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1.
Front Med (Lausanne) ; 8: 741204, 2021.
Article in English | MEDLINE | ID: mdl-34805207

ABSTRACT

Cancer patients are at a high risk of being infected with COVID-19 and have a poor prognosis after infection. Breast cancer is one of the most common cancers. Since vaccination is an effective measure to prevent the spread of COVID-19, we studied the vaccination rate among breast cancer survivors and analyzed their characteristics to provide evidence for boosting the vaccination rate. The researchers conducted a multicenter, cross-sectional study on 747 breast cancer survivors from six hospitals in Wuhan city between June 5, 2021, and June 12, 2021. The self-administrated questionnaires based on relevant studies were distributed. The researchers then compared differences in characteristics among vaccinated patients, hesitant patients, and non-vaccinated patients. Moreover, they performed univariable and multivariable logistic regression analyses to identify potential factors associated with vaccination hesitancy. The researchers assessed a total of 744 breast cancer survivors -94 cases in the vaccinated group, 103 in the planning group, 295 in the hesitancy group, and 252 in the refusal group. The vaccination rate was 12.63% (95% CI 10.25-15.02%) and 37.23% (95% CI 27.48-47.82%) patients reported adverse reactions. The vaccination hesitancy/refusal rate was 73.52% (95% CI 70.19-76.66%), which was independently associated with current endocrine or targeted therapy (odds ratio [OR] = 1.52, 95% CI 1.03-2.24), no notification from communities or units (OR = 2.46, 95% CI 1.69-3.59) and self-perceived feel (general vs. good, OR = 1.46, 95% CI 1.01-2.13; bad vs. good, OR = 4.75, 95% CI 1.85-12.16). In the hesitancy/refusal group, the primary reason was "I did not know who to ask whether I can get vaccinated" (46.07%), the person who would most influence decisions of patients was the doctor in charge of treatment (35.83%). Effective interaction between doctors and patients, simple and consistent practical guidelines on vaccination, and timely and positive information from authoritative media could combat misinformation and greatly reduce vaccine hesitancy among breast cancer survivors.

2.
Oncol Lett ; 10(3): 1277-1280, 2015 Sep.
Article in English | MEDLINE | ID: mdl-26622663

ABSTRACT

Gefitinib is an epidermal growth factor receptor (EGFR) inhibitor, which is used to treat patients with advanced non-small cell lung cancer (NSCLC) harboring EGFR mutations. Dermatological reactions are the most common adverse events associated with gefitinib treatment; other adverse effects, including diarrhea, nausea, stomatitis and an asymptomatic elevation of liver enzymes have also been reported. The present study describes a patient with intestinal obstruction who was successfully undergoing treatment with gefitinib for primary and metastatic neoplasms. Gefitinib-induced intestinal obstruction has not been previously reported; therefore, careful monitoring of gastrointestinal symptoms should be conducted throughout the course of gefitinib-treated malignancies.

3.
Oncol Rep ; 32(6): 2687-95, 2014 Dec.
Article in English | MEDLINE | ID: mdl-25310770

ABSTRACT

Progestin and adipoQ receptor family member III (PAQR3) is a regulator that negatively modulates the Ras/Raf/MEK/ERK signaling cascade and the GPCR Gßγ subunit signaling pathway. The role of PAQR3 in hepatocellular carcinoma (HCC) has not been elucidated. The present study investigated the expression of PAQR3 and its prognostic value in primary HCC patients. Furthermore, the functional aspects of PAQR3 were also studied using an in vitro cell model. PAQR3 expression was examined in paired HCC and adjacent noncancerous tissues using real-time quantitative RT-PCR (62 pairs) and western blotting (26 pairs). We also analyzed PAQR3 expression in 132 additional HCC samples by immunohistochemistry. The functional impact of PAQR3 on the proliferation and colony formation of an HCC cell line was analyzed by transfecting cells with a full-length PAQR3 expression vector or siRNA targeting PAQR3. The expression of PAQR3 was significantly decreased in the cancer tissues. Clinicopathological analyses showed that the expression of PAQR3 was significantly correlated with expression of serum α-fetoprotein (AFP), mitotic count, tumor size, histological grade and recurrence. Notably, Kaplan-Meier survival curves revealed a correlation between decreased expression of PAQR3 and the poor prognosis of HCC patients. Multivariate analyses showed that PAQR3 expression is an independent prognostic marker for overall and disease-free survival of HCC patients. Furthermore, restoring PAQR3 expression in HCC cells significantly diminished Hep3B cell proliferation and colony formation. Silencing PAQR3 expression in hepatic normal cell line LO2 significantly enhanced cell growth. PAQR3 may play an important role in the progression of HCC and serve as a potential candidate for the targeted therapy of HCC.


Subject(s)
Carcinoma, Hepatocellular/genetics , Intracellular Signaling Peptides and Proteins/genetics , Liver Neoplasms/genetics , Membrane Proteins/genetics , Neoplasm Recurrence, Local/genetics , Receptors, Cell Surface/biosynthesis , Adult , Biomarkers, Tumor , Carcinoma, Hepatocellular/pathology , Cell Proliferation/genetics , Disease-Free Survival , Female , Gene Expression Regulation, Neoplastic , Genes, Tumor Suppressor , Hep G2 Cells , Humans , Liver Neoplasms/pathology , Male , Middle Aged , Receptors, Cell Surface/genetics , alpha-Fetoproteins/metabolism
4.
Eur J Ophthalmol ; 24(2): 279-81, 2014.
Article in English | MEDLINE | ID: mdl-24170512

ABSTRACT

PURPOSE: To observe the curative effect of Xeloda in meibomian gland carcinoma. METHODS: We treated a 53-year-old woman, who had recrudescent meibomian gland carcinoma, with Xeloda. RESULTS: The mass was much smaller with decreased amount of overflow pus after 4 cycles of chemotherapy with Xeloda. CONCLUSIONS: Xeloda played a significant role in treating recrudescent meibomian gland carcinoma in this patient.


Subject(s)
Adenocarcinoma, Sebaceous/drug therapy , Antimetabolites, Antineoplastic/therapeutic use , Deoxycytidine/analogs & derivatives , Eyelid Neoplasms/drug therapy , Fluorouracil/analogs & derivatives , Meibomian Glands/drug effects , Neoplasm Recurrence, Local/drug therapy , Adenocarcinoma, Sebaceous/diagnostic imaging , Adenocarcinoma, Sebaceous/secondary , Capecitabine , Deoxycytidine/therapeutic use , Eyelid Neoplasms/diagnostic imaging , Eyelid Neoplasms/pathology , Female , Fluorouracil/therapeutic use , Humans , Lymphatic Metastasis , Meibomian Glands/diagnostic imaging , Meibomian Glands/pathology , Middle Aged , Neoplasm Recurrence, Local/diagnostic imaging , Neoplasm Recurrence, Local/pathology , Prodrugs , Tomography, X-Ray Computed , Treatment Outcome
5.
J Huazhong Univ Sci Technolog Med Sci ; 33(6): 845-851, 2013 Dec.
Article in English | MEDLINE | ID: mdl-24337846

ABSTRACT

The effects of class I PI3K inhibitor NVP-BKM120 on cell proliferation, cell cycle distribution, cellular apoptosis, phosphorylation of several proteins of the PI3K/AKT signaling pathway and the mRNA expression levels of HIF1-α, VEGF and MMP9 in the acquired gefitinib resistant cell line H1975 were investigated, and whether NVP-BKM120 can overcome the acquired resistance caused by the EGFR T790M mutation and the underlying mechanism were explored. MTT assay was performed to detect the effect of gefitinib, NVP-BKM120, NVP-BKM120 plus 1 µmol/L gefitinib on growth of H1975 cells. The distribution of cell cycle and apoptosis rate of H1975 cells were examined by using flow cytometry. The mRNA expression levels of tumor-related genes such as HIF1-α, VEGF and MMP9 were detected by using real-time quantitative PCR. Western blotting was used to detect the expression level of phosphorylated proteins in the PI3K/AKT signaling pathway, such as Ser473-p-AKT, Ser235/236-p-S6 and Thr70-p-4E-BP1, as well as total AKT, S6 and 4E-BP1. The results showed that the NVP-BKM120 could inhibit the growth of H1975 cells in a concentration-dependent manner, and H1975 cells were more sensitive to NVP-BKM120 than gefitinib (IC50:1.385 vs. 15.09 µmol/L respectively), whereas combination of NVP-BKM120 and gefitinib (1 µmol/L) did not show more obvious effect than NVP-BKM120 used alone on inhibition of cell growth (P>0.05). NVP-BKM120 (1 µmol/L) increased the proportion of H1975 cells in G0-G1 phase and the effect was concentration-dependent, and 2 µmol/L NVP-BKM120 promoted apoptosis of H1975 cells. There was no significant difference in the proportion of H1975 cells in G0-G1 phase and apoptosis rate between NVP-BKM120-treated alone group and NVP-BKM120 plus genfitinib (1 µmol/L)-treated group or between DMSO-treated control group and gefitinib (1 µmol/L)-treated alone group (P>0.05 for all). It was also found that the mRNA expression levels of these genes were down-regulated by NVP-BKM120 (1 µmol/L), and NVP-BKM120 (1 µmol/L) or NVP-BKM120 (1 µmol/L) plus gefitinib (1 µmol/L) obviously inhibited the activation of Akt, S6 and 4E-BP1 as compared with control group, but single use of gefitinib (1 µmol/L) exerted no significant effect. These data suggested that NVP-BKM120 can overcome gefitinib resistance in H1975 cells, and the combination of NVP-BKM120 and gefitinib did not have additive or synergistic effects. It was also concluded that NVP-BKM120 could overcome the acquired resistance to gefitinib by down-regulating the phosphorylated protein in PI3K/AKT signal pathways in H1975 cells, but it could not enhance the sensitivity of H1975 cells to gefitinib.


Subject(s)
Aminopyridines/pharmacology , Antineoplastic Agents/pharmacology , Drug Resistance, Neoplasm/drug effects , Morpholines/pharmacology , Phosphoinositide-3 Kinase Inhibitors , Quinazolines/pharmacology , Adenocarcinoma/metabolism , Apoptosis/drug effects , Cell Line, Tumor , Cell Proliferation/drug effects , Gefitinib , Humans , Hypoxia-Inducible Factor 1, alpha Subunit/genetics , Hypoxia-Inducible Factor 1, alpha Subunit/metabolism , Lung Neoplasms/metabolism , Matrix Metalloproteinase 9/genetics , Matrix Metalloproteinase 9/metabolism , RNA, Messenger/genetics , RNA, Messenger/metabolism , Vascular Endothelial Growth Factor A/genetics , Vascular Endothelial Growth Factor A/metabolism
6.
J Huazhong Univ Sci Technolog Med Sci ; 33(5): 770-774, 2013 Oct.
Article in English | MEDLINE | ID: mdl-24142735

ABSTRACT

This study explored the role of radiation-induced autophagy in low-dose hyperradiosensitivity (HRS) in the human lung cancer cell line A549. A549 cells, either treated with an autophagic inhibitor 3-methyladenine (3-MA), or with a vehicle control, were irradiated at different low doses (≤0.5 Gy). The generation of autophagy was examined by laser scanning confocal microscopy. Western blotting was used to detect the expression of microtubule-associated protein l light chain 3B II (LC3B-II). Flow cytometry (FCM) and clonogenic assays were used to measure the fraction of surviving cells at the low irradiation doses. Our results showed that there was a greater inhibition of autophagic activity, but a higher degree of low-dose HRS in A549 cells treated with 3-MA than in control group. Our data demonstrated that radiation-induced autophagy is correlated with HRS in A549 cells, and is probably one of the mechanisms underlying HRS.


Subject(s)
Autophagy/radiation effects , Radiation Tolerance/radiation effects , Adenine/analogs & derivatives , Adenine/pharmacology , Autophagy/drug effects , Blotting, Western , Cell Line, Tumor , Cell Survival/drug effects , Cell Survival/radiation effects , Dose-Response Relationship, Radiation , Flow Cytometry , Green Fluorescent Proteins/genetics , Green Fluorescent Proteins/metabolism , Humans , Lung Neoplasms/genetics , Lung Neoplasms/metabolism , Lung Neoplasms/pathology , Microscopy, Confocal , Microscopy, Electron, Transmission , Microtubule-Associated Proteins/genetics , Microtubule-Associated Proteins/metabolism , Phagosomes/drug effects , Phagosomes/radiation effects , Phagosomes/ultrastructure , Radiation Tolerance/drug effects
7.
Zhonghua Zhong Liu Za Zhi ; 30(7): 552-4, 2008 Jul.
Article in Chinese | MEDLINE | ID: mdl-19062728

ABSTRACT

OBJECTIVE: To evaluate the efficacy of zoledronic acid combined with local radiotherapy for limited metastatic bone cancer. METHODS: Forty-five patients with limited bone metastatic cancers were randomly divided into two groups: 23 in the combination group who received intravenously administration of zoledronic acid and local radiotherapy, the other 22 in the radiotherapy alone group who underwent local radiotherapy only. RESULTS: The response rate of pain relief was 91.3% in the combination group versus 86.4% in the radiotherapy alone group, without statistically significant difference between two groups (P > 0.05). However, the recalcification rate was significantly higher in the combination therapy group (52.2%) than that in radiotherapy alone group (22.7% P < 0.01), and the proportion of patients with new bone metastasis formation was significantly lower in the combination group (13.0%) than that in the radiotherapy alone group (40.9%, P < 0.05). The common side-effects were transient pyrexia and nausea. CONCLUSION: Zoledronic acid combined with local radiotherapy is effective in relieving pain, improving bone recalcification and reducing the formation of new bone metastasis.


Subject(s)
Bone Density Conservation Agents/therapeutic use , Bone Neoplasms/drug therapy , Bone Neoplasms/secondary , Diphosphonates/therapeutic use , Imidazoles/therapeutic use , Pain Management , Adult , Aged , Bone Neoplasms/complications , Bone Neoplasms/radiotherapy , Bone Regeneration/drug effects , Breast Neoplasms/pathology , Combined Modality Therapy , Female , Humans , Lung Neoplasms/pathology , Male , Middle Aged , Nasopharyngeal Neoplasms/pathology , Pain/etiology , Radiotherapy , Zoledronic Acid
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