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

2021 ◽  
Vol 5 (2) ◽  
pp. 312-319
Author(s):  
Irawan Sastradinata ◽  
Andrijono ◽  
Mohamad Farid Aziz ◽  
Wan Lelly H ◽  
Sri Hartini ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Hydatidiform Mole ◽  
Annexin V ◽  
Trophoblast Cell ◽  
Proliferation Index ◽  
Good Growth ◽  
Time Observation ◽  
Β Hcg ◽  
And Control ◽  
Cell Proliferation Index

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.

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

2021 ◽  
Vol 5 (4) ◽  
pp. 359-366
Author(s):  
Irawan Sastradinata ◽  
Andrijono ◽  
Mohamad Farid Aziz ◽  
Wan Lelly H ◽  
Sri Hartini ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Hydatidiform Mole ◽  
Trophoblast Cell ◽  
Proliferation Index ◽  
Good Growth ◽  
Trophoblast Cells ◽  
Proliferation And Apoptosis ◽  
Β Hcg ◽  
Cell Proliferation Index

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.

Noninvasive Carcinoma of the Breast: Angiogenesis and Cell Proliferation

2004 ◽  
Vol 128 (8) ◽  
pp. 893-896 ◽  
Author(s):  
Ying Cao ◽  
Gladell P. Paner ◽  
Leonard B. Kahn ◽  
Prabha B. Rajan
Keyword(s):  
Cell Proliferation ◽  
Microvessel Density ◽  
Carcinoma In Situ ◽  
Nuclear Grade ◽  
Proliferation Index ◽  
Carcinoma Of The Breast ◽  
Cell Proliferation Index ◽  
Noninvasive Carcinoma ◽  
Mib 1

Abstract Context.—Angiogenesis and the cell proliferation index can predict the prognosis of invasive breast carcinoma; however, little is known of their roles in noninvasive tumor. Objective.—To investigate the correlation of microvessel density and cell proliferation index with other histologic parameters (histologic type, nuclear grade, and mitotic count) in 65 cases of noninvasive carcinoma of the breast. Design.—Formalin-fixed, paraffin-embedded tissues from 65 cases of carcinoma in situ of the breast were immunostained with antibody against factor VIII antigen and proliferation-associated nuclear antigen MIB-1. The microvessel density was measured by counting the total number of microvessels around the carcinoma in situ per 10 low-power microscopic fields. The cell proliferation index was calculated by counting MIB-1–positive nuclei in 100 tumor cells. A χ2 test and Spearman rank correlation test were used for statistical analysis. Results.—The microvessel density and cell proliferation index of comedo-type, high-nuclear-grade ductal carcinomas in situ are significantly higher than those of either noncomedo type ductal carcinomas in situ or lobular carcinoma in situ (P < .001). Conclusions.—Angiogenesis and the cell proliferation index are active biological processes and may be considered as markers to separate low- and high-risk patients with noninvasive breast carcinomas.

scholarly journals Current Paradigm of Treatment for Pancreatic Neuroendocrine Tumor

2021 ◽  
Vol 26 (1) ◽  
pp. 24-32
Author(s):  
Min Je Sung ◽  
Moon Jae Chung
Keyword(s):  
Cell Proliferation ◽  
Medical Treatment ◽  
Neuroendocrine Tumor ◽  
Standard Treatment ◽  
Pancreatic Neuroendocrine Tumor ◽  
Somatostatin Analogues ◽  
Proliferation Index ◽  
Ki 67 ◽  
Grade 3 ◽  
Cell Proliferation Index

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.

Telomerase activity and cell proliferation index in cholesteatoma

2005 ◽  
Vol 125 (7) ◽  
pp. 707-712 ◽  
Author(s):  
Seung Hwan Lee ◽  
Young Ho Jang ◽  
Kyung Tae ◽  
Yong Wook Park ◽  
Mi Jung Kang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Telomerase Activity ◽  
Proliferation Index ◽  
Cell Proliferation Index

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

2021 ◽  
Vol 57 (1) ◽  
pp. 20
Author(s):  
Puguh Setyo Nugroho ◽  
Muhtarum Yusuf ◽  
Titiek Ahadiyah Hidayati
Keyword(s):  
Cell Proliferation ◽  
Nasopharyngeal Carcinoma ◽  
Protein Expression ◽  
Statistical Significance ◽  
Proliferation Index ◽  
Ki 67 ◽  
Node Status ◽  
Interaction Factor ◽  
Spearman Test ◽  
Cell Proliferation Index

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.

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

2020 ◽  
Vol 4 (10) ◽  
pp. 2236-2244
Author(s):  
Patrick W. Mellors ◽  
Moritz Binder ◽  
Rhett P. Ketterling ◽  
Patricia T. Greipp ◽  
Linda B. Baughn ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Cell Proliferation ◽  
Risk Stratification ◽  
Proliferation Index ◽  
Newly Diagnosed ◽  
Cytogenetic Abnormalities ◽  
Improve Risk Stratification ◽  
Risk Scoring ◽  
Risk Scoring System ◽  
Cell Proliferation Index

Abstract 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.

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

2019 ◽  
Vol 76 ◽  
pp. 1
Author(s):  
Juliana Portes ◽  
Danielle Castex Conde ◽  
Eliane Pedra Dias
Keyword(s):  
Systematic Review ◽  
Cell Proliferation ◽  
Odontogenic Keratocyst ◽  
Proliferation Index ◽  
Ki 67 ◽  
Cell Proliferation Index

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

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