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Ovarian Cancer - Science topic

Discussion about research related ovarian cancer topics
Questions related to Ovarian Cancer
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Hello all.
I work in the field of Bioinformatics and help create pipelines that analyze sequencing data for ovarian cancer. I am interested in reviewing articles related to ovarian cancer/bioinformatics but do not have an idea of how to start this process. Any advice would be greatly appreciated, thank you.
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I do not have experience in these journals but with many journals, esp higher-ranking, they are exactly as Dr Chunfeng Xu and Dr Jobin Thomas describe - they call/invite you if you are well-published or well known in that field.
Some journals, though, have a link on their site where you can apply and state your experience. They usually ask you to also state your relevant publications.
This link also has more info on becoming a reviewer:
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I want ask question what is one method in ovarian cancer
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Dear Doctor
Go To
Temkin SM, Bergstrom J, Samimi G, Minasian L. Ovarian Cancer Prevention in High-risk Women. Clin Obstet Gynecol. 2017 Dec;60(4):738-757. doi: 10.1097/GRF.0000000000000318. PMID: 28957949; PMCID: PMC5920567.
[Conclusions
Improved understanding of the development of ovarian cancer has accelerated prevention strategies in high risk women and potentially, the general population. Many women have a risk of ovarian cancer that is difficult to define. Known mutations in BRCA1/2 confer the highest known risk and surgical removal of the tubes and ovaries is recommended in these women. With increased availability of molecular and genetic testing, new low and moderate penetrance genetic abnormalities are being identified and increasing the numbers of women who may be at risk for the development of ovarian cancer. However, decision making has becoming increasing complex as technology has advanced more rapidly than our understanding of the clinical consequences of these genetic mutations. Further research is needed to understand the risk of lower penetrance genes, the interactions between genetic and environmental risk and the additive or synergistic risks of multiple risks factors in combination. The long-term clinical effects from the surgical interventions to reduce the development of ovarian cancer as well as an understanding of the clinical outcomes from the genetic and environmental risks are needed to better quantify and individual woman's risk of ovarian cancer. Looking forward, personalization of surgical and medical prophylaxis strategies based upon an individual's risk factors will be possible in order to maximize ovarian cancer prevention and minimize toxicity associated with surgical removal of the ovaries.]
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I need a subject in the fields of nanostructures, ovarian cancer, and paclitaxel
please help me to find a good review article title
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To write a review article, consider selecting a topic based on recent advancements in your field or gaps in existing research. Our website provides comprehensive guidance on choosing a subject, formulating a hypothesis, and selecting the right tools for your research. You can explore detailed resources here - https://researchbrains.com/research-in-future/ and https://researchbrains.com/recent-research-updates-3/.
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Hello everyone,
I'm working with a PA-1 ovarian cancer cell line xenograft model in female nude mice. My cells are at 372 passages, the cell repository bank themselves gave at 352th passage. Injection protocol involves a 1:1 Matrigel mixture with 0.5*10^7 cells suspended in 10% FBS-supplemented DMEM media per flank, it has been administered thrice with a observation period of 10 days per tumor induction. The route of injection is subcutaneous. However, I'm encountering issues with low tumor take and even tumor regression in some animals after it reaches ~70mm3. what could contribute to low tumor take or Could there be any improvements or troubleshooting to achive the tumor in the animals?
Thank you for the insights.
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Hello Johanna Miks,
1. The cell lines often lose their original biological characteristics such as growth rate, tumorigenicity, gene and protein expression patterns, and cellular signaling pathways through many passages, or they may be altered with increasing cell passage number. I suggest you use cells of lower passage number.
2. If you are using aged nude mice, then it is very much possible that such mice may develop small populations of extrathymic T cells also called “leaky” which are capable of rejecting tumor grafts.
3. While injecting cells into nude mice, suspend cells either in PBS or media without FBS. While the nude mice has no adaptive immune response, they still retain functional B cells and a fully intact innate immune response. So, the innate immune system may recognize components in FBS that in turn may help clear your tumor xenograft before it is fully formed.
4. Tumor regression is mainly caused by immune reponses.
5. The viability of your cells is important for tumor formation. While injecting the cells into mice ensure that minimum damage is done to the cells.
6. While injecting the cells make sure that the cell suspension is a homogeneous mixture.
7. Confirm the quality of nude mice that you are using to make sure that the mice is not the cause of the problem.
Follow the above measures, and I hope that these may be able to solve your problem.
Best.
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A very Emergency case, The Mother of my best friend, the results of her MRI said that she had nodular peritoneal thickening that suggested peritoneal serosal carcinoma, and ovarian cancer, also she has ascites, what is the source of ascites in case of high CA-125? We are suggesting a surgery to remove the ovarian, peritoneal biopsy and taking different samples to histology laboratory for culture and characterization, Any Informations would be helpful and well Appreciated, Many Thanks
Ali
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I am NOT a doctor but as compter science professional, little more AI provided detail:
In cases where there is nodular peritoneal thickening, ovarian cancer, and ascites, the source of ascites can be the result of various factors, including the presence of cancer cells in the peritoneal cavity.
CA-125 is a tumor marker that is often elevated in cases of ovarian cancer, although it can also be elevated in other conditions. The presence of high CA-125 levels, along with the imaging findings of nodular peritoneal thickening, suggests the possibility of peritoneal serosal carcinoma, which is a type of cancer that affects the lining of the abdominal cavity (peritoneum). Ovarian cancer can sometimes spread to the peritoneum, leading to peritoneal serosal carcinoma.
Ascites refers to the accumulation of fluid in the abdominal cavity. In the context of ovarian cancer, ascites can occur due to several reasons, including:
1. Peritoneal involvement: Cancer cells can spread to the peritoneum, leading to inflammation and the production of fluid.
2. Impaired lymphatic drainage: The presence of cancer can disrupt the normal flow of lymphatic fluid, leading to its accumulation in the abdomen.
3. Liver involvement: Advanced ovarian cancer can involve the liver, leading to impaired liver function and fluid accumulation.
Surgery, as you mentioned, is often a crucial component of the treatment plan for ovarian cancer. The specific surgical procedures performed can vary depending on the individual case, but they may include removal of the ovaries (oophorectomy), peritoneal biopsy, and collection of various samples for histological examination. These procedures aim to obtain a definitive diagnosis, determine the extent of the disease, and guide further treatment decisions.
Please consult qualified healthcare professionals who can provide personalized advice and guidance based on the specific details of your best friend's mother's case. They will be able to provide the most accurate information and help determine the most appropriate course of action.
Hope it helps
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Hello. I need a dataset of ovarian ultrasound images of healthy people and people with ovarian cancer. Does anyone have the dataset of ovarian ultrasound of healthy people or ovarian ultrasound of people with ovarian cancer to provide me? How should I find this dataset?
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Hi. I would suggest you get the data from :
1. https://www.cancerimagingarchive.net/ (open source data to run any preliminary research)
2. Any Radiology department at hospitals, clinics with ultrasound machines, or cancer centers in your place of area. You must grant ethics approval first from the ethics committee member of the hospital
3. Collaboration with other experts in the field and create a team member before you conduct the research. Make sure there are few clinicians involved in this team.
All the best.
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Can anybody help me find articles which revolves around the idea of: mutations in a cell proliferative pathway which increases the risk of ovarian cancer occurence mediated by increased expression of Anxa1 protien?
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I am working onovarian cancer drug -resistance research , and I need a well animal-model to Improve my project depth. Thus, I plan to carry out the PDX model on my work. It would be great if someone could offer some tips for this experiment.
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Hello Yang Meng
The problem of using the classical models for cancer drug screening which include cultured human tumor cell lines and rodent xenografts comprising human cells grown subcutaneously in immunodeficient animals, is the artificial nature of tumor cell lines, typically passaged for many generations in enriched culture media. These models generally may not be representative of the genetic and epigenetic heterogeneity of the original primary tumor. I am happy that you have taken up the PDX model for your work which is widely used in oncology drug discovery.
You could transplant tumor samples collected from patients either during diagnostic biopsy or debulking surgery into immunocompromised mice either orthotopically or non-orthotopically.
Orthotopic ovarian cancer mouse model accounts for transplantation of tumor cells either into ovarian bursa (intrabursally, IB), or into mouse peritoneal space (intraperitoneally, IP). The non-orthotopic locations for ovarian cancer include mammary fat pad, sub renal capsule, and subcutaneous (SC) space.
The advantage of using orthotopic model allows one to assess tumor development in a relevant environment and evaluate efficacy in a preclinical tumor model that mimics the disease process in humans. With orthotopic models, we can closely monitor and accurately quantify primary tumor growth, metastatic activity, and response to therapy scenarios. On the other hand, in non-orthotopic models different microenvironment surrounding non-orthotopic tumor grafts can lead to different transplantation outcome or phenotype.
The orthotopic implantation of tumor fragments directly into the organ of origin to better mimic the complexity of human malignancy has become a hot topic as a preclinical model for oncology drug research.
Please find attached a few references that may be helpful for your experiments.
Good Luck!
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Hi;
I am looking for a Systematic Anti-Cancer Treatment Dataset for ovarian cancer. I have applied to NHS but it takes too long. I also contacted many hospitals, but they do not record agent information. It doesn't matter which part of the earth, does anyone know a place that I can apply?
Best
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Any US claims data set would include information on drug treatments. It should be possible to acquire a license for use relatively quickly but they tend to be costly. Do you have a budget limit?
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Hello everyone,
We are doing a research on efficacy of iota score on ovarian cancer.
We are calculations the sensitivity, specificity, PPV, NPV etc.
But we are stuck with ROC. Any suggestions how to draw ROC curve.
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Thanks sir for the reply.
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Is CA 125 a reliable marker for Ca ovary in a postmenopausal women with large lesion in ovary?
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A large ovarian lesion requires the use of a wide range of tumor markers to identify neighboring areas and the degree of their damage during metastasis. Check out free consultations by mail: nps@udm.ru
Diagnostic Information www.fertilityecology.ru
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After establishing the appropriate dose, clinicians wish to assess the efficacy and safety of a new intravenous agent in patients with recurrent, platinum-resistant ovarian cancer. The primary endpoint was Response Evaluation Criteria in Solid Tumour (RECIST) overall response rate (ORR). The researchers wish to exclude the uninteresting rate of 10%, with a more desirable response rate of 20%. They decide to use a significance level of 10%.
a) The investigators have asked you to calculate a sample size for this study. Write out an appropriate formula.
b) Using a 10% significance level, how many subjects would be required to exclude a response rate worse than 10%?
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Hi James
Thanks for your help. This is not a live exam question.
kind regards
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Hello!
I would really appreciate some wider knowledge on my issue.
I am running a meta-analysis to look at the risk ratios associated with the risks of incidence/mortality of breast or ovarian cancers in BRCA2+ and BRCA1/2+ carriers. Due to how I must split the data into groups (BRCA2+ and OC risk for example), I get lots of small groups.
My issue is, some of the sets only contain 2/3 studies. I tried random effects using Revman but because I have a low number of studies I am unsure whether it can be accurate. When I used fixed effects I couldn't produce the charts the same way which was what initially prompted me to use random effects.
Really at a loss just now as to whether I can keep this as random effects but explain the different weights of my results...how would you approach this?
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Hello!
It seems that you are familiar with the concepts of the fixed- and random-effects models. Then, you probably have considered the random-effects model to be more appropriate, because having one true effect size is rarely a logical assumption. However, in your situation, it seems that the random-effects model may not be appropriate. With three effect sizes, your estimate of the true variance (tau-squared) will have very poor precision. But can you use the fixed-effect model instead? Yes. However, you should interpret the results as descriptive statistics (i.e., the weighted average of the effect sizes you have). Although you are willing to estimate the population effect size (in the random-effects model, the distribution of the population's true effect sizes), your data do not allow for such an inference.
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Our lab has been trying to get OAW28 ovarian cancer cell line for months. It seems they do not grow well so many labs do not have them. We ordered some from the ECACC through Millipore-Sigma, but were informed that the cell line went out of stock and subsequently failed QC, so it needs to be re-banked and we are looking at waiting until August or later for the cells to be available. Does anyone in ovarian cancer research have this cell line?
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  1. If you can contact someone directly at Genentech or Broad Institute which is mentioned in the ncbi links, that might be an option.
  2. https://www.accegen.com/product/oaw28-abc-tc0864/
  3. https://www.culturecollections.org.uk/products/celllines/generalcell/detail.jsp?refId=85101601&collection=ecacc_gc
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Hello everyone,
I am fairly new to cell culturing. For my experiments, I plate cells in 35 mm dishes. A crucial step in data analysis is cell-segmentation using the Stardist plug-in on ImageJ. However, I am struggling to obtain proper segmentation because all my cells tend to grow in clusters, making the segmentation processes highly unprecise.
To overcome this, when plating cells, I'd like to obtain single cells (similar to the image I attached.)
Does anybody have any suggestion on how this can be done?
I usually work with OVCAR cells.
Thank you in advance,
Giammarco
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Wash the cells with PBS without Ca2+/Mg2+ at the time of trypsinization and preferably use trypsin with EDTA. Clumps form because of the presence of free DNA in cell suspension which are released from dead cells. Free DNA attracts cells which bind altogether forming clusters.
You can use DNase I at concentrations from 20-100µg/ml to avoid formation of clusters. For each cell type, the working concentration must be determined individually.
Hope this is helpful.
Best.
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I am updating my earlier review on the role of Fluoride doped Hydroxyapatite in Cancer and my current focus is on Psammoma Bodies which have been found, and identifed as high risk, in a very wide range of Cancers. These include Cancers of the Bone, Spine, Brain, Choroid Plexus, Dura Mater, Gliofibroma, Medulloblastoma, Meningioma, Cervix and Endometrium, Ovary, Kidney, Lung, Mesothelioma, Pancreas, Skin, Hemangioendothelioma, Olfactory Neuroblastoma, Duodenal Somatostatinoma, Stomach and Thyroid. Early studies did not have the benefit of advanced analytical techniques, or did not even consider the Fluoride content or composition of the mineralization. Can anyone help by supplying analytical data based on Raman spectroscopy, neutron activation, x-ray or wet analysis?
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Hello, Dear Geoff.
We continue to work on the subject you mentioned. There are methods that can analyze this.
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I am trying to establish an ovarian cancer preclinical model through peritoneal injection into C57BL/6 mice.
The parental ID8 p53-/- cell line was modified through lentiviral infection in order to express OVA peptide and GFP-luciferase. We injected 5·10e^6 cells per mice.
In day 40 after injection we did not get any tumor in any of the mice.
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Couple things.... the ID8 cells you generated are expressing 3+ new proteins, each on their own can potentially slow tumor growth by increasing the immunogenicity of the tumor (especially for OVA). Knowing this, you should have included a set of mice with the parental ID8 p53 -/- along side as a positive control.
If you failed to see tumors in your positive control group, you either didn't inject as many cells as you thought (i.e. counting errors, substantial cell death) or you were working with a different cell line.
The original parental ID8 cell line grows very slowly (8-10 weeks), and the ID8-OVA cells are sooooo much slower (12-15).
Check these papers out.
The original ID8 p53-/- paper
Walton, J. et al. CRISPR/Cas9-Mediated Trp53 and Brca2 Knockout to Generate Improved Murine Models of Ovarian High-Grade Serous Carcinoma. Cancer Res 76, 6118–6129 (2016).
ID8-Luc2
Baert, T. et al. The dark side of ID8-Luc2: pitfalls for luciferase tagged murine models for ovarian cancer. J Immunother Cancer 3, 57 (2015).
ID8-GFP
Lee, W. et al. Neutrophils facilitate ovarian cancer premetastatic niche formation in the omentum. J Exp Med 216, 176–194 (2018).
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Kindly explain what kind of contamination is seen in the attached files. This is SKOV3 cell line. To remove the contamination we have treated it with Gentamycin but couldn't get rid of it.
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It is most probably bacterial contamination. Treat it with Penicillin group of drugs.
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I am currently testing Acriflavine anticancer activity in mice (in a model of ephitelial ovarian cancer). The powder is dissoved in 10% DMSO in physiological solution (ps). Is there anyone working with this compound? I would like to know if there is a difference between using Acriflavine and Acriflavine hydrochloride, specially talking about the stability in ps.
Here there is the link to Sigma, where they have both.
Thank you!!
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Dear Maria,
These data below should help:
Which is more harmful acriflavine or hydrochloride?
Infobox references. . Acriflavine ( INN: acriflavinium chloride) is a topical antiseptic. It has the form of an orange or brown powder. It may be harmful in the eyes or if inhaled. It is a dye and it stains the skin and may irritate. The hydrochloride form is more irritating than the neutral form. It is derived from acridine.
Acriflavine - Wikipedia
Which is more harmful in the eye acriflavine or hydrochloride?
Acriflavine ( INN: acriflavinium chloride) is a topical antiseptic. It has the form of an orange or brown powder. It may be harmful in the eyes or if inhaled. It is a dye and it stains the skin and may irritate. The hydrochloride form is more irritating than the neutral form.
Acriflavine - Wikipedia
How is acriflavine used in the treatment of cancer?
Acriflavine is used in biochemistry for fluorescently labeling high molecular weight RNA. It is used as treatment for external fungal infections of aquarium fish. In an animal model, acriflavine has been shown to inhibit HIF-1, which prevents blood vessels growing to supply tumors with blood and interferes with glucose uptake and use.
Acriflavine - Wikipedia
How is acriflavine used to treat hepatocellular carcinoma?
Antitumor activity of acriflavine in human hepatocellular carcinoma cells. Lee CJ (1), Yue CH (2), Lin YY (3), Wu JC (4), Liu JY (5). Patients suffering from advanced hepatocellular carcinoma can generally be treated only by targeted therapy to achieve a survival rate that lasts a few months more than that achieved with conventional therapy.
Antitumor activity of acriflavine in human hepatocellular ...
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Hi,
I am currently working on a project that involves characterizing FT190 and FT194 cell lines, but I can't find much information about them. I want to know as much as I can about them, including the patient's nationality from which they were derived from and if they are chemo and radiation naive. Thanks!
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These are immortalized FT secretory cells we developed a few years ago from women who had surgery for non-cancer indications.
A comprehensive characterization of these lines (WGS, RNA-Seq, scRNA-Seq, etc) will be submitted soon. The cells have been sent to ATCC for easier access. Some are already available on their website. Hope this helps.
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During single-cell dissociation of tissue with Subtisilin A, a cold-active protease, at 6ºC, I find that the enzyme stops working beyond 30 min. Also once I do flow on my population, I find that the epithelial cells, positive for Epcam, are almost depleted from my sample, suggesting that this protease is not kind to the Epcam epitope. This is controversial given the fact that there are two papers published out there in which they use the enzyme to dissociate kidney and ovarian cancer samples (both of which contain epithelial cells) and they are able to show an increase in the epithelial population and the enzyme works for them up to 3 hours. Has anyone had a similar experience? Thank you very much beforehand.
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Hi Ivo Röwekamp I followed exactly the same protocol from that paper you are posting but I still find those problems. I repeated the experiments over and over and my epithelial population gets depleted. Thanks, Rae Farnsworth for your input although I have tried a very similar approach and never worked, I also think the epitope is being degraded for some reason!
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Generally, in advanced ovarian cancer inhibition of autophagy is beneficial. Went through few articles which have suggested that cellular senescence could be used as a therapy for ovarian cancer. But according to the current literature, the inhibition of autophagy prevents cellular senescence. Can anyone tell me What is the relationship between Cellular senescence and autophagy in ovarian cancer?
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Estrogens (E2) are concerned with the etiology of ovarian cancer. Estrogens make production and anti-estrogens slow down ovarian cancer growth in vitro and in vivo. Estrogens increased the generation of reactive oxygen species (ROS), Autophagy blocked ROS inhibition. Kindly find the attached article.
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I am processing high-grade serous ovarian cancer samples and trying to grow tumor cell culture for subsequent functional assays. Any recommendation on the dissociation process, enzyme mix and/or culture media?
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...in addition to the previous comments following papers may help
doi:10.1038/nprot.2006.328
DOI: 10.1038/ncomms8419
Good luck
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Is the levels of beclin 1 and LC3 increased or decreased during autophagy in ovarian cancer?
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Ertan Kanbur Thank you, any idea about beclin 1?
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Hi,
I am trying to isolate platelets from ovarian cancer ascites. In literature I didn't found protocols for the isolation of platelets from ascites. The only protocols/kits are disponiles for whool blood. Can anyone help me?
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Hi everyone!
My current project involves measurements of CA-125 and some of the apparatus we use gives an output in pg/ml whereas the standard measurement unit of concentration in serum for this antigen is u/ml.
u/ml is a unit usually used for measurement of enzymes and for concentration of immunoglobulins. CA-125 is neither of those. It has no enzymatic activity one can measure.
So, how do I convert between the two units of concentration if I want to compare?
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Thank you Rabeah Al-Temaimi !
Yes, I saw that question asked in the past. There were two main answers given there: one that talks about the enzymatic activity (doesn't seem very applicable as so far I haven't seen any mention of CA-125 being an enzyme)
Another person gives a straight answer that 1 kU/L = 2.4 ng/ml.
This number refers to the value that I found in this paper:
However, my concern is that 2.4ng/ml only applies specifically to immunoglobulin E that that paper I linked above is about.
Thank you for finding the paper from TL Klug. This is useful, even if it is missing the arbitrary unit designation. And also, thank you for replying. I was not sure how active this part of Researchgate is.
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Women undergoing risk reducing bilateral salpingo-oophorectomy especially if they are BRCA1 or BRCA2 pathogenic variant carriers are warned of a residual risk of primary peritoneal cancer. A meta-analysis of studies showed only a 79% reduction in risk of ovarian type cancer after BSO in BRCA1 and BRCA2 carriers. Meaning for a BRCA1 carrier there could still be a 10% risk of primary peritoneal cancer with a high likely mortality rate. Having been involved in referring women to a gynaecological service that undertakes very careful surgery with bagging of the tubes and ovaries we have only now seen our first primary peritoneal cancer after more than 38 years of operations on nearly 600 carriers. Given that it is now thought that the great majority of high grade serous ovarian cancers originate from fimbrial precursor cells rather than for instance ovarian rest cells we feel that if careful surgery is undertaken early enough before the main risk period that this risk reduction is likely to be >95% rather than only 79%. This means a residual risk of only around 2% for BRCA1 and 1% for BRCA2. Do fellow clinicians agree?
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Risk of peritoneal cancer after risk reducing SO in BRCA mutation carries depends on timing and technique of surgery ranging from 1to 10%.Counselling and patient selection is important.
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Hello
Recently, I am curious to know about mechanisms of endometriosis and signaling pathways.
I have a question about the difference between signaling pathways in benign tumors and malignant tumors.
Since I studied, I noticed that the signaling pathway involved in benign and cancerous cells is similar, like MAPK signaling, Wnt Signaling, Apoptosis, Cell adhesion and angiogenesis.
So, what is the difference between endometriosis and ovary cancer in terms of pathway ?
Thank you in advance.
Kimiya
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It would be better to compare benign and malignant conditions in the same organ/tissue: endometriosis vs endometrial cancer, for example, instead of uterus compared with ovary tissue.
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Dear, researchers i want to introduce ovarian cancer in Swiss mice, because most of carcinogens are not organ specific, can anyone tell me which drug/carcinogens i try to introduce cancer?
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Yes because i would like to looking erythrocytes turnover in ovarian adenocarcinoma induced mice.
how ovarian cancer alter the erythropoiesis and erythrocytes turnover in cancerous mice?
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For example, I have a dataset of HE4 in the form of a numerical variable. and I want to apply it to a survival analysis for ovarian cancer prognosis. How can I find a cut off of HE4 value which is the best for prognosis of survival outcome?
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this paper may help you figure out some methods.
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Is there any specific kit?
Can I do sequencing?
What are the exons responsible?
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  1. Sanger
  2. PCR
  3. MLPA
  4. NGS : most commonly used
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What will be the levels of below-mentioned biomakers during autophagy activation? Specifically in ovarian cancer
Beclin-1,
p62/sqstm1,
SNAP 23,
Annexin-A2,
LC3B,
Syntaxin-17 and
VAMP 8
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Hi Luxitaa,
Here is a link to a colleague from Cardiff University who does a lot on autophagy, some of his papers may be useful to you: https://www.cardiff.ac.uk/people/view/126767-tee-andrew
BW
Stephen
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From total number of ovarian cancer cell lines present, for how many cell lines, sequencing data is available?
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There are quite a few. Some are frequently referenced. But it more important that what question you want to answer and then you look for a right cell line. Sometime we use patient's derived cell lines too.
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We have mice injected w/ specific cancer cell lines. The cancer cell lines failed to pick up the luciferase bioluminescent tag. We have a rubric of categories to measure the mice, but I was curious to see if there were any other variables that we could measure that would give proxy measurement for changes in tumor size.
thank you.
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We inject the tumor cells in the flank and we measure the palpable tumor after 7 days using a caliper as said previously. We also use bioluminescence imaging to quantitate the data.
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I'm trying to grow PDX-derived cells from a SCCOHT model and I need them to survive short-term (7-14days) ex vivo
After tumor digestion I platted 7,000,000 cells in a 10cm ULA dish
In the following day they were forming spheroids but the spheroids were aggregating/clumping (First picture)
I filtered through a 40uM strainer and collect the portion that remained in the filter, washed with PBS, added 0.5mL of trypsin for 40s, neutralized with 1mL of 10% FBS media and them diluted in the serum reduced media (Counted with trypan blue and had >90% viability - Second picture)
I repeated this one more time after 3 days but they keep forming these giant aggregates every 2-3 days
I'm unsure if it is worse to separate them into single cells and lose the cell-cell contact or to let them grow in aggregates of spheroids
Does anyone know how to procced in this situation?
I digested the PDX tissue in Dispase/DNAse for 30min, filtered through a 100uM strainer, lysed the RBCs, minimized the debris with Ficoll and them platted in Advanced DMEM + 5% FBS
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Do you want to generate independent spheroids .
Varying concentration of serum with methyl cellulose
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Thanks to the US Government Comparative Toxicogenomics Database based in North Carolina, over 2000 Human genes impacted by Fluoride chronic poisoning are linked to Diseases resulting from the disruption of normal cellular and systemic processes.
Looking at just one of these genes, mTOR, Mammalian-homolog-Target-Of-Rapamycin, a known cause of Dental Fluorosis, we find the following diseases listed:
Cancer, features Hepatocellular Carcinoma, Adenocarcinoma, Ovarian Neoplasms, Mesothelioma, Mantle-Cell Lymphoma, Small Cell Carcinoma, Precursor T-Cell Lymphoblastic Leukemia - Lymphoma, Uterine Cervical Neoplasms, Renal Cell Carcinoma, Breast Neoplasms, Colonic Neoplasms, Non-Small-Cell Lung Carcinoma, Lymphatic Metastasis, Glioblastoma.
Damage to the Brain is listed under the general heading Neurotoxicity Syndromes, then Glioblastoma, Malformations of Cortical Development, Schizophrenia, Focal cortical dysplasia of Taylor (Epilepsy requiring surgery),
Other listed diseases include Congenital Capillary Malformations, Hypertension, Left Ventricular Hypertrophy.
Please let me know of any more Fluoride induced diseases you have found linked to mTOR.
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A recent paper implicates mTOR as a cause of reduced IQ in children.
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I'm interested in finding out if there are data available regarding mutations affecting 53BP1 that are known - or supposed to - cause resistance to PARPi in the contest of breast or ovarian cancer. So far, most of the data I've found, did not really show specific mutations ( or the domains affected ) but rather the only showed the loss of 53BP1 expression. I would be interested in knowing where those mutations were occurring and how they were compromizing 53BP1 function so that HR could be restore.
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Non
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I need to predict disease with the help of deep learning. If you know about these then please help me find my way. In the following, I add my dataset of ovarian cancer. It's taken from a hospital in Bangladesh. Now I am trying to use this dataset for predicting ovarian cancer in early-stage using deep learning.
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Does anyone have experience uding He4 tumor marker for ovarian cancer?
I ve read some papers it seems interesting.
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As per one recent research:
In patients with benign diseases, abnormal serum levels of HE4 and CA 125 were found in 1.1% (3 of 285) and 30.2% (86 of 285) of patients, respectively. CA 125 false positive results were mainly found in premenopausal women with abnormal serum levels in 32.3% of the patients with gynaecological benign diseases in contrast to 22% of them found in postmenopausal women. The use of ROMA algorithm reduces the proportion of CA 125 false positive results in the total group as well as in pre- or postmenopausal women
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So...I am running immunohistochemistry assays of ovarian cancer tissues that are fixated and prepared by someone else (same person every time). Lastly, between different runs with the auto stainer I have had two of the same slides (very same cut) run in two different times with the same concentration and the same program (those were the positive control) and there is a difference in staining between the two slides. This shouldn't be the case since the operator is the same, the procedure was the same and the dilution was the same. Also, same batch of antibody, so I have no clue of what can possibly be going on and how to fix it.
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We have the Dako Autostainer and have started to notice in consistent staining. We ran duplicates using 1 Central drop zone and 2 drop zones either side.
We also run the same slides on our old Dako strainer and the staining was fine.
We think the reagents are not spreading evenly across the slide and tissue, more so on small tissue samples.
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It would really help if you can help me understand how do we decide on any cell lines, in my case cancer cells.
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LNCaPs are widely used.
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I used calcein AM and Ethidium to do viability test for ovarian cancer spheroid but it seems that Calcein AM doesn't penwtrate to center of spheroid which may due to lack of gap junctional intracellular communication(GJIC) so it that can be a possible reason for ovarian cancer spheroid and what can be suitable viability test in this case
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We have used MTT assay for evaluating viability of cells in spheroids subjected to different treatments. The protocol followed is given in DOI: 10.1007/s12668-014-0157-2.
Also, fluorometric as well as colorimeteric based viability assay kits are available with R & D systems for measuring viability in tumor spheroids. You can refer : www.rndsystems.com
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Has anyone conducted a Puromycin kill curve on the mouse ovarian cancer ID8 cell line? I will be needing to do one before transfection, and am trying to decide the concentrations to vary treatment at. What concentrations have worked for you?
Thanks in advance.
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I performed my own kill curve analysis using this Lentivirus: https://shop.essenbioscience.com/products/nuclight-red-lentivirus-reagent-ef1a-puro
Concentrations were 0, 2, 5, and 10ug/mL Puromycin. 2ug concentration was ideal in this scenario, though 5 and 10 work as well given more time
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I have given 12 hrs of Rapamycin treatment (100 nM) to ovarian cancer cells after which I see a decrease in both phospho as well as the total levels of mTOR. Why does the total level go down? is there any literature available?
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A prolonged treatment of cells with rapamycin, an inhibitor of mTOR, inhibits protein synthesis. Thus, depending upon the half-life of a protein, it is predicted to decrease the levels of proteins in cells. In certain cell types, the mTOR protein half-life is short (1.5 - 3 h). This could account for an observed decrease in the levels of mTOR following rapamycin treatment of ovarian cancer cells.
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I checked 3AO cells online (ATCC ECACC and some company website) could not find this cells‘ background information.
eg. ES2
(Morphology)fibroblast
(disease)clear cell carcinoma
(age)47 years
(Ethnicity)black
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It is a human epithelial ovarian carcinoma cell line. It can be purchased from the Chinese Academy of Sciences Type Culture Collection, Shanghai, China.
Please see link:
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Hello all,
I'm relatively new to research and just started growing my own Ovarian cancer cells from a pleural effusion.
It's been about 2 weeks now since I've had them in a flask and have changed the media about twice a week. At first the growth was extremely slow, I suspect because of the enviromental change?
However, withing the last few days they began to proliferate much quicker than the previously and now I see one particularly interesting mass and I have no idea if it's just a collection of dead cells or if it's something else. It looks nothing like the regular ovarian cancer cells nor the fibroblasts so not sure if it is and I'm just mistaken.
If anyone could tell me what this is I'd greatly appreciate it!
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As you've provided a nice big clear image of what the cells look like that's fairly easy to answer. That is just a big clump of cells that are growing on top of each other. It's a bit easier to see if you adjust the contrast a bit like I have. You can see single cells that you're expecting to see then if you look carefully around the edges in particular where I've drawn white rectangles you can see these cells haven't spread out as much and the further in you go the less spread out they become until it just looks like a shapeless mass.
Cells only spread out like what you typically see in 2D culture on flat hard substrates. On very very soft substrates or in 3D culture they adopt a more rounded appearance. You can see that here, the ones on the very outside have a single cell underneath them they are adhering to between them and the plastic culture dish. They can still feel that hard substrate but because there is a soft cell between them they don't spread out as much. The further into the clump you go the more cells there are, they feel a softer substrate beneath them and there's also less room for them to spread out so they have a more blob like structure.
There is nothing you can (or should) do at this point but when they become confluent enough to split and you've got them in suspension in a falcon tube pipette them up and down 20-30 times with a 1ml pipette. If you use slow deliberate strokes it provides enough shear force to break up cell clumps into more of a single cell suspension without damaging them too much. This should help prevent clumping like you've got here.
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Hi all,
Currently I am working on a project where I inject GFP-expressed ovarian cancer cells into zebrafish embryos. I injected cells at 2dpf, and took images at 2dpi and 4 dpi. And I am tracking tumor progression by taking green fluorescence images.
However, I found a really weird thing today when I was imaging by uninjected control: clearly there are spherical regions that both emits green and red along axis of fish, but I don't understand what is causing this problem... because I am tracking green dots to verify my hypothesis and this is interfering my results...
Any thoughts on why this is happening? I am currently using EK strain and the images were taken at 4dpi.
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These are developing pigment cells; the stripe along the dorsal surface is quite characteristic. They autofluoresce in both the green and red channels, and you can see this in the image– most dots have both colors.
To remove this, you must inhibit pigment development from 1 dpf on (we use PTU solution) or use an albino strain of fish. And one must always take comparable images of negative controls (same stage, no injections) using the same illumination.
Finally, I would check on your injected cells much earlier. At 2 dpf the zebrafish already has a working innate immune system, which means thousands of macrophages and neutrophils that can kill foreign cells. Unless you are inhibiting the innate immune system or using a immunocompromised strain of fish there may be no injected cells alive by the time you are trying to see them (48 or 96 hours later). So you need to confirm that the injected cells are viable and for how long. I would inject and then image much earlier-- such as 1 hour, 2 hours and 4 hours, for a start.
Good luck with your experiment.
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I am planning to use nu/nu nude mice, but I also read that NSG or NOD/SCID are good for xenografting. Can anyone offer any advice?
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We use either athymic balb/c mice or NOD/SCID mice in our ovarian cancer xenografts (http://altogenlabs.com/xenograft-models/ovarian-cancer-xenograft/). You don't want to have the host immune system attacking the tumor as its growing, and preventing regression through immunodeficient mice is the best way to do so.
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Hello,
I have been trying to grow spheroids and have not had any luck. I wanted to see if anyone had a link to an article/document that outlines the procedure.
More information.
I am using ovarian cancer cell lines A2780 and SKOV3. The medium used is DMEM/F-12 supplemented with insulin, EGF, FGF, and .4% BSA. For the A2780 I can get aggregates that resemble spheroids, but when I attempt to dissociate and replate for a 2nd generation the spheres do not reform. I tried a cell count after dissociating the first generation and the result was nearly identical to that of the seeding density. So I was thinking the medium was the issue seeing as it would seem that the cells are not proliferating to form the 2nd generation. When trying to count the 2nd generation it appears that the cells are dead (trypan blue counting) even though medium was being replaced either ever 2 or 3 days. I saw some references that also used B27 supplement in the medium as well, but I am unfamiliar with this.
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There are many different protocols for making spheroids. This is quite nice publication about different types of 3D cultures and methods of making them: https://www.clinicalkey.com/#!/content/playContent/1-s2.0-S1476558614001948?returnurl=https:%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS1476558614001948%3Fshowall%3Dtrue&referrer=https:%2F%2Fwww.ncbi.nlm.nih.gov%2F
In my case, when nothing works I try 3D Bioprinting method and add fibroblasts together with cancer cells.
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Interested ONLY in non-probabilistic based computation technologies which use already proven markers/marker sets and other diagnostic procedures.
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Am interested in this work...
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Genetic testing for hereditary cancer predisposition:
what are studies (or guidelines) focused on panels of genes for breast cancer, ovarian cancer, colorectal cancer and polyposis?
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Hi Tatiyana
some key points you are searching for are focused at:
hue this helps
fred
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I have had success using DO-1 and higher dilutions of Pab240 (lower dilutions yield non-specific cytoplasmic signal) to detect nuclear p53, and I have read that DO-7 is another reliable antibody for nuclear p53 detection. Has anyone had reproducible success with antibodies to detect cytoplasmic p53 in IF experiments? I have read that BP53-12 (sc-263) could potentially be a good candidate - can anyone vet this?
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Hi,
I can not give you a hint for a specific antibody, but if an antibody should specifically detect cytoplasmic p53 it has to be an antibody against a modification that is specific for cytoplasmic p53. Unfortunately, most modifications (phosphorylation) I know, are more or less specific for nuclear p53. I would suggest that "normal" p53 antibodies like DO1, DO7 should detect also cytoplasmic p53, if it is present.
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Can someone please suggest me some research articles for the detection of lung and ovarian cancer using Surface plasmon resonance (SPR)? I found lot of research papers on prostate, breast and colorectal cancer detection, but found only one article for lung cancer (V. Sahu et. al. 2016) and one on ovarian cancer (J. Yuan et. al. 2012) detection using SPR.
I am only interested in SPR detection method.
Thanks in advance!
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Dear Shawana
You may find this article useful
Talanta. 2011 Oct 30;86:377-83. doi: 10.1016/j.talanta.2011.09.031. Epub 2011 Sep 22. Surface plasmon resonance based immunosensor for the detection of the cancer biomarker carcinoembryonic antigen.
Altintas Z1, Uludag Y, Gurbuz Y, Tothill IE.
Good luck
Sivakumaran
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Hello,
Has anyone authenticated the cell line Cov362(ovarian cancer)? We received our results back from ATCC however the cells are not in their data base so the results were inconclusive.
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We provide comprehensive cell profile library to help identity your cell lines.
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Human papilloma virus, sexual behaviour and logical places of infection and malignancy
The locations on the body of sexual transmitted infections with human papilloma viruses, can correlate with "inovationes" in sexual behaviour.
It is logical that the viral affects (condilomata, precancerous lesions and carcinoma) can be located on cervix, vulva, glans penis, prostata, anal region, oral region and tongue, head and neck, larynx, oesophagus and breast.
Very important is the possible causal connection between human papilloma virus infection and breast carcinoma.
Data show that apart from the heart and the kidney, the virus has been found in all other organs that have been analyzed so far, i.e., prostate, urinary bladder, oral cavity, larynx, esophagus, stomach, colon, liver, vagina/vulva, endometrium, ovary, breast, penis, anus, skin, and lung. Some of the detection rates are remarkable, e.g., colon cancer up to 97%, lung cancer 80%, and breast cancer 74% (Petersen I, Klein F., 2008)*.
Double primary carcinomas (cervix and breast) in the same person is not rare.** The occurrence of a second malignancy in a patient with a known malignant tumor is not uncommon.
It could be supposed the same or similar etiology (Viral?, HPV ??***) or coincidence of different etiological factors.
Maybe the new antiviral therapy and the Gardasil vaccination can be helpful for different types of malignancy, especially for very frequent and dangerous breast, anal and ovarian cancers.
* Pathologe. 2008 Nov;29 Suppl 2:118-22.
** http://www.google.com/search?q=double+carcinoma+cervix+breast&rls=com.mi... -us:IE-SearchBox&ie=UTF-8&oe=UTF-8&sourceid=ie7&rlz=1I7ADBS
***British Journal of Cancer (2006) 94, 338–338. ***Breast Cancer Research and Treatment (1992), Vol.21, No 2
Competing interests: None declared
Competing interests: No competing interests
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I try to undestand.
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I had transfected Ovarian Cancer cell line along with pCMV6-AN-HA tag vector along with my GOI POTEB in PD60mm.
I have seen expression within 24 hrs after infection and it shows >90% transfection efficiency. However, because I am not just interested in protein expression, stable expression is more important to me. I am using G418 (250ug) to generate a stable cell line. My cells reached 90% confluency and every going fine for the continuous fifth day but after fifth day massive cell death occurred. I had changed the media after 24hours of post transfection by every second day. What could be the probable reason for the death? What could be done to avoid massive cell death?
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First generate a kill curve which is highly recommended before establishing stable cell line; which is a dose responsive experiment where u treat your cells with an increasing amounts of antibiotic to determine the minimum antibiotic conc that can kill your all cells over the course of one week.
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Are gene mutation (BRAF, KRAS, PTEN, and TP53) analyses required to define type 1 and type 2 ovarian cancers? Or, cell morphology is enough to define ovarian cancer types. Thanks.
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Think same as Mohammed. Usually the cell morphology is accepted.
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I'm doing differential expression analysis of TCGA Ovarian Cancer between tumor and normal. For transcriptome profiling, however, there is no data for normal (either blood normal or solid tissue normal).
But when I read some people, I saw people did this analysis. They never mention this problem.
How did they do the analysis without control???
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Hi,
maybe you can use following data portals:
Regards,
Norman
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BRCA1 and BRCA2 are considered as tumour suppressor genes but mutations of these genes are selectively increase the risk of breast and ovarian cancers, compare to other type of tissue cancers.is there any reason for tissue specificity?
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Hi Kamalathasan.
The organs are all expressing ER during embryonic development, certain cell phenotype differentiation and maintenance of the adult organs. And BRCA genes may be involved in ER signaling. Thus, Epigenetic regulation of BRCA genes appear to be related to ER-activated other gene regulation.
Regards.
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It is known that phenol red mimics the action of some steroid hormones, particularly estrogen. What is the impact of using media with phenol red on the results of breast or ovarian cancer cells concerning cell growth, viability and proteins expression assays? has anyone noticed any difference in results when compared with media without phenol red?
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I have used media with phenol red to culture MCF-7 cells, but the phenol red free media for tests for estrogen potency of chemicals. I think it is only needed to use the phenol red media for experiments there the purpose is to use the estrogen dependant response of the cell. In the culture of MCF-7 cells the media have to be added an estrogen for the cells to grow and here the phenol red has no effect.
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I saw that you were interested in my new project on THz spectroscopy for Ovarian cancer detection in tissue samples.  Is this related to your projects?  Are you interested in collaborating?
Thanks,
Tatiana
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Setting priorities to reduce maternal morbidity and mortality for our health plan.
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I’m finishing my PhD project, which I analysed high grade serous ovarian carcinoma on patients with different clinical responses to carboplatin using transcriptome and I found MMP14 differentially expressed. On protein analysis, higher levels of MMP14 immunostaining were associated with better prognosis (OS and PFS survival analysis). I’m struggling to understand how MMP14 could initiate intraperitoneal metastases, with initial detachment of tumour spheroids from the surface of the ovary (Lengyel 2010) and at the meantime, be a protective factor of better prognosis in high grade serous ovarian carcinoma.
Have someone a hypothesis to share about this?
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Hi Mariana, these are very interesting results!.
I have not worked with MMP14, but I have worked with MMP9 and MMP2. For these MMPs, TIMPs play a major role in controlling their activities.
I have not been active in this field, but a paragraph in
caught my eye:
"Others have since demonstrated that MMP-14, a protein anchored to the cell membrane of stromal cells, binds to TIMP-2 through its catalytic domain and then uses it as a receptor for pro-MMP-2, a protein also initially produced by the stromal cells. Free adjacent MMP-14 can then cleave the Asn37-Leu38 bond of pro-MMP-2 leading to MMP-2 intermolecular autocatalytic cleavage of the Asn80-Tyr81 bond. This process leads to an active and soluble form of MMP-2 called MMP-2a. MMP-2a can then bind to cancer cells via an αvβ3 integrin (7 , 26 , 43)"
If this holds up, then high MMP-14 and low TIMP-2 will not activate other MMPs, leading to less invasive properties.
Hope this helps.
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i´m looking for a human (ovarian cancer) cell line expressing MRP2
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thank you!!!
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Lambeck et al., (2007) detected that the median concentration of serum IL-7 in healthy patients is 2.9pg/ml. They have also detected that the median concentration of serum IL-7 in ovarian cancer patients is 5.3 pg/ml.
While Xie et al., (2004) have estimated that the median serum level of IL-7 in ovarian cancer patients is 32.49 pg/ml, and the median peritoneal level of IL-7 (mainly by tumor cells) in ovarian cancer patients is 17.39 pg/ml.
I need both the shedding rate and shedding fraction for IL-7, can I get them from its level (conc.) in the serum or the peritoneal fluid? 
Trinder et al., (1999) have estimated that the production rate for IL-7 in renal cancer cell lines is ranging from 3.9 to 15.1 pg/ml/10^(6) cells/day. Can I benefit from this information in estimating the production rate for IL-7 in ovarian cancer?
Thanks in advance.
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Sorry. No idea.
I am a clinician.
Regards
Bernardo Rapoport
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A 33 years primigravida with a family history of two first degree relatives with epithelial ovarian cancer, BRCA status not known, wants me to perform BSO during elective Caesarean section
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BRCA1/2 gene status should be known to the best of my knowledge. Around 10 - 15 %  chance of inheritence exists with ovarian cancers in this case.  Screening with annual mammography from age 30 and breast MRI from age 25 for BRCA1 and BRCA2 mutation carriers are suggested by some authors.
Also bilateral salpingo-oophorectomy can be offered to women with a BRCA1 or BRCA2 mutation once they have complete the desired number of children, around 35 - 40 years of age. Youngest age when the ovarian cancer appeared in the family should be questioned and considered.  However, at 33 year old, inducing menopause may adversely effect heart and bone status of the patient seriously and should be decided by a council of the doctors if the patient insists on having the bilateral salpingoophorectomy.  Early menopause may also affect the cognitive function, so if this women is a professional using cognitive functions/decision making processes, this should be taken into account. 
A single physician should not decide on bilateral salpingoophorectomy of a 33 year old patient just by the desire of the patient to the best of my understanding. 
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As i am using 500ml of RPMI + penicillin1% + FBS 10 % .
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hi Serag. Can u provide me the reference for using this media ? i have not seen this media in contents. 
Thanks.
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Hi, I want to do a cycle/viability assay for ID8 ovarian cancer cells after treatment with the epigenetic drug Decitabine, on various doses. Has anyone done it and if yes, do you know the optimal dose for Edu? And does Edu incubation need to take place before PI incubation? Thank you, Pavlina.
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Hi Pavlina,I tested 10uM
I tested 10uM concentration for different cell lines for 1 h and a half. It has given me very good results in a combination with PI staining (20ug/ml). 
If it does not work well, you can either double the Edu concentration or incubation time. 
Hope it works for you properly.
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A SNP variant for a cysteine protease was identified and investigated in two independent studies. The SNP is located at the miRNA binding site. One study associates this variant with a reduced risk of ovarian cancer  whereas the other study associated this variant with a more progressive version of Crohns' diseases. This would only make sense if the SNP results in an increased interaction between miRNA and the variant, thus decreasing the protein expression. My question is, can a SNP variant in the miRNA binding site actually increase the affinity between miRNA and the transcript? Or do miRNA SNP variants only lead to defective degradation?
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It might be important to  understand where the miRNA binding site  is positioned , since it could overlap with other motifs. 
But in response to your question it can be theoretically possible, as miRNA have a preference to what RNA motifs they bind too and a SNP within a motif can shift it
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For CAM assay, is it crucial to incubate eggs at 70% humidity. Cant we use Tissue culture incubators ?
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You need 60% humidity for the CAM assay.
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I have thought if patient with ovarian  cancer needs compulsorily  lymph node ressection when surgery is performed after neoadjuvant chemotherapy or of rescue once disease is already advanced and para aortic and pelvic lymph node ressection increase morbidity to surgery process.
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Dear Dr.Batista. its regarding the removal of lymphnodes after NACT, prophyactically lymphadenectomy  is required if the tumour mass is more than of 2cm size in the pelvic region.
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Dear all, according to Grimes DA et al., 2014 ( http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD006134.pub5/abstract;jsessionid=B22DED607EDF16AB77AF3505560F19B1.f04t02 ), treatment of functional ovarian cysts (FOC) with OCP appears no better than watchful waiting. But it's evident that some progestagens (I guess it especially may be refered to 19-norsteroids) have a definite anti-gonadotropic effect. What about this? Does anybody have a reliable information about the positive influence of some OCP or progestagens on FOC? Thanks a lot!
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 Dear Maksim 
greetings
We need to qualify different types of progestagens to draw a solid conclusion about usefulness of these medications
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Hi everyone. I am trying to grow A2780/Adr cells in NCr nu/nu mice and would like to know if someone has experience in growing the tumors. I am interested to know how many cells were injected, when did the tumor start growing and how fast did they grow to reach 1 cc.
Thank you.
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Thank you very much Krzystztof Ksiazek!
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I am separating ovarian cancer cells from primary cell tissue and I do not have a FACS machine or any magnetic bead. Is there any suggestions to separate the fibroblast and mesenchymal cells from the ovarian cancer cells.
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Givon - good morning.  My first question is about the source of your tissue.  Is this animal model material, or are you working with primary material from patients?  If the latter, are you satisfied with your strategy for producing a more-or-less single cell suspension, or do you think you still have islands of cells and fibrosis that may make sorting difficult?
My second question is why magnetic beads aren't an option.  Is it the lack of an appropriate antibody, or is there another reason?  
If you do have an antibody with sufficient specificity for the cells you're looking for, microbubble separation would be another approach.  We're working on this technology currently and have a 'universal' streptavidin-coated low-density microbubble that can buoyantly sort cells from complex suspensions.   They've been used in positive selection (e.g., capture the cancer cell) and depletion (e.g., capture the fibroblasts and mesenchymal cells), so might be an additional option.
I'm happy to discuss the technology further.  If it would be helpful, feel free to message me or reach out via the website.
Best, John
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Is it frequently used Ca 125? Is there any other cheap and efficient OC biomarker ?
Thank you
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i think here we are digressing fro the quetion of Edlira refgarsding Ca125 FROM CA15-3 AS A PROSGNOSTIVC MARKER IN CA OVARY EPITHELIAL TUMOURS.