Expression of p53, Ki-67, and EGFR in odontogenic keratocysts before and after decompression

2006 ◽  
Vol 35 (9) ◽  
pp. 568-572 ◽  
Author(s):  
Pia Clark ◽  
Peter Marker ◽  
Henning Lehmann Bastian ◽  
Annelise Krogdahl
Keyword(s):  
Ki 67 ◽  
Odontogenic Keratocysts ◽  
Before And After

scholarly journals Changes in Cellular Regulatory Factors before and after Decompression of Odontogenic Keratocysts

2020 ◽  
Vol 10 (1) ◽  
pp. 30
Author(s):  
Slmaro Park ◽  
Han-Sung Jung ◽  
Young-Soo Jung ◽  
Woong Nam ◽  
Jung Yul Cha ◽  
...  
Keyword(s):  
Recurrence Rate ◽  
Biological Behavior ◽  
Nuclear Antigen ◽  
Epithelial Cyst ◽  
Ki 67 ◽  
Proliferation Markers ◽  
Odontogenic Keratocysts ◽  
Wide Range ◽  
Before And After ◽  
Cyst Lining

Decompression followed by enucleation, which is one of the treatments used for odontogenic keratocysts (OKCs), is frequently used in OKC lesions of large sizes. This method offers the advantage of minimizing the possibility of sensory impairment without creating a wide-range bone defect; moreover, the recurrence rate can be significantly lower than following simple enucleation. This study aimed to assess the changes in histology and expression of proliferation markers in OKCs before and after decompression treatment. A total of 38 OKC tissue samples from 19 patients who had undergone decompression therapy were examined morphologically and immunohistochemically to observe changes in proliferative activity before and after decompression. The markers used for immunohistochemistry (IHC) staining were Bcl-2, epidermal growth factor receptor (EGFR), Ki-67, P53, PCNA, and SMO. The immunohistochemistry positivity of the 6 markers was scored by using software ImageJ, version 1.49, by quantifying the intensity and internal density of IHC-stained epithelium. The values of Bcl-2, Ki-67, P53, proliferating cell nuclear antigen (PCNA), and SMO in OKCs before and after decompression showed no significant change. No correlation between clinical shrinkage and morphologic changes or expression of proliferation and growth markers could be found. There was no statistical evidence that decompression treatment reduces potentially aggressive behavior of OKC within the epithelial cyst lining itself. This might indicate that decompression does not change the biological behavior of the epithelial cyst lining or the recurrence rate.

Antitumor effects of Auraptene in 4T1 tumor‐bearing Balb/c mice

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Mohammad Reza. Shiran ◽  
Davar Amani ◽  
Abolghasem Ajami ◽  
Mahshad Jalalpourroodsari ◽  
Maghsoud Khalizadeh ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Body Weight ◽  
Tumor Volume ◽  
Serum Levels ◽  
Ki 67 ◽  
Tumor Bearing ◽  
Paraffin Oil ◽  
Anti Cancer ◽  
Before And After ◽  
Ifn Γ

Abstract Objectives Breast cancer is a common malignant tumor in women with limited treatment options and multiple side effects. Today, the anti-cancer properties of natural compounds have attracted widespread attention from researchers worldwide. Methods In this study, we treated 4T1 tumor-bearing Balb/c mice with intraperitoneal injection of Auraptene, paraffin oil, and saline as two control groups. Body weight and tumor volume were measured before and after treatment. Hematoxylin and eosin (H & E) staining and immunohistochemistry of Ki-67 were used as markers of proliferation. In addition, ELISA assays were performed to assess serum IFN-γ and IL-4 levels. Results There was no significant change in body weight in all animal groups before and after treatment. 10 days after the last treatment, Auraptene showed its anti-cancer effect, which was confirmed by the smaller tumor volume and H & E staining. In addition, Ki-67 expression levels were significantly reduced in tumor samples from the Auraptene-treated group compared to the paraffin oil and saline-treated groups. In addition, in tumor-bearing and normal mice receiving Auraptene treatment, IL-4 serum production levels were reduced, while serum levels of IFN-γ were significantly up-regulated in tumor-bearing mice after Auraptene treatment. Conclusions In the case of inhibition of tumor volume and Ki-67 proliferation markers, Auraptene can effectively inhibit tumor growth in breast cancer animal models. In addition, it might increases Th1 and CD8 + T cell responses after reducing IL-4 serum levels and IFN-γ upregulation, respectively. However, further research is needed to clarify its mechanism of action.

scholarly journals The Change of Soluble Programmed Cell Death-Ligand 1 (sPD-L1) in Glioma Patients Receiving Radiotherapy and Its Impact on Clinical Outcome

2020 ◽  
Author(s):  
Xing-chen Ding ◽  
Liang-liang Wang ◽  
Yu-fang Zhu ◽  
Jia Yang ◽  
Jin-ming Yu ◽  
...  
Keyword(s):  
Checkpoint Inhibitors ◽  
Progression Free Survival ◽  
Enzyme Linked Immunosorbent Assay ◽  
Murine Models ◽  
Isocitrate Dehydrogenase 1 ◽  
Ki 67 ◽  
Kaplan Meier ◽  
Programmed Death ◽  
Potential Biomarker ◽  
Before And After

Abstract Background: It has been proved that the levels of soluble programmed death-ligand 1 (sPD-L1) are associated with prognosis in extracranial malignancies. However, the expression of sPD-L1 in glioma patients receiving radiotherapy (RT) still remains unclear.The purpose of this study is to evaluate the concentration of sPD-L1in the plasma of glioma patients before and after RT, and to explore its relationship with clinical outcomes.Methods: Between October 2017 and September 2018, the glioma patients treated with RT (30 ± 10 Gy, 2 Gy/f) were enrolled and the blood samples were collected before and after RT. We quantified the sPD-L1 levels by enzyme-linked immunosorbent assay (ELISA). The isocitrate dehydrogenase-1 (IDH-1) promoter status and Ki-67 expression were evaluated by immunohistochemistry. The murine models of glioma were used to address whether circulating sPD-L1 molecules are directly targeted by the anti-PD-L1 antibody. The associations between sPD-L1 and clinical features were assessed with Pearson or Spearman correlation. The progression-free survival (PFS) and overall survival (OS) were determined by Kaplan-Meier method.Results: Sixty glioma patients were included, with the median age 52-year-old. The proportion of grade I, II, III, IV were 6.7%, 23.3%, 28.4% and 41.6%, respectively. The baseline sPD-L1 levels were significantly associated with tumor grades, IDH-1 mutation status and Ki-67 expression. Using 14.35 pg/mL as the cutoff, significantly worse PFS and OS were both observed in patients with higher baseline level of sPD-L1 (P = 0.027, 0.008, respectively). RT significantly increased the mean level of sPD-L1 (P < 0.001). Further analysis showed that increased level of sPD-L1 in IDH-1 mutation patients was higher than that in wide-type ones. Furthermore, the murine models of glioma indicate that sPD-L1 can be blocked by anti-PD-L1 antibody. Conclusion: This study reported that sPD-L1 might be a potential biomarker to predict the outcome in glioma receiving RT. The elevated level of sPD-L1 after RT suggested that the strategy of combination with immune checkpoint inhibitors and RT might be promising for glioma, especially for patients with IDH-1 mutation.

The changes in expression of ICAM-3, Ki-67, PCNA, and CD31 in psoriatic lesions before and after methotrexate treatment

2005 ◽  
Vol 297 (6) ◽  
pp. 249-255 ◽  
Author(s):  
Ayca Cordan Yazici ◽  
Umit Tursen ◽  
Duygu Dusmez Apa ◽  
Guliz Ikizoglu ◽  
Hale Api ◽  
...  
Keyword(s):  
Ki 67 ◽  
Before And After ◽  
Methotrexate Treatment ◽  
Psoriatic Lesions

Phase II breast cancer chemoprevention study with celecoxib in women at increased risk for breast cancer

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 1010-1010
Author(s):  
B. Arun ◽  
V. Valero ◽  
G. Yin ◽  
G. Babiera ◽  
J. L. Murray ◽  
...  
Keyword(s):  
Breast Cancer ◽  
High Risk ◽  
Atypical Hyperplasia ◽  
Post Treatment ◽  
Short Term ◽  
Ki 67 ◽  
High Risk Women ◽  
Before And After ◽  
The Difference ◽  
Er Expression

1010 Background: Short-term chemoprevention trials offer a convenient model to screen chemopreventive agents and identify endpoint biomarkers. One of the potential agents is celecoxib (C), which has antiproliferative and apoptosis inducing properties. In this prospective study, our primary aim was to evaluate changes in proliferation induced by C in breast tissue of high risk women. Here, we report changes in estrogen receptor (ER) proliferation index. Methods: 42 eligible high risk women were enrolled into the study, underwent fine needle aspiration (FNA) and started celecoxib treatment at 400 mg BID. Median age: 51.9 years. Risk factors: Gail risk > 1.67% (n=13), lobular carcinoma insitu (n=13), atypical hyperplasia (n=11), previous history of breast cancer (n=5). For ER and Ki-67 testing, thin preparations slides were incubated with primary mouse monoclonal antibody 6F11 against the ER and clone MIB-1, respectively. Appropriate negative and positive controls were included. At least 100 epithelial cells were evaluated per slide. Immunoreactivity for each marker was scored as the percentage of positive nuclei. We assessed the difference in ER and Ki-67 levels before and after treatment using a Wilcoxon signed rank test. Results: The average pre-treatment ER expression in FNA samples was 35.9% and Ki-67 was 2.4%. 19 (45%) showed hyperplasia or atypical hyperplasia. 39 patients underwent also post-treatment FNAs. The pre-and post treatment ER expression in this group was 35.7% (range 0–100%) and 27.4% (range: 0–100%), respectively. The difference in ER levels was statistically significant (p = 0.04). Twenty-six patients had Ki-67 levels measured both before and after treatment. The median difference in Ki-67 levels was 0 (range 0- 5). This change was not statistically significant (p = 0.63). Conclusions: We have completed accrual to a prospective short-term chemoprevention trial with celecoxib. We have found a significant downregulation of ER expression with 6 months celecoxib. Since ER expression is a marker of proliferation, this finding confirms celecoxibs antiproliferative properties. Currently, we have not observed a change in Ki-67; this could be partly due to the small number of samples and the fact that Ki-67 is low in normal epithelium. [Table: see text]

scholarly journals Prospective Monitoring of Circulating Epithelial Tumor Cells (CETC) Reveals Changes in Gene Expression during Adjuvant Radiotherapy of Breast Cancer Patients

2021 ◽  
Vol 28 (5) ◽  
pp. 3507-3524
Author(s):  
Matthias Mäurer ◽  
Katharina Pachmann ◽  
Thomas Wendt ◽  
Dorothea Schott ◽  
Andrea Wittig
Keyword(s):  
Breast Cancer ◽  
Single Cell ◽  
Tumor Cells ◽  
Early Stage ◽  
Breast Cancer Patients ◽  
Ki 67 ◽  
Epithelial Tumor ◽  
Before And After ◽  
Epithelial Tumor Cells ◽  
Cell Expression

Circulating epithelial tumor cells (CETC) are considered to be responsible for the formation of metastases. Therefore, their importance as prognostic and/or predictive markers in breast cancer is being intensively investigated. Here, the reliability of single cell expression analyses in isolated and collected CETC from whole blood samples of patients with early-stage breast cancer before and after radiotherapy (RT) using the maintrac® method was investigated. Single-cell expression analyses were performed with qRT-PCR on a panel of selected genes: GAPDH, EpCAM, NANOG, Bcl-2, TLR 4, COX-2, PIK3CA, Her-2/neu, Vimentin, c-Met, Ki-67. In all patients, viable CETC were detected prior to and at the end of radiotherapy. In 7 of the 9 (77.8%) subjects examined, the CETC number at the end of the radiotherapy series was higher than before. The majority of genes analyzed showed increased expression after completion of radiotherapy compared to baseline. Procedures and methods used in this pilot study proved to be feasible. The method is suitable for further investigation of the underlying molecular biological mechanisms occurring in cells surviving radiotherapy and possibly the development of radiation resistance.

Impact of biomarkers in predictivity of the efficacy and toxicity of a combination of panitumumab plus FEC 100 followed by docetaxel in a phase II neoadjuvant trial for triple-negative breast cancer (TNBC) patients.

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. 1051-1051
Author(s):  
Jean-Marc A. Nabholtz ◽  
Marie-Melanie Dauplat ◽  
Catherine Abrial ◽  
Beatrice E. Weber ◽  
Marie-Ange Mouret-Reynier ◽  
...  
Keyword(s):  
Ductal Carcinoma ◽  
Skin Toxicity ◽  
Ki 67 ◽  
Cutaneous Toxicity ◽  
Before And After ◽  
Hand Foot Syndrome ◽  
Grade Ii ◽  
Cutaneous Toxicities ◽  
Grade Iii

1051 Background: We evaluated the combination of a standard chemotherapy with panitumumab as neoadjuvant therapy of operable TNBC. Complete pathologic response (pCR) was the primary endpoint, with toxicity and biologic ancillary studies as secondary endpoints. Methods: Sixty patients with stage II-IIIA disease were prospectively included in this multicentre pilot study. Systemic therapy (ST) consisted of 4 cycles of FEC 100 (500/100/500 mg/m2) q.3 weeks followed by 4 cycles of T (100 mg/m2) q.3 weeks, in combination with panitumumab (9 mg/kg) for 8 cycles q.3 weeks. All patients underwent surgery at completion of ST. Paraffin-embedded samples and frozen samples have been systematically realised before and after neaodjuvant treatment in order to evalutate the biological profile of the tumor. Patients characteristics are : median age 50 ; median tumor size : 40 mm ; invasive ductal carcinoma : 96% ; Scarff-Bloom-Richardson Grade III : 70%, grade II : 30%, ki-67-positive : 100%, EGFR-positive : 78%, cytokeratine5-6-positive : 48% and p53-positive : 59%. Pathological response showed a pCR according to Sataloff’s classification of 52.38% and according to Chevallier’s classification of 46.52%. Skin toxicity was the main side-effect : Cutaneous toxicity grade IV : 5%, grade III : 30%, grade II : 20%. Neutropenia grade IV : 27% ; febrile neutropenia : 5%. Infection : 0%. Hand-foot syndrome grade III : 3.3%. Ungueal toxicity grade III : 1.6%, grade II : 20%. Results: We have tested the predictive value of ki-67, EGFR, cytokeratine 5-6 and p53. Only ki-67 is predictive of a pCR according to Chevallier’s classification (p=0.026), with a cut-off of 40% of positive cells (ROC curve): 62% of pCR if ki-67> 40% versus 23% if not (relative risk : 2.7). Low EGFR, high p53, and high cytokeratine 5-6 tended to be associated with poor reponse. No correlations were found between cutaneous toxicities and these biomarkers. The cutaneous toxicities were not predictive. Conclusions: HighKi-67 is predictive of more pCR. High EGFR, low p53 and low cytokeratine 5-6 tended to be associated with better response, but the data are not significant.

Dynamic molecular changes with VEGF targeted therapy in metastatic clear cell renal cancer.

2013 ◽  
Vol 31 (6_suppl) ◽  
pp. 437-437 ◽  
Author(s):  
Thomas Powles ◽  
Kevin Sharpe ◽  
Dan Berney ◽  
Irfan Kayani ◽  
Rukma Doshi ◽  
...  
Keyword(s):  
Targeted Therapy ◽  
Renal Cancer ◽  
Fdg Pet ◽  
Clear Cell ◽  
Ki 67 ◽  
Molecular Changes ◽  
Immune Parameters ◽  
Before And After ◽  
Metastatic Sites ◽  
Cell Renal Cancer

437 Background: The purpose of this study was to investigate for specific molecular changes associated with VEGF targeted in metastatic clear cell renal cancer (mRCC). This was achieved by taking tissue before and after VEGF TKI therapy. Methods: The study combined the data from 3 similar phase II prospective studies, investigating the role of VEGF therapy (pazopanib or sunitinib) prior to planned nephrectomy in untreated mRCC. A structured treatment break occurred during the planned nephrectomy (4 weeks). Paired tumour samples before and after 12-16 weeks of pazopanib or sunitinib were collected from these studies. Histopathology assessment (Furman grade, Ki-67, vascular density [CD31]), growth factor expression [FGF-2, c-MET, S-6-protein kinase] and immune parameters (CD3, 4, 8, PDL-1, FOXP3) before and after therapy were compared. Sequential functional imaging [FDG-PET] was performed to address the relationship between the primary tumour and metastatic sites. Results: Overall 62 patients had sequential tissue taken from these 3 prospective trials. Adequate quantities of sequential tissue were available from 48 patients. Pathological examination of the matched pairs before and after VEGF TKI showed a significant increase in tumour grade, Ki-67, lymphocyte infiltrate, and necrosis (p>0.05), there was also a significant decrease in CD31 (p<0.05). Significant changes to FGF-2, c-MET and FOXP3 expression was seen in the treated samples (p<0.05). FDG-PET results from 23 patients showed a significant correlation in the response seen in the primary renal tumour and metastatic sites with sunitinib (r=0.46 p<0.001). During the structured treatment break for nephrectomy (4 weeks) 37% of patients had disease progression (RECIST v1.1) underlining the aggressive nature of the disease after VEGF TKI therapy. This was associated with an increased risk of death on multivariate analysis (HR: 3.17; 95% CI, 1.46-6.86, p<0.03). Conclusions: These results suggest VEGF targeted therapy is associated with a more aggressive tumor phenotype. Changes to immune parameters and up regulation of growth factors potentially implicated in resistance to VEGF targeted therapy occurred.

scholarly journals Markers of cell proliferation in a GH-producing adenoma of a patient treated with pegvisomant

2005 ◽  
Vol 153 (2) ◽  
pp. 203-205 ◽  
Author(s):  
W M Drake ◽  
D M Berney ◽  
K Kovacs ◽  
J P Monson
Keyword(s):  
Cell Proliferation ◽  
Cellular Proliferation ◽  
Single Case ◽  
Tumour Size ◽  
Pituitary Tumour ◽  
Labelling Index ◽  
Ki 67 ◽  
Before And After ◽  
Gh Receptor Antagonist ◽  
Serum Gh

We report our findings on markers of cell proliferation (Ki-67 labelling index and topoisomerase-α expression) in a somatotroph pituitary tumour before and after exposure to pegvisomant, a GH receptor antagonist developed for the treatment of acromegaly. Specimens from two separate pituitary operations, separated by a period of 17 years that included 4 years of pegvisomant treatment, were stained for markers of cellular proliferation. Ki-67 labelling index and topoisomerase-α expression were both markedly greater (1–3% compared with 0–0.5% and 15–80% compared with 2–10% respectively) in the pegvisomant-exposed tumour compared with the earlier specimen. Clearly, caution must be exercised when interpreting findings from a single case, particularly one sufficiently refractory to conventional therapies to require treatment with pegvisomant. However, our data reinforce the requirement for careful radiological surveillance of the pituitary in the context of a drug that does not target the tumour responsible and where serum GH cannot serve as a marker of disease activity or tumour size.

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