Correlation between Cell Proliferation with Cervical Lymphoid Node Status in Nasopharyngeal Carcinoma Patients

Several studies showed that the index of nasopharyngeal carcinoma (NPC) cell growth could be used to assess the carcinogenesis interaction factor, development and prognosis of NPC. Cell proliferation index could always be assessed with Ki-67 protein expression test. This research was conducted to study the correlation between cell proliferation index with cervical lymphoid node status in NPC in clinical manifestation to asses the progressivity and prognosis on NPC patients. This study used cross sectional design. Biopsy tissue specimen were acquired from 35 NPC patients clinically divided into four criteria of cervical lymphoid node status (N0, N1, N2 and N3). Expression of Ki-67 protein was acquired by immunohistochemistry test using monoclonal rabbit antibody anti-human Ki-67 clone 901-325-091911 (Biocare Medical, LCC. 4040 Pike Line, CA 94520 USA). The measurement of Ki-67 protein was conducted by pathology consultant. Spearman statistic test was performed to asses the correlation between Ki-67 protein expression and cervical lymphoid node status. The statistical significance was defined as p<0.05. Positive expression of Ki-67 protein was found in 33 patients; 4 patients with N0 (11.43%), 5 patients with N1 (14.29%), 9 patients with N2 (25.71%), and 15 patients with N3. Negative expression of Ki-67 protein was found in 2 patients with N0 (5.71%). The Spearman test resulted at p=0.0001 with correlation coefficient of 0.758. The correlation between Ki-67 protein expression with cervical lymphoid node resulted in a significant correlation (p<0.05). In conclusion, cell proliferation index has correlation with cervical lymphoid node status in NPC patients.

Expression of Osteopontin and Cyclooxygenase-2 in relation to cellular proliferation, in non-tumor colonic mucosa, colonic adenomas and colon adenocarcinoma

Introduction: the participation of Cyclooxygenase-2 (COX-2) and Osteopontin has been postulated in the development of colon cancer, which play an important role in the progression and could be biomarkers for its prognosis, but their role remains controversial. Objective: to determine and to compare the expression of Osteopontin and COX-2 in non-tumor colonic mucosa, colonic adenomas and colon adenocarcinoma, in relation to the cell proliferation index. Methods: the immunohistochemical expression of COX-2, Osteopontin and Ki-67 in formalin fixed paraffin embedded tissue of non-tumor colonic mucosa, colonic adenomas and colon adenocarcinoma were determined and compared. Results: were included 65 cases: 19 of non-tumor colonic mucosa, 13 colonic adenomas and 33 colon adenocarcinomas. There was increased expression of Ki-67 in dysplastic and tumor cells. There was positive expression for COX-2 in adenomas (30.7%) and adenocarcinomas (27.3%), without significant difference between non- tumor colonic mucosa, adenomas and adenocarcinoma (p = 0.888). Osteopontin showed more frequent positivity in adenocarcinomas (72.7%) and adenomas (84.6%) than in non-tumor mucosa (10.5%), (p = <0.0001), without significant differences in its expression between subtypes and grades of adenoma dysplasia, nor between grades of differentiation, extension and proliferation of adenocarcinomas. There was a significant association between Osteopontin expression and the cell proliferation index. No association was observed between the expression of COX-2 and Osteopontin (p = 0.96). Conclusions: Osteopontin overexpression in colon adenocarcinoma and adenomas in comparison with non-tumor colonic mucosa, and its significant relationship with the cell proliferation index, constitutes additional evidence of its possible participation in the colonic carcinogenesis process.

Current Paradigm of Treatment for Pancreatic Neuroendocrine Tumor

Pancreatic neuroendocrine tumor (PNET) refer to tumors originating from the islet of Langerhans and shows various prognosis based on the presence or absence of symptoms due to hormone secretion, the Ki-67 cell proliferation index, and the histologic grade, and according to the degree of disease progression defined by the tumor-node-metastasis (TNM) stage classification. The purpose of medical treatment for PNET is to control symptoms or inhibit tumor growth. Somatostatin analogues can be administered for the purpose of controlling symptoms caused by the secretion of specific hormones, and are accepted as effective drugs for inhibiting the progression of G1/G2 tumors based on World Health Organization (WHO) classification with a Ki-67 cell proliferation index less than 20%. Among the molecularly targeted agents, everolimus and sunitinib can be considered in patients with WHO G1/G2 PNET showing progression after somatostatin analog therapy. Cytotoxic chemotherapy is generally administered to patients with large tumor volume and rapidly progressing metastatic NET, and etoposide/cisplatin combination therapy has been considered as a standard treatment. For the patient group of Grade 3 PNET (well differentiated) newly classified by the WHO 2017 classification, guidelines for standard treatment have not yet been established. As it has been reported, studies are needed to evaluate the treatment response rate of somatostatin analogues or molecularly targeted therapies for the patient with Grade 3 PNET. It is important to consider a multidisciplinary approach with all possible treatment options including medical treatment, radical resection of primary or metastatic lesions, liver-directed therapies, and peptide receptor radionuclide therapy for the patients with PNET.

The Effect of Ethynil Estradiol and Desogestrel on Proliferation and Apoptosis Hydatidiform Mole Trophoblast Cell

Background: To explore the effect of ethynil estradiol and desogestrel on proliferation and apoptosis hydatidiform mole trophoblast cell. Methods: From April 2008 until March 2009, we collected 15 samples of hydatidiform mole tissue. Trophoblast cells was isolated and culture at RPMI 20% FBS medium. Only 7 samples (46%) shown good growth. Cell was identified using cytology and β HCG test. Trophoblast cells good quality than devided into three groups observation. First group get ethynil estradiol 10 nmol/mL, second group get desogestrel 100 nmol/mL, Third group get DMSO 1%. Cells incubated and observe at 24, 48, 72, 96 hours. Cell cycle, apoptosis and β HCG was evaluated at each time observation. Cell cycle evaluation using BD cycle test plus DNA reagent, apoptosis evaluation using FITC-Annexin V. Analyze using FACSCalibur flowcytometer. β HCG evaluation using Abbott AxSym total β-HCG reagent pack. Results: The group of cell that get ethynil estradiol in concentration 10 nmol/mL had cell proliferation index, amount cells and β HCG level higher than control after 72 hours observation. The group of cell that get desogestrel in concentration 100 nmol/mL have cell proliferation index, amount cells and β HCG level lower than control after 48 hours observation. There are no differences of apoptosis between the two group and control. Conclusion: Ethynil estradiol will increase proliferation of hydatidiform mole trophoblast cell, while desogestrel will decrease proliferation of hydatidiform mole trophoblast cell. There are no effect of ethynil estradiol and desogestrel on apoptosis of hydatidiform mole trophoblast cell.

The Effect of Ethynil Estradiol and Desogestrel on Proliferation and Apoptosis Hydatidiform Mole Trophoblast Cell

A B S T R A C TIntroduction To explore the effect of ethynil estradiol and desogestrel onproliferation and apoptosis hydatidiform mole trophoblast cell. Methods: From April2008 until March 2009, we collected 15 samples of hydatidiform mole tissue.Trophoblast cells was isolated and culture at RPMI 20% FBS medium. Only 7samples (46%)shown good growth. Cell was identified using cytology and β HCG test.Trophoblast cells good quality than devided into three groups observation. Firstgroup get ethynil estradiol 10 nmol/mL, second group get desogestrel 100 nmol/mL,Third group get DMSO 1%. Cells incubated and observe at 24, 48, 72, 96 hours. Cellcycle, apoptosis and β HCG was evaluated at each time observation. Cell cycleevaluation using BD cycle test plus DNA reagent, apoptosis evaluation using FITC-Annexin V. Analyze using FACSCalibur flowcytometer. β HCG evaluation usingAbbott AxSym total β-HCG reagent pack. Results: The group of cell that get ethynilestradiol in concentration 10 nmol/mL had cell proliferation index, amount cells andβ HCG level higher than control after 72 hours observation. The group of cell thatget desogestrel in concentration 100 nmol/mL have cell proliferation index, amountcells and β HCG level lower than control after 48 hours observation. There are nodifferences of apoptosis between the two group and control. Conclusion: Ethynilestradiol will increase proliferation of hydatidiform mole trophoblast cell, whiledesogestrel will decrease proliferation of hydatidiform mole trophoblast cell. Thereare no effect of ethynil estradiol and desogestrel on apoptosis of hydatidiform moletrophoblast cell.

Metaphase cytogenetics and plasma cell proliferation index for risk stratification in newly diagnosed multiple myeloma

Metaphase cytogenetic abnormalities, plasma cell proliferation index (PCPro), and gain 1q by fluorescence in situ hybridization (FISH) are associated with inferior survival in newly diagnosed multiple myeloma (MM) treated with novel agents; however, their role in risk stratification is unclear in the era of the revised International Staging System (R-ISS). The objective of this study was to determine if these predictors improve risk stratification in newly diagnosed MM when accounting for R-ISS and age. We studied a retrospective cohort of 483 patients with newly diagnosed MM treated with proteasome inhibitors and/or immunomodulators. On multivariable analysis, R-ISS, age, metaphase cytogenetic abnormalities (both in aggregate and for specific abnormalities), PCPro, and FISH gain 1q were associated with inferior progression-free (PFS) and overall survival (OS). We devised a risk scoring system based on hazard ratios from multivariable analyses and assigned patients to low-, intermediate-, and high-risk groups based on their cumulative scores. The addition of metaphase cytogenetic abnormalities, PCPro, and FISH gain 1q to a risk scoring system accounting for R-ISS and age did not improve risk discrimination of Kaplan-Meier estimates for PFS or OS. Moreover, they did not improve prognostic performance when evaluated by Uno’s censoring-adjusted C-statistic. Lastly, we performed a paired analysis of metaphase cytogenetic and interphase FISH abnormalities, which revealed the former to be insensitive for the detection of prognostic chromosomal abnormalities. Ultimately, metaphase cytogenetics lack sensitivity for important chromosomal aberrations and, along with PCPro and FISH gain 1q, do not improve risk stratification in MM when accounting for R-ISS and age.

Analysis of cell proliferation index using the Ki-67 Antigen in odontogenic keratocyst: a systematic review

Objetivo: analisar artigos científicos sobre o índice de proliferação celular usando o anticorpo anti-Ki-67 em ceratocistos odontogênicos e comparar esses trabalhos para estimar um índice médio para essa lesão. Material e Métodos: dois pesquisadores realizaram a busca literária de forma independente na base de dados MEDLINE/PubMed e 28 artigos contendo dados relevantes foram selecionados. Resultados: a análise imuno-histoquímica utilizada nos artigos avaliados mostrou-se muito variável, não apresentando metodologias claras e unificadas, tornando a comparação entre os diferentes resultados difícil. Conclusão: Considerando o ceratocisto odontogênico uma lesão de comportamento clínico incomum, uma classificação adequada é necessária, assim como um tratamento apropriado com um bom prognostico deve ser estabelecido para o paciente de acordo com sua natureza. Dessa forma, um protocolo de análise imuno-histoquímica deve ser estabelecido para que possamos obter dados confiáveis sobre essa lesão

H. PYLORI INFECTION, ENDOSCOPIC, HISTOLOGICAL ASPECTS AND CELL PROLIFERATION IN THE GASTRIC MUCOSA OF PATIENTS SUBMITTED TO ROUX-EN-Y GASTRIC BYPASS WITH CONTENTION RING: a cross sectional endoscopic and immunohistochemical study

ABSTRACT Background Morbid obesity treatment through vertical gastroplasty Roux-en-Y gastric bypass initially used a contention ring. However, this technique may create conditions to the development of potentially malign alterations in the gastric mucosa. Although effective and previously performed in large scale, this technique needs to be better evaluated in long-term studies regarding alterations caused in the gastric mucosa. Objective To analyze the preoperative and postoperative endoscopic, histological and cell proliferation findings in the gastric antrum and body mucosa of patients submitted to the Roux-en-Y gastric bypass with a contention ring. Methods We retrospectively evaluated all patients submitted to Roux-en-Y gastric bypass with a contention ring with more than 60 months of postoperative follow-up. We compared the preoperative (gastric antrum and body) and postoperative (gastric pouch) gastric mucosa endoscopic findings, cell proliferation index and H. pylori prevalence. We evaluated cell proliferation through Ki-67 antibody immunohistochemical expression. Results In the study period, 33 patients were operated with the Roux-en-Y gastric bypass using a contention ring. We found a chronic gastritis rate of 69.7% in the preoperative period (gastric antrum and body) and 84.8% in the postoperative (gastric pouch). H. pylori was present in 18.2% of patients in the preoperative period (gastric antrum and body) and in 57.5% in the postoperative (gastric pouch). Preoperative cell proliferation index was 18.1% in the gastric antrum and 16.2% in the gastric body, and 23.8% in the postoperative gastric pouch. The postoperative cell proliferation index in the gastric pouch was significantly higher (P=0.001) than in the preoperative gastric antrum and body. Higher cell proliferation index and chronic gastritis intensity were significantly associated to H. pylori presence (P=0.001 and P=0.02, respectively). Conclusion After Roux-en-Y gastric bypass with contention ring, there was a higher chronic gastritis incidence and higher cell proliferation index in the gastric pouch than in the preoperative gastric antrum and body. Mucosa inflammation intensity and cell proliferation index in the postoperative gastric pouch were associated to H. pylori presence and were higher than those found in the preoperative gastric antrum and body mucosa.