OBJECTIVE: To investigate the efficiency of recombinant human epidermal growth factor (rhEGF) on burn wound healing and to explore the effective density of the ointments. METHODS: A total of 120 cases of burn in superficial II degree and profound II degree were randomly divided into 2 groups. In the first group of 15 cases of superficial II degree, the wounds were treated by rhEGF ointments of different density, 0.5 microgram/g, 10 micrograms/g and 50 micrograms/g, to screen out the effective density. And in the other 105 cases of the second group, optimal density of the ointments based on the result of the first group were employed to treat the burn wound in superficial II degree and profound II degree, with the self-corresponding wounds of the same degree as control, to study the efficiency of rhEGF on wound healing, according to the wound healing time, and adverse reaction of the ointment. RESULTS: In the first group, the average healing time of superficial II wound treated by ointments of 10 micrograms/g and 50 micrograms/g significantly shortened when compared with that treated by ointments of 0.5 microgram/g(P lt; 0.01), but there was no obvious difference between the cases treated by ointments of 10 micrograms/g and 50 micrograms/g. In the second group, the healing time of superficial II wound treated by ointments of 10 micrograms/g was (8.39 +/- 2.25) days, (9.52 +/- 2.56) days in the control (P lt; 0.01); and healing time of profound II burn treated by ointments of 10 micrograms/g was (16.80 +/- 2.99) days, (18.27 +/- 3.17) days in the control (P lt; 0.01). And healing rates of burn wound at different periods were higher than those of the control. CONCLUSION: The above results indicate that rhEGF ointments can enhance burn wound healing significantly, and the ointment of 10 micrograms/g is a good choice for clinical application.
Objective:To study the effects of growth factor on the proliferation of the cultured huamn retinal glial cells. Methods:EGF(0.5～100.0ng/ml) and NGF (0.5～10.0ng/ml) were added to cultures of human retinal glial cells and the proliferation rates of the cells were measured by MTT method. Results:EGF at a dosage ranging from 0.5ng/ml to 100.0ng/ml and NGF (0.05～10.0ng/ml) stimulated the cellular proliferation effectively with their EC 50 of 17ng/ml and 0.7 ng/ml respectively. Conclusion:Both EGF and NGF NGF had an effective stimulation on human retinal glial cell proliferation.They may play a role in the formation of PVR. (Chin J Ocul Fundus Dis,1998,14:33-34)
Objective To explore the effect of membrane surface nucleolin （NCL） on activation of epidermal growth factor receptor （EGFR） signaling. Methods Immunohistochemistry was used to identify the expressions of membrane surface NCL or EGFR in pallilary thyroid carcinoma （PTC） tissues. The level of phosphorlated EGFR in TPC-1 cells was observed by Western blot. TPC-1 cells invasion capacity was detected by Transwell assay. Results The posi-tive expression rates of membrane surface NCL and EGFR in PTC tissues were 100% （56/56） and 80.4% （45/56） respe-ctively， while the expressions of NCL and EGFR were related with lymph node metastasis （P＜0.05）. There was posi-tive correlation between the expressions of NCL and EGFR （r=0.635， P＜0.01）. Western blot showed that anti-NCL or anti-EGFR of TPC-1 cells could inhibit the expression of phosphorlation EGFR （P＜0.01）. Transwell assay showed the number of membrane-invading cells were reduced significantly in anti-NCL group anti-EGFR group （P＜0.01）. Conclusions Membrane surface NCL may be a kind of indispensable component in activation of EGFR signaling， by which EGFR can participate in growth and invasion of tumors. NCL can be used as a target for developing a new field of tumor treatment.
Objective To analyze the factors associated with the adoption of targeted therapy in patients with human epidermal growth factor receptor 2 (HER2)-positive breast cancer and to generate evidence to inform decision-making on public security policy regarding innovative anticancer medicines for the benefit of patients. Methods The study population comprised female patients diagnosed with HER2-positive breast cancer and treated at Fujian Cancer Hospital from 2014 to 2020. The patients were eligible for targeted therapy. The demographic and sociological characteristics and clinical information of patients were extracted from the hospital information system. We performed binary logistic regression analysis of factors associated with the adoption of targeted therapy in patients with HER2-positive breast cancer. We also divided the participants into two groups according to their tumor stage for subgroup analysis. Results A total of 1 041 female patients with HER2-positive breast cancer were included, among them, 803 received targeted therapy. In September 2017, molecular-targeted medicines for HER2-positive breast cancer began to be included in the local basic health insurance program. Only 282 (35.1%) patients adopted targeted therapy before September 2017, after which this number increased to 521 (64.9%). Among the patients who adopted targeted therapy, most were formally employed (45.8%) and enrollees of the urban employee health insurance program (66.0%). Among those who did not adopt targeted therapy, most were unemployed (42.4%) and enrollees of the resident health insurance program (50.0%). Binary logistic regression analysis revealed that patient occupation, gene expression of estrogen receptor, tumor stage, surgery or not, radiotherapy or not, and undergoing treatment before or after September 2017 were correlated with the adoption of targeted therapy (P<0.05). Conclusions Inclusion of targeted medicines for HER2-positive breast cancer in the health insurance program substantially increased the overall administration of these therapies. Individual affordability is a critical factor associated with the application of targeted therapy in eligible patients. Future policies should enhance the public security of patients with a relatively weak ability to pay and provide insurance coverage for innovative anti-cancer medicines.
【 Abstract 】 Objective Overexpressions of epidermal growth factor (EGF) and EGF receptor have been associated with progression and invasive phenotype of pancreatic cancer. However, the underlying molecular mechanism by which EGF worked in pancreatic cancer cells has not been completely understood. In this study, effect of EGF on the invasion and metastasis of pancreatic cancer cells and its regulatory mechanism were investigated. Methods The effects of EGF on the proliferation, adhesion and invasion of pancreatic cancer cells were detected by WST-1 proliferation assay, adhesion assay and invasive assay, respectively. The activity and expression of MMP-2 and MMP-9 were examined by zymography, Western blot and RT-PCR, respectively. The activity of NF- κ B was examined by EMSA. Results EGF could significantly promote the invasiveness of pancreatic cancer cells but did not affect cell proliferation or adhesion. The expressions of NF- κ B and MMP-9 were significantly increased by EGF, but EGF did not affect the activity and expression of MMP-2. Furthermore, EGF stimulated the NF- κ B binding activity. Pretreatment with NF- κ B inhibitors, pyrrolidine dithiocarbamate (PDTC), could significantly inhibit the activity of NF- κ B induced by EGF. Meanwhile, the EGF-induced expression and activity of MMP-9, as well as cell invasiveness were also inhibited by NF- κ B inhibitor. Conclusion EGF could increase the expression and promote the invasiveness of MMP-9 via the activation of NF- κ B in pancreatic cancer cells, which implies that NF- κ B inhibitant, such as PDTC, may diminish the invasiveness of pancreatic cancer cells.
Tyrosine kinase inhibitors (TKIs) are the standard of care for non-small cell lung cancer patients with epidermal growth factor receptor (EGFR) mutation. The efficacy of TKIs and prognosis of EGFR-mutated patients with compound EGFR mutation, oncogene mutation, suppresser gene mutation or other diver gene mutation are worse than those of patients with a single EGFR mutation. This article makes a review of related clinical researches aiming to provide references for clinical scenarios. To sum up, molecular alterations and clinical features should be correlated as accurately and dynamically as possible in the diagnostic and therapeutic process, and combined therapeutic strategies should be chosen flexibly and reasonably to improve patients’ survival and prognosis.
ObjectiveTo systematically evaluate the correlation of amplification of human epidermal growth factor receptor 2 (HER2) with the clinicopathological characteristics and prognosis of colorectal cancer patients.MethodsPubMed, EMbase, Cochrane Library, Chinese Biomedical Literature Database (CBM), Wanfang, and other databases were searched, and cohort studies focused on the relationship between HER2 amplification and clinicopathological characteristics and prognosis of colorectal cancer patients were included. The retrieval time limit was from October 2020, and RevMan 5.4 software was used for meta-analysis.ResultsA total of 9 studies (11 cohorts) were included for meta-analysis of 7 209 patients with colorectal cancer. Results of the meta-analysis showed that HER2 amplification was not associated with overall survival [HR=1.10, 95%CI (0.98, 1.24), P=0.11]. HER2 amplification was not correlated with gender [OR=0.98, 95%C1 (0.74, 1.31), P=0.90] and tumor differentiation [OR=0.80, 95%C1 (0.49, 1.32), P=0.39], but correlated with the tumor location [OR=1.85, 95%C1 (1.01, 3.37), P=0.04], RAS wild-type gene [OR=6.36, 95%C1 (3.41, 11.87), P<0.000 01], TNM stage [OR=0.45, 95%C1 (0.32, 0.64), P<0.000 01], lymph node metastasis [OR=1.54, 95%C1 (1.12, 2.13), P=0.008], and the depth of tumor invasion [OR=0.17, 95%C1 (0.05, 0.55), P=0.003].ConclusionCurrent evidence shows that HER2 amplification is not associated with OS in patients with colorectal cancer, but associated with tumor infiltration, lymph node metastasis, TNM stage, tumor site, and RAS genotype.