Association between ultra-processed food and osteoporosis: a cross-sectional study based on the NHANES database.

AIM: Nutritional characteristics and additives in ultra-processed foods (UPF) are directly related to bone health. Physical activity as a modifiable lifestyle intervention also plays a possible role in bone mineral density (BMD), but effect of physical activity on association between UPF and osteoporosis is not fully understood. Herein, this study aims to explore the association of UPF with osteoporosis, and assess the potential mediating effects of some related factors on this pathway. METHODS: Data of adults were extracted from the National Health and Nutrition Examination Survey (NHANES) database in this cross-sectional study. Associations of unprocessed/minimally processed food (MPF), processed culinary ingredient (PCI), processed foods (PF) and UPF with femur neck BMD, total femur BMD and osteoporosis were investigated using linear regression and weighted univariate and multivariate logistic regression analyses respectively. Subgroup analyses of age, gender, physical activity, poverty income ratio (PIR), hypertension, diabetes mellitus (DM), cardiovascular disease (CVD), and dyslipidemia were performed. The potential mediating and interaction effects of physical activity and related factors on association of UPF with osteoporosis were also assessed. The evaluation indexes were ß, odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: Among 10,678 eligible persons, 454 had osteoporosis. After adjusting for covariates, elevated UPF intake was associated with decreased demur neck and total femur BMD (ß=-0.003). A higher UPF intake level (> 57.51%) was linked to higher odds of osteoporosis (OR = 1.789). These relationships were also significant in different subgroups. Physical activity had a potential mediating effect on the association between UPF and osteoporosis (OR = 0.47, mediating proportion = 21.54%). CONCLUSION: UPF intake levels were associated with BMD and osteoporosis. Physical activity had an interaction effect with UPF, and had a potential mediating effect on relationship between UPF and osteoporosis.

Quality of life estimate in stomach, colon, and rectal cancer patients in a hospital in China.

The objective of this study was to investigate the outcome and coping patterns of patients with stomach, colon, and rectal cancer in a hospital in China. Health-related quality of life was assessed in 118 stomach, colon, and rectal cancer patients in Chinese People's Liberation Army General Hospital, Beijing, China, using the generic version of the European Organization for Research and Treatment of Cancer Quality of Life (QOL) Questionnaire Core 30 Items, Self-rated Anxiety Scores (SAS), Self-rated Depression Scores (SDS), Medical Coping Modes of Questionnaire (MCMQ), and Social Support Requirement Scale (SSRS) questionnaires. The overall QOL was 50.7 ± 6.5, 48.1 ± 7.7, and 47.6 ± 6.4, respectively, for stomach, colon, and rectal cancer groups. Correlations between QOL and SAS and SDS in stomach cancer patients were significantly higher than observed in the cohort of colon or rectal cancer patients (Spearman coefficient of 0.366 and 0.129, respectively). Cluster analysis of MCMQ data revealed four identifiable patterns (resign, confront, avoid-confront, and avoid-resign) of coping in the study group. Subjective support was significantly higher than objective support (p < 0.05); however, extent of using the support was significantly lower than either objective (p < 0.05) or subjective support (p < 0.01). SAS and SDS were negatively correlated to SSRS scores (p < 0.01 and p < 0.05, respectively). Stomach, colon, and rectal cancer patients had anxiety and depression stemming from their cancer diagnosis and postdiagnosis treatment, and sex dependency was prevalent in SSRS response. Coping patterns were reliable indicators of psychosocial side effects in patients with stomach, colon, and rectal cancers.

Long-term response to sintilimab, bevacizumab and chemotherapy in heavily pretreated microsatellite stable colon cancer.

Most advanced colorectal cancer patients with proficient DNA mismatch repair or microsatellite stability (MSS) are insensitive to immune checkpoint inhibitor therapy. This report describes a heavily pretreated refractory colon adenocarcinoma patient with MSS. After experiencing four lines of treatment, the patient received the fifth-line therapy with the combined sintilimab, bevacizumab and chemotherapy. She achieved a long-term clinical outcome. The patient's progression-free survival after the fifth-line therapy was approximately 9.3 months, and her overall survival was approximately 57 months. To the best of our knowledge, this case represents the first report of durable clinical benefit from combination of an immune checkpoint inhibitor, bevacizumab and chemotherapy in a heavily pretreated patient with refractory metastatic colon adenocarcinoma with MSS.

To date, little information is available on the efficacy of combination of immunotherapy, antiangiogenic therapy and chemotherapy in heavily pretreated refractory colon cancer patients with microsatellite stability (MSS). Here, we describe a heavily pretreated refractory colon adenocarcinoma patient with MSS. After experiencing four lines of prior treatment, the patient received the fifth-line therapy with the combined immunotherapy, an antiangiogenetic inhibitor and chemotherapy. She achieved a durable clinical outcome. To our knowledge, this case is the first report of successful treatment of a heavily pretreated refractory metastatic colon adenocarcinoma patient with MSS receiving the combined immunotherapy, antiangiogenic therapy and chemotherapy.

LncRNA HCG11 promotes 5-FU resistance of colon cancer cells through reprogramming glucose metabolism by targeting the miR-144-3p-PDK4 axis.

BACKGROUND: Colorectal cancer (CRC), one of the most common human malignancies, is a leading cause of the cancer-related mortality. 5-FU is a first-line chemotherapeutic agent against CRC. Although CRC patients responded to 5-FU therapy initially, a part of patients succumbed to CRC due to the acquired drug resistance. Thus, investigating molecular mechanisms underlying chemoresistance will contribute to developing novel strategies against colorectal cancer. OBJECTIVE: Accumulation evidence revealed pivotal roles of long non-coding RNAs (lncRNAs) in tumorigenesis and chemoresistance of CRC. However, the precise roles and molecular mechanisms of lncRNA-HCG11 in CRC remain unclear. This study aimed to investigate the biological roles and underlying mechanisms of HCG11 as well as its molecular targets in regulating the cellular metabolism processes, which facilitate the chemoresistance of CRC. METHODS AND RESULTS: This study uncovers that HCG11 was significantly upregulated in CRC tumors tissues and cell lines. Moreover, HCG11 was elevated in 5-FU resistant CRC tumors. Silencing HCG11 inhibited colon cancer cell proliferation, migration, invasion and glucose metabolism and sensitized CRC cells to 5-FU. In addition, we detected increased HCG11 expression level and glucose metabolism in the established 5-FU resistant CRC cell line (DLD-1 5-FU Res). Furthermore, microRNA-microArray, RNA pull-down and luciferase assays demonstrated that HCG11 inhibited miR-144-3p which displays suppressive roles in colon cancer via sponging it to form a ceRNA network. We identified pyruvate dehydrogenase kinase 4 (PDK4), which is a glucose metabolism key enzyme, was directly targeted by miR-144-3p in CRC cells. Rescue studies validated that the miR-144-3p-inhibited glucose metabolism and 5-FU sensitization were through targeting PDK4. Finally, restoration of miR-144-3p in HCG11-overexpressing DLD-1 5-FU resistant cells successfully overcame the HCG11-faciliated 5-FU resistance via targeting PDK4. CONCLUSION: In summary, this study reveals critical roles and molecular mechanisms of the HCG11-mediated 5-FU resistance through modulating the miR-144-3p-PDK4-glucose metabolism pathway in CRC.

Pancreatic cancer with synchronous liver and colon metastases: A case report.

BACKGROUND: Metastasis of pancreatic cancer to the colon is rare and the features need to be further elucidated. Herein, we report a rare case of pancreatic cancer with simultaneous liver and colon metastases. CASE SUMMARY: A 48-year-old man with intrahepatic space-occupying lesions based on a computed tomography scan was admitted to our hospital for further treatment. Abdominal magnetic resonance imaging revealed a 6.4 cm × 4.2 cm mass in the tail of the pancreas and multiple low-density masses in the liver parenchyma. In addition, a mass of 2.2 cm × 1.6 cm with surface congestive erosions in the sigmoid colon was detected by colonoscopy. Histopathological examination of biopsies from both the liver and colon lesions revealed a moderately to poorly differentiated adenocarcinoma. Immunohistochemical staining of the colon tumor was positive for cytokeratin (CK) 7 and CK, but negative for colorectal adenocarcinoma-related markers CK 20, CDX2, and SATB2, thus indicating that the metastasis originated from the pancreas. Next-generation sequencing for genomic profiling of the liver and colon metastases both found mutations in KRAS (p.G12D) and TP53 (c.376-1delG), with microsatellite stable and low tumor mutational burden without actionable or cancer-predisposing gene mutations detected. The patient was subsequently treated with 12 cycles of FOLFIRINOX which led to a sustainable response, followed by ongoing maintenance treatment with irinotecan plus fluorouracil. CONCLUSION: For this rare case, careful evaluation of histopathological and immunohistochemical staining results are required. The genomic profiling of colon lesions was revealed for the first time, and FOLFIRINOX showed good treatment efficacy in this patient.

Pancreatic cancer differential methylation atlas in blood, peri-carcinomatous and diseased tissue.

BACKGROUND: Pancreatic cancer is common in elderly persons, and less than 20% of patients present with localized, potentially curable tumors. METHODS: We compared the methylated sites and genes in pericarcinous tissues compared to cancer tissue, and blood compared to pericarcinous tissues in order to harvest methylation markers for putative diagnostic and therapy monitoring purposes. RESULTS: Of 15,397 CpG sites detected in 7,440 genes, 5,605 (36.4%, 5,605 of 15,397) CpG sites were hypomethylated and 5,870 (38.12%, 5,870 of 15,397) CpG sites were hypermethylated. We then performed Gene Ontology (GO) and KEGG analysis to systematically characterize the ten significantly differentially methylated genes: PTPRN2, MAD1L1, TNXB, PRDM16, GNAS, KCNQ1, TSNARE1, HDAC4, TBCD, and DIP2C. Meanwhile, function analysis of genes with differentially methylated sites located in promoter regions of overlap group was also performed. According to previous studies, we further screened 22 pancreatic cancer related key genes. The results suggested that these key genes can influence methylation. GO and KEGG analysis indicated that these genes are involved in a wide range of functions. CONCLUSIONS: The identification of differentially methylated genes in this study provides valuable information for liquid biopsy methylation markers in pancreatic cancer.

Clinical pain management by a multidisciplinary palliative care team: Experience from a tertiary cancer center in China.

To investigate the effect of multidisciplinary interventions on pain management in cancer inpatients.Four hundred thirty eight patients with cancer pain, who performed the multidisciplinary intervention were recruited. Before and after intervention, the Brief Pain Inventory (BPI) and the MD Anderson Symptom Inventory (MDASI) score as the primary endpoints and QOL scores as the secondary endpoint were all evaluated. To investigate the factors that led to different responses to multidisciplinary interventions, patients were classified as non-responders or responders.Finally, 92 patients (63 male and 29 female) scheduled for cancer pain management by inter-professional team were studied. After individualized multidisciplinary therapy, both pain and symptom severity was improved, as demonstrated by lowered BPI worst and average pain scores, as well as symptom severity score measured by MDASI (P = .017, P = .003, and P = .011, respectively). The proportion of patients with mild pain increased regarding the BPI worst and average pain at baseline and after treatment (P < .05). The QOL analyses showed multidisciplinary interventions could significantly improve the function and symptom scores (P < .001). More patients in responder group received chemotherapy (58, 70.7%, P = .003), while fewer received mini-invasive therapy (6, 7.32%, P = .011).Multidisciplinary interventions had certain beneficial effect on cancer pain management, especially in patients with moderate or severe pain.

Survival of patients with advanced pancreatic cancer after iodine125 seeds implantation brachytherapy: A meta-analysis.

BACKGROUND: Brachytherapy with iodine-labeled seeds (I-seeds) implantation is increasingly being used to treat tumors because of its positional precision, minimal invasion, least damage to noncancerous tissue due to slow and continuous release of radioactivity and facilitation with modern medical imaging technologies. This study evaluates the survival and pain relief outcomes of the I-seeds implantation brachytherapy in advanced pancreatic cancer patients. METHODS: Literature search was carried out in multiple electronic databases (Google Scholar, Embase, Medline/PubMed, and Ovid SP) and studies reporting I seeds implantation brachytherapy in pancreatic cancer patients with unresectable tumor were selected by following predetermined eligibility criteria. Random effects meta-analysis was performed to achieve inverse variance weighted effect size of the overall survival rate after the intervention. Sensitivity and subgroups analyses were also carried out. RESULTS: Twenty-three studies (824 patients' data) were included in the meta-analysis. I-seeds implantation brachytherapy alone was associated with 8.98 [95% confidence interval (CI): 6.94, 11.03] months (P < 0.00001) overall survival with 1-year survival of 25.7 ±â€Š9.3% (mean ±â€Šstandard deviation; SD) and 2-year survival was 17.9 ±â€Š8.6% (mean ±â€ŠSD). In stage IV pancreatic cancer patients, overall survival was 7.13 [95% CI: 4.75, 9.51] months (P < 0.00001). In patients treated with I-seeds implantation along with 1 or more therapies, overall survival was 11.75 [95% CI: 9.84, 13.65] months (P < 0.00001) with 1-year survival of 47.4 ±â€Š22.75% (mean ±â€ŠSD) and 2-year survival was 16.97 ±â€Š3.1% (mean ±â€ŠSD). I-seeds brachytherapy was associated with relief of pain in 79.7 ±â€Š9.9% (mean ±â€ŠSD) of the patients. CONCLUSIONS: Survival of pancreatic cancer patients after I-seeds implantation brachytherapy is found to be 9 months, whereas a combined treatment with I-seeds brachytherapy and other therapies was associated with approximately 12 months' survival. The majority of patients who underwent I-seeds brachytherapy had their pain relieved.

Specific growth inhibition of ErbB2­expressing human breast cancer cells by genetically modified NK­92 cells.

The natural killer cell line NK­92 shows great cytotoxicity against various types of cancer. Several types of solid tumor cells, however, can effectively resist NK-mediated lysis by interaction of major histocompatibility complex (MHC) molecules with NK cell inhibitory receptors. To generate a eukaryotic expression vector encoding chimeric antigen receptor scFv anti-erbB2-CD28-ζ and to investigate the expression and action of this chimeric antigen receptor in cancer cells both in vitro and in vivo, NK­92 cells were genetically modified with an scFv anti-erbB2-CD28-ζ chimeric recep-tor by optimized electro-poration using the Amaxa Nucleofector system. The expression of the chimeric receptor was evaluated by RT-PCR and immunofluorescence. The ability of the genetically modified NK­92 cells to induce cell death in tumor targets was assessed in vitro and in vivo. The transduced NK­92-anti-erbB2 scFv-CD28-ζ cells expressing high levels of the fusion protein on the cell surface were analyzed by fluorescence-activated cell-sorting (FACS) analysis. These cells specifically enhanced the cell death of the erbB2­expressing human breast cancer cell lines MDA-MB-453 and SKBr3. Furthermore, adoptive transfer of genetically modified NK­92 cells specifically reduced tumor size and lung metastasis of nude mice bearing established MDA-MB-453 cells, and significantly enhanced the survival period of these mice. The genetically modified NK­92 cells significantly enhanced the killing of erbB2­expressing cancer and may be a novel therapeutic strategy for erbB2­expressing cancer cells.