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1.
Biomed Environ Sci ; 36(8): 715-724, 2023 Aug 20.
Artigo em Inglês | MEDLINE | ID: mdl-37711083

RESUMO

Objective: This study aimed to reveal the insomnia burden and relevant influencing factors among informal caregivers (ICs) of hospitalized patients with lung cancer. Methods: A cross-sectional study on ICs of hospitalized patients with lung cancer was conducted from December 31, 2020 to December 31, 2021. ICs' burden was assessed using the Caregiver Reaction Assessment (CRA), Hospital Anxiety and Depression Scale (HADS), and Insomnia Severity Index (ISI). Linear and logistic regression models were used to identify the influencing factors. Results: Among 289 ICs of hospitalized patients with lung cancer, 83 (28.72%), 53 (18.34%), and 14 (4.84%) ICs experienced mild, moderate, and severe insomnia, respectively. The scores concerning self-esteem, lack of family support, financial problems, disturbed schedule, and health problems were 4.32 ± 0.53, 2.24 ± 0.79, 2.84 ± 1.14, 3.63 ± 0.77, and 2.44 ± 0.95, respectively. ICs with higher Activities of Daily Living Scale (ADLS) scores were associated with a lower risk of insomnia, with an odd ratio ( OR) and 95% confidence interval ( CI) of 0.940 (0.898-0.983). Among the ICs, female gender ( OR = 2.597), alcohol consumption ( OR = 3.745), underlying medical conditions ( OR = 11.765), long-term caregiving experience ( OR = 37.037), and higher monthly expenses ( OR = 5.714) were associated with a high risk of insomnia. Conclusion: Of the hospitalized patients with lung cancer, 51.9% experienced insomnia. Patients' ADL, ICs gender, alcohol consumption, underlying medical conditions, caregiving duration, and monthly expenses were influencing factors. Therefore, prompt screening and early intervention for ICs of patients with lung cancer is necessary.


Assuntos
Neoplasias Pulmonares , Distúrbios do Início e da Manutenção do Sono , Humanos , Feminino , Cuidadores , Atividades Cotidianas , Estudos Transversais , Distúrbios do Início e da Manutenção do Sono/epidemiologia , Neoplasias Pulmonares/epidemiologia
2.
Cancer Biomark ; 34(1): 41-53, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-34542064

RESUMO

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.


Assuntos
Neoplasias do Colo , Neoplasias Colorretais , MicroRNAs , RNA Longo não Codificante , Linhagem Celular Tumoral , Neoplasias do Colo/tratamento farmacológico , Neoplasias do Colo/genética , Neoplasias Colorretais/tratamento farmacológico , Neoplasias Colorretais/genética , Neoplasias Colorretais/patologia , Fluoruracila/farmacologia , Fluoruracila/uso terapêutico , Glucose , Humanos , MicroRNAs/genética , MicroRNAs/metabolismo , Proteínas Quinases , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo
3.
World J Clin Cases ; 9(33): 10265-10272, 2021 Nov 26.
Artigo em Inglês | MEDLINE | ID: mdl-34904098

RESUMO

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.

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