warranted to translate these findings into clinical settings.

Construction and characterization of a knock-down RNA interference line of OsNRPD1 in rice (Oryza sativa ssp japonica cv Nipponbare).

In plants, RNA-directed DNA methylation (RdDM) is a silencing mechanism relying on the production of 24-nt small interfering RNAs (siRNAs) by RNA POLYMERASE IV (Pol IV) to trigger methylation and inactivation of transposable elements (TEs). We present the construction and characterization of osnrpd1, a knock-down RNA interference line of OsNRPD1 gene that encodes the largest subunit of Pol IV in rice (Oryza sativa ssp japonica cv Nipponbare). We show that osnrpd1 displays a lower accumulation of OsNRPD1 transcripts, associated with an overall reduction of 24-nt siRNAs and DNA methylation level in all three contexts, CG, CHG and CHH. We uncovered new insertions of known active TEs, the LTR retrotransposons Tos17 and Lullaby and the long interspersed nuclear element-type retrotransposon Karma. However, we did not observe any clear developmental phenotype, contrary to what was expected for a mutant severely affected in RdDM. In addition, despite the presence of many putatively functional TEs in the rice genome, we found no evidence of in planta global reactivation of transposition. This knock-down of OsNRPD1 likely led to a weakly affected line, with no effect on development and a limited effect on transposition. We discuss the possibility that a knock-out mutation of OsNRPD1 would cause sterility in rice. This article is part of a discussion meeting issue 'Crossroads between transposons and gene regulation'.

Comparison of clinical outcomes between laparoscopic and open surgery for left-sided colon cancer: a nationwide population-based study.

The role of laparoscopic surgery for left-sided colon cancer has been supported by the results of randomized controlled trials. However, its benefits and disadvantages in the real world setting should be further assessed with population-based studies.The hospitalization data of patients undergoing open or laparoscopic surgery for left-sided colon cancer were sourced from the Taiwan National Health Insurance Research Database. Patient and hospital characteristics and perioperative outcomes including length of hospital stay, operation time, opioid use, blood transfusion, intensive care unit (ICU) admission, and use of mechanical ventilation were compared. The overall survival was also assessed. Patients undergoing laparoscopic surgery had shorter hospital stay (p < 0.0001) and less demand for opioid analgesia (p = 0.0005). Further logistic regression revealed that patients undergoing open surgery were 1.70, 2.89, and 3.00 times more likely to have blood transfusion, to be admitted to ICU, and to use mechanical ventilation than patients undergoing laparoscopic surgery. Operations performed in medical centers were also associated with less adverse events. The overall survival was comparable between the 2 groups.With adequate hospital quality and volume, laparoscopic surgery for left-sided colon cancer was associated with improved perioperative outcomes. The long-term survival was not compromised.

Erratum: Preclinical investigation of ovatodiolide as a potential inhibitor of colon cancer stem cells via downregulating sphere-derived exosomal ß-catenin/STAT3/miR-1246 cargoes.

[This corrects the article on p. 2337 in vol. 10, PMID: 32905416.].