Science topic
Ovarian Cancer - Science topic
Discussion about research related ovarian cancer topics
Questions related to Ovarian Cancer
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.
I want ask question what is one method in ovarian cancer
I need a subject in the fields of nanostructures, ovarian cancer, and paclitaxel
please help me to find a good review article title
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.
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

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?
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?
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.
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
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.
Is CA 125 a reliable marker for Ca ovary in a postmenopausal women with large lesion in ovary?
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%?
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?
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?
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

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?
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.
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.


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!!
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!
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.
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?
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?
Is the levels of beclin 1 and LC3 increased or decreased during autophagy in ovarian cancer?
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?
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?
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?
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
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?
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?
Is there any specific kit?
Can I do sequencing?
What are the exons responsible?
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
From total number of ovarian cancer cell lines present, for how many cell lines, sequencing data is available?
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.
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


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.
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.
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.

Does anyone have experience uding He4 tumor marker for ovarian cancer?
I ve read some papers it seems interesting.
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.
It would really help if you can help me understand how do we decide on any cell lines, in my case cancer cells.
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
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.
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?
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
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!

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.



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?
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.
Interested ONLY in non-probabilistic based computation technologies which use already proven markers/marker sets and other diagnostic procedures.
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?
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?
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!
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.
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
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?
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.
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???
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?
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?
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
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?
i´m looking for a human (ovarian cancer) cell line expressing MRP2
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.
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
As i am using 500ml of RPMI + penicillin1% + FBS 10 % .
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.
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?
For CAM assay, is it crucial to incubate eggs at 70% humidity. Cant we use Tissue culture incubators ?
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.
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!
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.
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.
Is it frequently used Ca 125? Is there any other cheap and efficient OC biomarker ?
Thank you