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Cervical Cancer - Science topic

A forum for cervical cancer research.
Questions related to Cervical Cancer
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In this case the young lady has a 9.5cm (bulky) tumor of a high vascularity, in the cervix
and it is technically impossible to induce an abortion by surgery, in order to proceed with radiochemotherapy. Could it be possible to proceed with radiochemotherapy even if the abortion doesn't take place?
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Depends:
Previous pregnancies? probably
Malign Tumor? Yes
Hysterectomy
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White patch with clear border is indication of cervical cancer. Whiteness range vary from image to image. 
Thanx in advance
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your can go for segmentation techniques to target ROI what will do your task , there are so many manual and automatic segmentation techniques like morphological and k- means, level set etc you can refer to my papers published for tumor detection and segmentation  also
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Nanotechnology based screening for cervical cancer women can be possible
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You do not really need nano-technology to deal with screening and treatment of .  cervical cancer. It was proven the relationship between HPV infection and development of cervical cancer (especially in women 35 years or older. Here it is not enough space to  go with more detailed explanation. With HPV testing for high risk HPV types and the new vaccine the cervical cancer, already showed decrease about 50%. The test is very easy and sensitive. However it is different between female vs. male patients. Again there is not enough space to elaborate further.  
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I am doing my research in cervical cancer diagnosis. I plan to use some ideas of Fuzzy LSM for segmentation .Please provide the relevant answers related to my question.
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Studying on cervical cancer
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From literature to be exposed about 5 to 10 years inhaling the silicon dust cause silicosis for human, but in the cancer treatment we have only short treatments period with chemo or herbal drugs and I assumed that there are no serious side effects, but it seems that the silicosis risk highly depends on the concentration and duration of treatment by used silica which should be considered.
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Please suggest me method of scoring quality of life (EORTC QLQ C30) raw data in cancer patients? scoring of EORTC QLQ C 30 in cervical cancer patients.
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There is a standard scoring protocol which you should be able to easily find online Akhilesh.
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How can we reverse engineer Stochastic Gene Networks of Cervical cancer system to study its dynamics more closely and inhibit the cancer progression at the transcriptional level.
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There are various ways to perform reverse engineering, depending on your input. If you are from Bioinformatics background, you can perform system biology based modeling of pathways on the basis of information available.
As you are working on cervical cancer, you can perform literature mining to connect the pathways. Results can be verified by  checking enzyme substrate interaction through kinetic studies.
You can also follow the approach defined in attached paper.
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would dr vinod shidham throw some light as we came across his work in cytojournal 2011 article 8;1
thanking you
yours
dr nandini manoli
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The IHC stain is assessed in epithelial cells
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I am researching on effect of some plants after innoculation of a xenograft cervical cancer cells. i need to induce immunoseppression to prevent rejection of the xenograft cells.
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Dear Julius
The best way to accomplish immunosupression is by using nude mice (which are already immunosupressed)
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I interest in DNA HPV and pre cervical cancer lesion , my questions?
1. method with DNA HPV hybrid capture 2, if cytology is LSIL and biopsy is CIN-1, the results is negative before and after cryotherapy,  are there etiology other than HPV or are false negative?
2. method with DNA HPV hybdrid capture 2 , after cryotherapy and CIN 2+ , DNA HPV negative , can it be false negative?
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1. Most likely you are dealing with LSIL associated with low risk HPV types. I am not keen on cryotherapy. Just follow the patient!
2. CIN2 ideally, should be triaged with p16 - some of it will be just LSIL or even metaplasia. True HSIL can also be HPV negative - with potential implications in the follow up. Although it is not incorrect, I do not support treating high grade disease with cryotherapy.
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This very urgent please! I'm working with cervical cancer images on android platform. After a successful segementation, I want to automtically crop out the largest size, which is of cource the ROI in the Image please How can I do this?
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Let me see if I understood correctly.....you did the segmentation and already have the ROI and what you want is to extract that ROI into another image???? or remove the ROI from the original image???? well if any of that is what you want you could do it by using Image Arithmetic....i mean for example if you multiply the original image with.. for example a binary image of the ROI were every pixel is 0 but the ones in the ROI it will result in a image with only the pixel values of the ROI... if you do it the other way i mean every pixel with value 1 and the ROI 0....the result will be the original image without the ROI....if you already have the ROI that step could be done automaticly
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Which is the best segmentation technique for cervical cancer images?
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we are working on cervical cancer ,we would see the expression levels of target genes in both control and patient samples.  we are planning to use internal control as Coiled-coil-helix-coiled coil-helix domain containing 1 [chchd1] here i attached the chchd1 reference file.
can any one suggest which house keeping gene is best for my studies
can we see the expression levels of target genes in matched samples  [i.e ]same patient tissue RNA and same patient blood RNA is this method is valid?
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Hi Deepthi,
the reference you provided gives an answer to the first half of your question. Those three suggested genes (CHCHD1, SRSF9, TMBIM6) appear useful for qPCR data normalization of cervical cancer samples. And don't pick just one gene, but better use the geometrical mean of all three to normalize your data.
The second half of your question remains open. The same three normalizers may not work optimally for blood samples. You have to perform test runs with your blood samples and analyze the stability their expression
If the expression of these three is not stabile in blood samples, then the easiest way would be to choose another set of three from housekeeping genes e.g. 18SrRNA, ACTB, B2M, GAPDH, GUSB, HPRT1, HSPCB, PPIA, RPL13A, RPLP0, TFRC, UBC. Look for a set of three genes which demonstrate the most stabile expression in your blood samples. Use the help of geNorm and NormFinder, just as it was done in your reference article. And then use the geometrical mean of these three genes as a normalizing factor. Geometrical mean is less sensitive to outliers than arithmetical mean.
BR, Einari 
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I am doing research in Medical image processing. As a very first step, i enhanced an image using genetic algorithm. I  do not know howto proceed further?.
Please provide some details about how to proceed research further....
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Mr.Sathish, Please send me list of segmentation algorithm used till april 2016
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I am working on monoclonal antibody treatment against cervical cancer. I want to use antibody as a positive control. Can anyone suggest antibody that kill all cells (normal and cancer cells).
Right now I am using Cisplatin as a positive control but Cisplatin takes long time to kill cells (48-72hrs) and my treatment takes (less than 24hrs). I am not getting good positive controls.
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How does cervical cancer transfer from mother to daughter. There are many cases in which every female member in the family (mother daughter) have developed cervical cancer. I would like to know how does the transmission occurs? Its is through pregnancy time of after that? Also what could be the reason fortranfer?
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Please have a look at this useful PDF attachment.
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Availability of agent, practicability of model,
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The common cervial cancer for compound screening is s.c. xenograft model (siHa cells or Hela cells) in nude mice. 
However, if you want to study the mechnistic aspect of cervial cancer, other virus infected in vivo models have to been considered.
How I write a chapter in an international book?
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Is any one working/ or writing a book in early detection of cervical cancer?
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Dear colleagues,
I am searching an appropriate primer for diagnosis of vaginal cancers in female dromedary camels. I encountered some cases with adenocarcinoma, squamous cell carcinoma and some other types of vaginal and cervical cancers. From literature (About half of vaginal cancers in humans is associated with human papillomavirus (HPV) detection, in contrast to cervix cancer which is essentially all associated with HPV). Papillomaviruses have been detected in camels. I tried to test two samples by Prof Robert D Burk (Albert Einstein College of Medicine - NY-USA), but I had a problem in sample transportation. Now, I would like to test the other cases in home, but I do not know what is the appropriate primer that should be used.
Thank you
Ali
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Quick search in scopus revealed that there are no genital PVs described yet for camels. Just skin ones.
It is quite likely that PVs may are actually reponsible for  genital SCC in camels. As PVs are extremely species specific there may well be camel "only" genital PVs responsible for the SCC. So you have a "real" project to discover those PVs.
This article where the same has been done for horses may serve as a description of the methology involved in this.
Scase, T., Brandt, S., Kainzbauer, C., Sykora, S., Bijmholt, S., Hughes, K., … Foote, a. (2010). Equus caballus papillomavirus-2 (EcPV-2): An infectious cause for equine genital cancer. Equine Veterinary Journal, 42, 738–745. http://doi.org/10.1111/j.2042-3306.2010.00311.x
Edmund
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When reading the following article 'Human papillomavirus is a necessary cause of invasive cervical cancer worldwide' , I am quite confused on what is the use of HPV serology and how it works ,may anyone can give me some details? thx a lot!
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Squamous carcinoma of the cervix (2 x 0,8cm). 
Left ovary - micrometastasis, tube - N
Righ adnexa - N
LN - metastasis (right  1/5, left 0/5).
What will be the pTNM?
TNM-book doesn't clarified ovarian metastasis.
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Any staging system not useful for patients or physician must change.
These rare cases of cervical cancer with ovarian metastases should be staged like M1. However, due to its rarity, only case reports exist. This is a great opportunity for a multi-institutional, even multinational, research to obtain many cases to evaluate evolution and surviving. With this information, TNM system must change.
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The original question was about terminology. It would definitely be wrong NOT to classify cervical cancer as cancer, because that is what they are, even though they are are induced by an infectious agent. There are many other examples of cancers induced by infectious agents, take all the retrovirus-induced tumors in birds, mice, cats, cattle etc and also the HTLV-induced adult T-cell leukemia/lymphoma in man. Why should these diseases, as well as cervical cancer, possibly some brain tumors and others, not be called cancers? They consist of bodily cells (not the causing infectious agents) with unlimited growth, that invade and destroy the surrounding tissues and metastasize, thus leading to death.
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we need establish cervical cancer primary cell lines can any one advise how to maintain primary cell lines
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thank you
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Where to find image cervical cancer image data set from pap smear ? I need  classified the cancer image to train my algorithm. Thanks
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Thank You Mr Manan....but my research is for pathology image. anyway thanks for your help.
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Doorbar et al. 2012 and  Moscicki et al. 2012
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Here you can check some publications regarding your question:
Sundström K, Ploner A, Dahlström LA, Palmgren J, Dillner J, Adami HO, Ylitalo  N, Sparén P. Prospective study of HPV16 viral load and risk of in situ and invasive squamous cervical cancer. Cancer Epidemiol Biomarkers Prev. 2013 Jan;22(1):150-8. doi: 10.1158/1055-9965.EPI-12-0953-T.
van der Weele P, van Logchem E, Wolffs P, van den Broek I, Feltkamp M, de Melker H, Meijer CJ, Boot H, King AJ. Correlation between viral load, multiplicity of infection, and persistence of HPV16 and HPV18 infection in a Dutch cohort of young women. J Clin Virol. 2016 Oct;83:6-11. doi: 10.1016/j.jcv.2016.07.020.
Chang L, He X, Yu G, Wu Y. Effectiveness of HPV 16 viral load and the E2/E6 ratio for the prediction of cervical cancer risk among Chinese women. J Med Virol. 2013 Apr;85(4):646-54. doi: 10.1002/jmv.23490.
Hong D, Liu J, Hu Y, Lu X, Li B, Li Y, Hu D, Lu W, Xie X, Cheng X. Viral E6 is overexpressed via high viral load in invasive cervical cancer with episomal HPV16. BMC Cancer. 2017 Feb 15;17(1):136. doi: 10.1186/s12885-017-3124-9.
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I am going to use normal balb/c mice to establish folate positive receptors cancerous mice. As 90% of cervical cancer are folate positive receptors, I was thinking that it consider as a good model. Any other suggestion would be appreciated. 
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TERT is a gene coding the enzymatic component of telomerase. The second component TERC is massively overexpressed in cervical cancer tissue.
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Hello Erik,
A wide number of genome studies suggest that TERT is a susceptibility gene for the development of many cancers. Essentially it promoter mutation is an early genetic event by activating telomerase. Deregulation of telomerase expression in somatic cells might involve in oncogenesis. Therefore, TERT inhibition has been proposed by many groups, as a target for cancer therapies, which is very popular as a telomerase-based anti-cancer strategy!
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We have shown that the presence of CYP enzymes (CYP 1A1, 2A6) in exosomes derived from cervical cancer cells (Ca Ski Cells). When we treated these exosomes to HIV-1 infected U1 macrophages, we observed a massive increase in HIV replication. We think the increase in the viral replication is occurring via a CYP-mediated oxidative stress pathway. If we could inhibit the specific CYP enzymes within the exosomes, it could clarify their role. I am curious if anyone has ideas about ways to inhibit CYPs within exosomes?
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Thank you Dr. Mezencev for your suggestions.
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Dear all,
Evidence shows that VIA/VILI screening tests are more economical in screening of cervical cancer in developing countries. Weather VIA alone will give better results or VILI alone will give better results or both?
Thank you
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We have conducted a study in our institute to establish the effectiveness of Visual inspection methods in comparasion to PAP smear for screening of cervical cancer..
In our study we found the sensitivity, specificity, PPV&  NPV of Pap smear was 81.36%, 93.79%, 29.63% & 99.37%, for VIA sensitivity, specificity, PPV&  NPV was86.75%, 86.06%, 16.34% & 99.43% whereas that for VILI was 86.44%, 84.38%, 15.09% & 99.49%respectively. Although the specificity and positive predictive value of Pap smear was slightly higher than the visual inspection methods there was no significant difference in the sensitivities and the negative predictive value.
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The oncogenic potential of the high risk HPV types lies in the oncoproteins early (E6 and E7) which can bind to and modulate a number of different gene products, in particular, the tumor suppressors proteins (p53 and pRb).
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If I understood your question right, you want to know if other HPV proteins (different from E6/E7) can induce cervical cancer. Besides E6 and E7, E5 has been showed to be an oncoprotein as well. One well explored mechanism of E5 is regarding the evasion of immune system. The high‐risk E5 protein interferes with classical MHC class 1 processing, but also has many other functions related to proliferation.
E5 as an oncogene has been largely investigated in bovine papillomavirus BPV:
Check the review from Dr. Doorbar below:
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Hi,
If anyone can help me on finding out a list of different types of cancer cell lines that aberrantly overexpress the cell surface associated mucin1 (MUC1) proto-oncogene and the percentages of the MUC1 overexpression.
I have already known that MUC1 is aberrantly overexpressed in breast cancer (MCF7), non-small cell lung cancer (A-549) , prostate cancer (PC3), colorectal cancer (SW742) and pancreatic cancer (Aspc-1).
In addition, MUC1 overexpression has been demonstrated in hepatocellular carcinoma (Hep-G2), cervical cancer (Hala) and osteosarcoma (G292).
Thank you in advance!
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The HPV infections are very prevalent so many times HPV might be rather just a side finding in cervical cancer than the causing agent. Is it possible? (As it is well-known, cervical cancer can develop without HPV infection.)
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HPV is always the cause of cervical cancer. A woman may have cancer but no longer have an active HPV infection. Many women (and men) have HPV but only a few develop cancer; however, all women who develop cervical cancer had an HPV infection (originally) which caused it.
Read: The causal relation between human papillomavirus and cervical cancer, Bosch et al. and HPV in the etiology of human cancer, Munoz et al. You can search for both on Google scholar and they are freely available on line to read.
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Dear Sir,
Thank you for availing the cervical cancer data set for research.
I have a question regarding the two fields:
1- Dx:Cancer; is this field means the case has a cervical cancer or not?
2- what is meant bt the Dx field.
3- Is the data set containing both positive and negative cervical cases or all are positive?
Thank you again for help.
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I have some sequencing data from patients with cervical cancer and we have been able to determine that a good number of them, but we are having trouble telling for sure between hpv 16 and hpv 18. I am looking for a specific sequence that can be used tell them apart, does anybody now of a sequence or a set of primers that can be used to set them apart?. Thank you very much
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Kindly go through this
Rapid real time PCR to distinguish between high risk human papillomavirus types 16 and 18 by
H A Cubie,1 A L Seagar,1 E McGoogan,2 J Whitehead,1 A Brass,2 M J Arends,2 and M W Whitley3
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Hi! I am a medical student looking for published data on MIC and ITC detection rate in early-stage cervical cancer patients who underwent robot-assisted surgery and can't seem to find any in pubmed.
It may be that there is nothing published on the subject but if there is, could someone point me towards where I can find that data?
Thank you!
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Thank you! Sorry for the late answer: I didn't receive any email notifying me of your answer. Will check the article right away!
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The kit previous work in cervical cancer!
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The USPSTF of USA recommends screening for cervical cancer in women age 21 to 65 years with cytology (Pap smear) every 3 years or, for women age 30 to 65 years who want to lengthen the screening interval, screening with a combination of cytology and human papillomavirus (HPV) testing every 5 years.
What are the Clinical Considerations for discussion of cytology method, HPV testing, and screening interval?
What should be done in the resource-poor countries?
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This is for an MSc thesis work
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We are starting the research concerning the prognostic significance of immune profile in HPV carcinogenesis.
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Hi Erick 
This articles may help you 
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I don't know how to adjust bonferroni correction to my data. 
Firstly, I tested the levels of several types of biomarker candidates in normal and cancer serum using ELISA. I found three types of potential biomarkers (A, B, C) for discriminating cervical cancer from normal cytology. 
Secondly, I combined three types of biomarkers using logistic regression model. 
Then, I wanna using bonferroni correction to reduce type I error but I have no idea how to adjust the bonferroni correction to my data. 
Is the bonferroni corrected p value < 0.016? (<0.05/3 biomarkers)
Thank you for anyone's help. 
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Yes, for Bonferroni correction you did correct. Basically, here are 2 ways of doing it and both lead to the same result: one way, as you did: when deviding threshold level (0.05) by number of tests. And the second way: to multiply obtained p-values for each test by the number of tests and if the adjusted p-value is still below 0.05, consider as significant. This is about Bonferroni correction.
But now, before doing the Bonferroni correction, clarify for yourself: did you do multiple logistic regression of univariate? If you did multiple logistic regression, you do not need any further correction. As I understood, you combined them, meaning that you did multivariate logistic regressoin analysis. So, just use the p-value you obtained. You could apply the Bonferroni correction to the initial analysis, when all biomarker were analysed between normal and cancer serum.
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I am wondering if somebody could assist/tell me on the methods how to determine the HPV DNA and its onchoproteins/mRNA from women having full blown cervical cancer.
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Dear respectful scholars,
Cervical cell lines; SiHa cell infected by HPV16. HeLa cell infected HPV18.
Does the HPV have an influence to the apoptosis process because some of anticancer agent may not have effect to SiHa but HeLa cells?
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Amended on 22 July 2017
Further, I have been always doubting about the link of Helicobacter pylori (gram-negative, microaerophilic bacterium) to human stomach cancer.   A gastritis patient (8mo, female) has no Helicobacter pylori in her serum.   Her gastritis seems to be occurred by co-infection of Replicase polyprotein 1ab (Human coronavirus 229E; HCoV 229E; +ssRNA) at 1.8% of serum protein, and Protein HXLF3 (Human cytomegalovirus 5; HHV-5; dsDNA) at 2.5% of serum protein.   Then, co-infection of Replicase polyprotein 1ab (with transcription factor (TF) activity; Human coronavirus 229E; HCoV 229E) and Gag-Pol polyprotein (HIV-1; with IN and RT) seems to be the origin of stomach cancer.
A common cold patient (12mo, female) has no influenza virus, but has Replicase polyprotein 1ab (Avian infectious bronchitis virus; IBV; ACoV; with TF activity) at 9.4 μg/mg of serum protein and Conserved hypothetical protein (Mycoplasma pulmonis; may be from gram-positive bacteria; without cell wall) at 12.2 μg/mg of serum protein (total 2.2% of serum protein).   Then, co-infection of Replicase polyprotein 1ab (HCoV; with TF activity) and Gag-Pol polyprotein (HIV-1; with IN and RT) seems to be the origin of lung cancer.
The gait disorder patient (with biotin deficiency and with kidney disease) has Genome polyprotein (HCV; Flavivirus; with TF activity) at 5.3 μg/mg of serum protein and Genome polyprotein (Yellow fever virus; YFV; +ssRNA; Flavivirus; seems to be no TF activity)  at 6.1 μg/mg of serum protein.   Then, co-infection of Genome polyprotein (HCV; with TF activity) and Gag-Pol polyprotein (HIV-1; with IN and RT) seems to be the origin of kidney cancer.    
The GSD-1b patient (with biotin deficiency) has Protein TAT/Transactivating regulatory protein (Simian IV; SIV; with Transcription Factor (TF) activity) at 7.6 μg/mg of serum protein.   Then, the infection of Protein TAT (SIV or HIV-1; with TF activity) and Gag-Pol polyprotein (HIV-1; with IN and RT) seems to be the origin of pancreatic cancer.  
A human breast milk (from a healthy Japanese mother) has Protein Bel-2 (Macaque simian foamy virus; SFV; retrovirus; with Transcription Factor (TF) activity) at 21.9 μg/mg of milk protein.   Then, the infection of Protein Bel-2 (Macaque simian foamy virus; SFV; with Transcription Factor (TF) activity) and Gag-Pol polyprotein (HIV-1; with IN and RT) seems to be the origin of human breast cancer.
A bovine milk of Japan has no retrovirus, though Genome polyprotein (Dengue virus 3; DENV-3、flavivirus, +ssRNA; seems to be no TF activity) is found at 4.6 μg/mg of milk protein.   Therefore, drinking the bovine milk of Japan seems to be safe or no risk for inducing breast cancer. 
Therefore, Japanese edible fucoidan (sulphated poly-fucose; derived from brown seaweed Mozuku) is also expected to be effective on these cancers in addition to liver cancer of rat (please see file; Rat DEN Np-Fuco).
By the way, integrase (IN) and reverse transcriptase (RT) of retrovirus HIV-1 are essential to induce cancer.   Virus of bacteriophage or plasmid is integrated into host DNA to induce lysogenic conversion to change the glycochain of host cells (please see file; phage conversion 2).   Integration of HCV seems to be performed by the help of reverse trascriptase (RT) and integrase (IN) of HIV.   Integrated virus HIV-1 and HCV similarly changes the glycochain of host cell (fucosylation of host cell glycochain in HCC; please see file; Dr. Aoyagi Fucose).   Therefore, integrase of HIV-1 is essential to induce the human cancer via lysogenic conversion.   On the other hand, HPV and Helicobacter pylori do not possess integrase (IN).   Thus, many markers of cancer are related to glycochain-region of glycochain-containing molecules (glycoproteins and glycolipids).        
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Looking any information whether there is rapid point of care molecular methods to screen/diagnose cervical cancer associated with HPV infection. 
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Hi, everyone. I'd like to learn about that How to build and optimize production platform of HPV-VLPs (cervical cancer vaccine) depolymerization and reunion?Who has the relevant suggestions and information? Thanks for your share in advance.
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Can i get a dataset of cervical cancer images??
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Need coding of Fuzzy Level Set Method.I am doing my research in Cervical Cancer using an Image Processing. Completed Confirmation Meeting. I could not able to carry forward my research further. Pls provide some useful information to continue my research.
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I have so much passion for Cervical Cancer Research. Can any one tell me what are the current research gaps in this Field of cervical cancer. Which areas have to be answered. I,m more interested in Epidemiological gaps or issues and management related issues towards cervical cancer!
Thank You!
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Sir, it is more fruitful when you will get study on those part which you may want to work.. You will realize, and make a good hypothesis by studying current research.
All the best
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I am developing two different cancer models in immunocompetent balb/c mice by subcutaneusly injection of Hela and SK-BR-3 cell lines. Appreciate any suggestions.Is there any option to generate tumor in an immunocompetent balb/c mice?. Can we make them immonodeficient? If there is no possibility to use immunocompetent balb/c mice then which type of mice is suggested?  
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Hi Rozita,
1. Immunocompetent balb/c can't be injected human cancer cell lines.
2. Human cancer lines must be injected to immunodeficient mice.
3. 4T1 and EMT6 are very good models in balb/c mice.
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Cervical Cancer is sexually transmitted, and condoms are not preventive. Could some form of contact tracing be applied here?
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I disagree. Firstly males are the reservoir for HPV in terms of cervical cancer, males pass the virus onto females which then may develope cervical cancer. So vaccination of boys will be useful in protecting unvaccinated females and contribute to herd immunity. Secondly there are other genotypes of HPV that can cause cancer other than HPV 16 and 18 which are covered by the vaccines (HPV 6 and 11 are also covered by the Gardasil vaccine and these cause 90% of genital warts), however recent data suggests that there is some cross protection for some of these other types. Finally I do not believe that other genotypes will fill in the space and cause more cancer by the removal of HPV 16 and 18. I spoke at length about this to Ian Frazer and he agrees that because these viruses are old and have co-evolved with us it is unlikely that another genotype will substitue for these. The epidemiolgy also would suggest that this substitution will not happen. For example in a Western Australian study, HPV 18 was in found in lower prevalence (2.6%) compared to other high risk HPv genotypes, for example HPV 52 (6.6%) in the normal population (no dysplasia or cancer). However, HPV 18 was found in 15.6 % of cancers while HPV 52 was not found in cancers at all. This suggests that the onogenic potential of the other non HPV 16 and 18 genotypes is less and that they will not fill a niche left by HPV 16 and 18. Sexual behavior will not be changed by the vaccine but the vaccine will protect against cervical cancer. Australian data is already showing a decline in the number of pre-cancerous lesions.
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In resource poor countries like India.
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Based on systematic reviews and metanylisis and taking account some facts:
1. Among those newly diagnosed with cervical cancer, 30–60 % have never had a screening test. (1)
2. Up to 15 % have had inadequate follow up after an abnormal Pap smear.(1)
3. 60 to 80 % of women diagnosed with advanced cervical cancer have not had a screening test within the past 5 years. (1)
4. The population-level impact of screening (i.e., reduction in the incidence and mortality of cervical cancer) was most influenced by the level of coverage. (2).
It is evident that due to the already established relationship between high-risk oncogenic HPV and cervical cancer, the possibility of primary screening using HPV DNA test, specially in places where cytology has not been used or where, for some reason , has not been adopted appropriately is very cost-effective. (3)
1- Glick et al, 2012
2- Goldie et al, 2006
3- Luhn ; Wetzensen, 2013
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For a case of unilateral serous multilocular ovarian cyst with multifocal dermoid cysts incorporated in the wall of the cyst in a 29 years old female with 2 living children?
what about differential diagnosis and possible ones ?
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A possible differential diagnosis are also endometriomas, which are often multilocular. However the most frequent diagnosis are cystadenofibromas or cystadenomas.
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The main reasons associated with the poor uptake of the vaccine are cost, physician recommendation, acceptability, and concerns. How can I address them?
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Low cost, convenience, Clinician's strong recommendation
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A high level of agreement and or concordance is observed for high risk HPV than low risk HPV when HPV detected with self-collected samples are compared to those detected with a doctor's collected samples. Please provide citation if available
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Dear Adolf,
Follows the paper that Prof. Eleuterio has mentioned.
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I need some meaningful contributions please.
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Yes
The HPV virus has to reach the basal cells of the cervix. Therefore, there must be some form of break in the epithelium for the HPV to reach the basal cells. Cervicitis is one way in which there can be a break in the epithelium. A similar situation exists in throat cancer and the relationship between smoking and drinking spirits. The smoking and spirit drinking results in a break in the epithelium and therefore HPV can reach the basal cells. In cervical cancer it does not have to be cervicitis and the process of metaplasia is also thought to be associated.
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I was wondering if there is more ongoing research involving newer biomarkers for earlier detection of tumours. As much as one hears about the newer ongoing cancer therapeutic research or late stage cancer, one doesn't hear or follow much about the newer cancer diagnostic biomarker studies. I would like to get your feedback on this issue.
As an example, the overexpression of p16 (INK4a), in initiation of neoplastic transformation of HPV infected cervical epithelial cells has been useful in the early detection of cervical cancer using Immunohistochemistry and has been very helpful in the clinics. On the other hand, targeted molecular research application of cancer therapy for breast and lung cancers, such as HER2/Neu or EGF receptor 1 inhibitors, do reduce the tumours but at that point the tumours are already very aggressive in nature and also such therapies become very expensive for the patient and have a lot more side effects that also limit their efficacy. Also cancer is curable when detected early and prevention is better than cure.
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It a great view, thank you for the comment. Yes, I truly believe the challenge lies in understanding, analyzing and the mass data generated by hi-througput studies of specific cancers both at the genomic and expression levels. As of now we have to depend a lot on the specific scanning data using PET or CT scans to identify tumour masses or metasatsis at the clinics. While there are few new specific diagnostic biomarkers to follow up the specific lesions for diagnostic or prognostic views, well that's how it appears..
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Human Papilloma Virus (HPV) is the main cause of cervical cancer. In addition, HPV is also responsible for many other cancers including vulval, vaginal, anal, penile and oropharyngeal cancers. However, now we have a powerful tool against HPV in the form of a vaccine. Thus, HPV vaccination at a mass scale will not only eradicate cervical cancer but also probably eradicate/substantially reduce a number of other cancers in both men and women.
However, HPV related cancers are more common in low- and middle-income countries (LMICs) and due to prohibitive costs, cultural reasons etc. the access, availability and uptake of HPV vaccine remains low in LMICs. I would welcome your thoughts regarding figuring out ways in which HPV vaccination can be made cheaper and more widely available. We also need ideas which will encourage LMIC governments to include this vaccine in the country immunization programs, and to overcome cultural barriers so that we can imagine a time when cervical cancer (and the other related cancers as well) have been eradicated.
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Mr. Skaete is not correct. Both Gardasil and Cervarix data show that women previously exposed (seropositive) do gain efficacy and increased immune titers after vaccination. Cervarix is better than Gardasil for antibody induction and disease prevention. But the efficacy is less than if the woman had been seronegative and DNA negative at vaccine administration.
A combination of screening (must and is first priority) with vaccination for those who choose to be vaccinated is how the message of cervical cancer prevention (not eradication) can be accomplished.
New screening methods with HPV testing as primary provide the near 100% sensitivity for CIN 3 disease that cytology cannot. Fewer screens in a woman's lifetime with the more sensitive test (and resulting increase in false positives and trips to colposcopy) will allow the rate of cervical cancer to drop below the 2-3/100,000 that is now possible with cytology alone.
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I am currently carrying out a project examining the potential effect HPV has on keratin expression in HeLa cells and C33a's which will be divided into those transfected with a HPV plasmid, and those not including the plasmid. I'm finding it difficult to pinpoint the markers used for keratin expression, would someone be able to point me in the right direction. I understand a panel may be necessary, but which immunohistochemical markers for cytokeratin would be the main ones to use here?
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To really understand effects of HPV on keratins, you will need to include a broad panel that reflects both reserve cell and squamous cell keratins. I would include 5, 7, 8, 14, 17, 18 and 19. I would not include k1 or k10, since squamous cells do not differentiate significantly in monolayer culture. I don't understand why you want to look at HeLa cells, since they already contain HPV 18 and express the viral E6 and E7 genes.
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I am looking at the acetowhitening dynamics observed in dysplastic cervical tissue. For my experiments I need to source cervical fibroblasts and keratinocytes (preferably both, though only one or the other will do).
Is anybody aware of any companies etc where I might be able to order these cells from? At this point, obtaining biopsies from which to isolate cells is not an option.
Failing that, I am also looking for oral keratinocytes and fibroblasts. Does anybody know where I might be able to source these other than via punch biopsies. I.e. are there any cell culture companies who might supply these cell lines?
Thanks.
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I don't think no company is preparing oral fibroblasts or keratinocytes,but it is easier to isolate fibroblasts from oral cavity especially from gingiva. Only hinderance is you have to harvest under aseptic condition otherwise whole sample go waste. Gingiva has abundant fibroblasts and keratinocytes and also can be easily harvested by punch biopsy
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How do nurses care for women with cervical cancer?
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With a caring heart. Answering question as honestly as you can.
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A 43 years old patient presents squamous carcinoma IN SITU from vaginal cupola and HPV signals post-total abdominal hysterectomy due to NIC III performed more than 10 years ago. Witch would be the better treatment option for?
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So this is not a recurrence. This is a vaginal cancer. (She had TAH <33 years old?)
Was a cervical cancer documented in the specimen after the TAH?
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Can someone recommend a simple protocol for preparing HeLa culture? Or can you give some details?
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Hi Ashraf Ali. Sorry for d late response.
Some links below for your use.
http://www.abcam.com/ps/pdf/protocols/cell_culture.pdf (This is a general guideline but u'll find it useful, I did.)
All d best.
P.S. I forgot somehow to mention that t DMEM makes the remaining 89% volume of the culture medium.
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I am considering doing my masters thesis on this topic but as a new masters student, I would greatly appreciate some guidance. Thank you!
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RLB is used for HPV Detection
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I am coordinator of an FP7 RAIDs project (rational assessment and innovative drug section) on cervical cancer. The project involves genomic and proteomic as well as tumor micro environment definition. As model systems we shall also phenotype cell lines and assess single or double drug targeting strategies.
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Please see my profile if you think we can talk in details
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I am currently studying HeLa and C33a cervical cancer cultured cell lines. I have observed interesting immunohistochemical staining pattern of cytokeratins in C33a cell line. To understand these findings I am trying to establish whether these patterns are related to cell cycle stages.
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Hi Debashish, thank you for your reply. I have looked at few report in the setting of cervical cancer and other types, which do suggest this varying cytokeratin profile. However, I was hoping to find some correlation of this to cell cycle, or something else. Perhaps phenotypical changes through different passages may contribute to a varying cytokeratin expression within a cell line? any suggestions on that?
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The first thing we must keep in mind that one micro-RNA can only be used for diagnostics if it getting overexpressed or or underexpressed only in cancer tissue and not in normal one. But in your case as I can understand you have a single micro-RNA, with one micro-RNA from one data-set its difficult to access its diagnostic relevance. In such cases important aspect is to look for its disease association, that how the micro-rna is associated to the disease. If it is expressing then it must have some role in any of the hallmarks of cancer. Many times a kind of micro-RNA signature is predictive of a cancer stage or kind of disease, e.g. many microRNA signatures are distinct for metastatic and non-metastatic cancers. So you need to dig more before declaring it of a diagnostic relevance.
Oral contraceptives & cervical cancer
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What is your opinion: do oral contraceptives increase a risk of cervical cancer? answer only yes or not
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I have at least 3 patients (female 11-13 yo) who received the first dose of Gardasil in 2009 or 2010 and just now (second semester of 2012) are coming back for the two doses left. What do you think we should do?
Should we re-initiate the three doses scheme?,
Give the two missed doses with a six months separation?,
Do not give more doses?,
Other solution?
Thank you for your input...
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No vaccine series needs to be restarted because of an interval that is longer than recommended (with the exception of oral typhoid vaccine in certain circumstances). You should continue the series where it was interrupted. In rr5515.pdf (Recommendations of the Advisory Committee on Immunization Practices (ACIP)) from 2006 look the paragraph Lapsed Vaccination Schedule p11
If the HPV vaccine schedule is interrupted, the vaccine series does not need to be restarted. In mm5920.pdf (CDC/ MORBITIDY AND MORTALITY WEEKLY REPORT)
page 19
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I research oligometastases and oligo-recurrence.
Oligometastases is the state that cancer patients with 1 - 5 recurrent or metastatic lesions, which could be treated by local therapy directly, often combined with sophisticated systemic therapy and to achieve long-term survival or even cure. Oligo-recurrence is the state that cancer patients 1-5 recurrent or metastatic lesions with primary lesions contorol. Then, local therapy is more effective for oligo-recurrent state to achieve better survival than other types (with active primary lesions) of oligometastases.
I am targeting breast cancer and NSCLC.
Which other types of cancer are good candidates to research oligometastases and oligo-recurrence?
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If your focus is on acute laboratory or imaging results then you can select cases of sufficient number, either all of one diagnosis or some for each diagnosis, depending on your research questions. However, if your focus is on down-stream effects and survival/survivorship, then you need engaged patients and possible more of them. It depends on your focus. If you clarify that then further advice can be offered.
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Is HDAC overexpressed in cervical cancer? What is the mechanisms of oncoprotein E6 and E7 of HPV influence the activity of HDAC?
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Dear Abi,
To answer this question beyond a single research article, I strongly recommend you to search the NCBI GEO profiles database, it is a free database.
For example, I did a search for HDAC9 (you can try other types) and cervi* (truncated term so I can get cervix, cervical) and there seems to be a sligh upregulation when compare to normal samples and as one moves towards late stages (high grade vs invasive) http://www.ncbi.nlm.nih.gov/geo/tools/profileGraph.cgi?ID=GDS3292:205659_at
However, did not find significant differences in terms of expression of HDAC9 btween HPV-positive and HP-negative samples for squamous cell carcinoma http://www.ncbi.nlm.nih.gov/geo/tools/profileGraph.cgi?ID=GDS1667:205659_at
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More than ten percent of the female population has been involved worldwide in bacterial vaginosis, but the cervical cancer is considerably less frequent. So the hypothesis that bacterial vaginosis predisposes to cervical intraepithelial neoplasia does not have a strong possibility according to the statistical data mentioned above.
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I agree with Federico Nave that statistically significant association doesn't mean diagnosis.
Only HPV infection is etiological factor of cervical neoplasia.
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I used EORTC questionnaires to assess changes in quality of life over time in various domains.I need a graphic method to present these changes.Any suggestions?
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I think you simply use  Ecell Matrix . Though you genterate graphics including curves and bars.
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Which test should be preferred over the other in combination with LBC? Should one do a HPV DNA or a E6/E7 mRNA detection?
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The preferred screening depends on the resources available, the population screened and also the objective. HPV DNA is relatively less expensive and easily applied to the community based screening programme. But the problem is that it is often nonspecific, especially at younger age (<30 years) and mere presence of DNA is not necessarily translated into the progression to CIN or higher lesion. E6/E7, on the other hand is very much specific, as they are expressed preferentially in the cells that are on the process of neoplastic transformation and so can detect the women who are going to develop CIN soon. But the main constraint is the cost. 
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Can someone provide me with cervical cancer dataset?
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Hi, can you explain a bit what you want to do?  The topics suggest pre-treatment and data mining.  How big of a data set do you need?
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need the database for analysis
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We are trying to extract HPV DNA from cervical swabs (ThinPrep) using MagNA Pure 96 equipment from Roche and we are encountering a serie of dificulties.
We have tried several approaches regarding sample preparation:
 - 2 ml or 1 ml of cell suspension, wash with PBS, external lysis (1 hour or overnight incubation with Prot. K), take 500 ul directly to the equipament -> 50 or 100 ul of elution
 -  500 ul of cell suspension directly to the equipment, without any sample preparation
 - 500 ul of cell suspension directly to the equipament, without any sample preparation, and adding 50 ul of PBS 10x
We have used several protocols: Viral Universal, Pathogen Universal, DNA Cells, Viral NA Plasma. 
The best results obtained were an agreement rate of 50% with the current extraction: manual protocol using Virus MinElute Kit from QIAGEN. The amplification system is a real time PCR with SYBR Green (Master Mix from Applied Biosystem) or a commercial kit INNO-LIPA from Fujirebio. 
Does anyone have a tip to improve this agreement rate to 90 or 100%?
For other types of samples the results are good (plasma, urine, dried swab,  LCR) except for the fact that in External Quality Assessment programs the extraction efficiency is very low: the diference in the Ct values are as big as 6 units. 
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How did you determine the 50% value? Was it purely based on PCR, or did you quantify the DNA using some other method?
If you have access to a NanoDrop or other spectrophotometer, you can estimate the quantity and purity of DNA. 
A fluorescence based assay, such as Qubit, is good for more accurate quantification of your extract. 
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We are listening different types of cancer for example brain, blood, lymph nodes, lungs, bone, breast and, cervical cancer but why then, we are not hearing heart cancer? Is there any special mechanism responsible for that? I have studied some of the research works on that and got that tumors produced in the heart but those didn't converted to malignant stage. A sarcoma is a type of tumor that originates in the soft tissues of the body; a rhabdomyosarcoma occurs in the muscle tissue of the heart. But its incidence is not frequent for example less than 0.1%.
Please help to why do we never hear about heart cancer??
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Dear Béatrice Marianne Ewalds-Kvist , I am working in Labaid Cardiac Hospital and everyday lots cardiac patients come here for treatment as well as for services. But I haven't got the any patients regarding to Cancer disease. In Bangladesh there is no proper facilities to do such type of higher research. But I got some information that some research has been done on it and found rare cases regarding heart cancer.
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Cervical lesions
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Thank you, Beatrice. 
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What is the special properties of cervical cancer cells taken from Henrietta Lacks?
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The cell line is still continuous line submitted by Gey in ATCC. Though, I heard most of the HeLa is contaminated. Now, you can get variant HeLa for example 293. If we culture from others its not called as HeLa. Even though cellular origin and carcinogenicity are similar, Cell line vary from each other in expressing varying levels of proteins. Like human cervical cancer cell line HeLa doesn't express CD40, where as similar cervical cancer cell line obtained from human SiHa expresses CD40.
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I am working with HeLa and CasKi cell which contain HPV18 and 16 respectively. The MTT results of my plant extracts showed better outcomes on HeLa cells than CaSki cells that was a bit surprising for me because HeLa cells seemed to be more invasive and fast growth. I could not find any article about difference between treatment of cervical cancer caused by HPV 16 and 18. would be grateful if any one let me know which type is more invasive and harder to treat with anticancer agents.   
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Neda, you have noticed the fact a tumor is less reponsive to chemoradiotherapy does not mean it cannot be more responsive to other agents. Please keep on research on herbal extracts and possible other agents. Include other climates and local ecosystems too. Important conclusions could arise.
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An 62 yrs old woman with bulky melanoma of cervix with extension to endometer and distal vagina. metastatic work up is negative.
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Dear Dr Go J Yoshida
if inguvinal nodes clinicaly is negative ,do you recommend sentinle lymphe node biopsy via technecium?
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We are looking into use the cell line for a mouse model but I was unable to find it on ATCC or elsewhere. Are there issues with the model that I should be aware of ? If you could also suggest an alternative HPV cell line for mouse model, I would be grateful. Thank you so much !
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Hi Sri - unless it is for some health and safety reason (a cell line expressing oncogenes) I don't know why it is unavailable. What about Caski or SiHa cell lines (although human)?
Best wishes
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Hi, i need cervical cancer benchmark images
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Cervical cancer is staged clinically. That is, it is assessed by direct visual inspection of the cervix and by palpation by digital pelvic examination and then also by some broad clinical markers of kidney function or other organs being compromised. If you google search for "cervical dysplasia picture atlas" who should find many published books. If you are talking about benchmark for Cervical cancer in Cat Scan or MRI imaging I'm not aware if these have been assembled into an atlas but a radiology text might be a good place to start.
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I have perform my IHC on cervical cancer tissues (PF), following that I have also got the slides evaluated from the pathologist. The pathologist have scored the slides on the basis of the protein expression (i.e. +1, +2, +3).
For further validation or quantification what further analysis can be done?
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We use the Aperio positive pixel for all clinical trials.  It is a FDA approved algorithm.  You must first have the slides scanned via the Aperio system.  Then download the image scope  app to open the slides.   Free....The positive pixel algorithm is there.
It is the easiest  image analysis system there is.  Easier than  Image  J, Metamorph, and Image Pro plus.
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Hello dear community,
I have a question for all biologists, physiologists, physicians, pharmacists, gynecologists
My sister is 12 years old and the doctors say they should be vaccinated against HPV (human papillomavirus), not later than in two months.
My question is, I have read in various sources that vaccination is harmful and can cause cancer. I'm looking for the truth, I know that the only vaccination against human papillomaviruses, which Cervical cancer can prevented. I want to know from you what is true and like I want to be able to have evidence to understand that.
I hope for a fast answer
Thank you,
Petr Kirpeit
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What I have learned about HPV and this vaccine I can suggest to give it....it will probably protect from  HPV and as Ru-Jeng Teng sad no there are REAL evidences about vaccine causing cancer!
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I am having trouble growing tumors on NOD/SCID mice with HeLa Cells. Has anyone tried growing tumors with this cell line? There is considerable inconsistency I am observing with the tumor growth and would be glad if I could get any suggestions or help.
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We've done NOD/SCID xenografts with HeLA (http://altogenlabs.com/xenograft-models/other-bladder-cervical/hela-xenograft-model/). Matrigel is of course a necessity, and the inconsistency of results is usually resolved by letting the tumors reach a certain volume before beginning any kind of treatment. The resulting growth patterns (if the treatment is effective) are substantially different, and appropriate statistical tests help establish significance.
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What is the main HPV types in cervical cancer women who are HIV positive?
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You might want to check the following paper:
Human papillomavirus types among women infected with HIV: a meta-analysis.
By: Clifford GM, Gonçalves MA, Franceschi S; HPV and HIV Study Group.In: AIDS. 2006 Nov 28;20(18):2337-44.
It says:
The six most common high-risk HPV types were 16 (4.5%), 58 (3.6%), 18 (3.1%), 52 (2.8%), 31 (2.0%) and 33 (2.0%). HPV16 was also the most common type in 2053 HIV-positive women with ASCUS/LSIL and 295 with HSIL.
A more recent article may be of interest as well but it does not seem to answer your question directly:
Human papillomavirus infection and increased risk of HIV acquisition. A systematic review and meta-analysis.
Houlihan CF, Larke NL, Watson-Jones D, Smith-McCune KK, Shiboski S, Gravitt PE, Smith JS, Kuhn L, Wang C, Hayes R.
AIDS. 2012 Nov 13;26(17):2211-22
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If so, what is the cut-off level for HPV types to be defined as high risk?
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Yes. Subtypes HPV 16 and 18 are found in over 70 percent of all cervical cancers. 
High-risk (oncogenic or cancer-associated) types
Common types: 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 69, 82
Low-risk (non-oncogenic) types
Common types: 6, 11, 40, 42, 43, 44, 54, 61, 72, 81
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For cervical cancer, it is infected by human papillomavirus that contain two structural proteins and other oncoproteins. But there are about 20% of patients are anti-HPV16 E7 negative. However HPV16 E7 protein is oncoprotein. Why is it? Could anyone give me the answer? Thanks. 
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Cervical cancer is developed only with presence of HPV. Absence of Anti HCV antibodies are explained by locality of infection.
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I am currently working on stem cell markers (5 markers) on cervical cancer patient tissue. Some one suggested me to run all the markers together for one tissue then proceed with next tissue sample.
OR
I can run one whole batch of samples with one antibody then other.
Will it make any difference?
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I would also recommend to stain one antibody after the other. From technical point of view it is better to know first, that the marker works on all types of tissue. If one of it fails because of the need of a different AB-titer (eg high expression vs low expression), you have to restain all your specimens with the new titer for a valid comparison.
And there are usually less variations, if you provide one larger amount of working solution instead of serveral times making a small amount.
Do you work on FFPET? Have in mind, that the prepared sections for IHC should be stained within maximal 2 weeks. Too long storage can influence your antigens.
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There is a high burden of HPV infection in women coming to the antenatal clinic of a referral hospital I mentor. Since I do clinical consultation of HIV and STI related cases they usually keep them for me to see. However we could not provide screening services for CIN and we know that HPV contributes to 90% of cervical ca cases. However we do not provide screening services which means we could not offer the opportunity of treating early cases of CIN thereby preventing advanced ca. Recently I took an online course and exam which I passed on VIA (visual inspection of the cervix using aceton) and the screening involves treating of suspicious cases using cryo therapy which I also could administer. cryotherapy is highly effective and well tolerated. So my question here is that if there is anyone here willing and able to assist me to set up the screening and early treatment as well as prevention of advanced ca of the service in this resource poor setting. Thank you.
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I think that the best way is combination of PAP smear (ecto- and endo-cervical) and Colposcopy.
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We encountered in the camel clinic during gynecological examination of infertile females some cases with vaginal growth. By routine histological examination,   vaginal adenocarcinoma and squamous cell carcimoma were diagnosed. I would like to know the predisposing factors for these cases? Are the mating behavior (frictional for 10-15 min, the penis is fibroelastic type=hard) and the chronic vaginal inflammation contributing factors? What about the condition in women or in the other animals?    
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Interesting question. Could the traditional bedu (and somali) treatment against camel sterility: cutting with an unsterilized razor blade any small protruding area found in the vagina play a predisposing role?  
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Sexual behavior and HPV virus infection by cervical, breast and duoble carcinomas....
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Hig risk HPV types (HR-HPV) are implicated as direct causal agents in the carcinogenesis of different types of cancers. Persistent infection with HR-HPV (mainly HPV 16 & 18) is the major cause of the main types of cervical cancer (up to 70%).
However, HPV infection alone is not sufficient cause. Thus, long term virus persistence and the participation of other cofactors are needed to increase the risk of cancer progression. These include; high parity, cigarette smoking, long term of using hormonal contraceptives and nutritional factors.
Breast cancer (BC) is accounted as a multifactorial aetiology disease. Some of the risk factors are: mutations in the BRCA1 & BRCA2 genes (inherited genes), radiation, exogenous hormones, increasing age, alcohol, diet and lack of physical activity. Additionally, reproductive events such as early menarche, late menopause and late age at first pregnancy could be also implicated as risk factors for BC.
We've already detected some of the high risk HPV types in breast cancer cases. However, HPV and Breast cancer development is still controversial. Currently, we are aiming to investigate the definitive relationship between HPV and BC development.
Regards .
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Could someone help me with the case of a patient who underwent surgery of Wertheim-Meigs for cervical cancer for 15 days ago, and has been showing urinary retention. She referred to feel of bladder fullness but can't urinate. We are making intermittent catheterization.
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in my opinion good urine microscopic examination and culture sensitivity to rule out any infection. micturating cystourethrogram to rule out any injury.some time Bladder atonicity can occure because of denervation, so ratherthan intermittent catheteraisation i feel catheterise the patient and investigate and treat the cause accordingly. 
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I want to do gene clustering in R using the dataset from GEO. About 2433 datasets are available.  If I want to do it, how should I select the dataset. Is possible to select two cell line dataset and do clustering. I want to know the logical errors behind the selecting the dataset. 
I am following the given below steps for clustering
1: Downloaded the 2433 available dataset from GEO
2: Or else direct fetching of all the dataset from GEO in R
3. Loading and normalizing the data
4: Quality check
5: Filtering dataset
6: Finding deferentially expressed dataset
7: Annotating the dataset
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Probably you could first visualise each dataset in an eye-pleasing manner. I have an R/Bioconductor package (http://supfam.org/supraHex/) which can help you a little bit. 
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tumor markers for fgs histochemistry
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Please check:
Cervical cytology as a diagnostic tool for female genital schistosomiasis: Correlation to cervical atypia and Schistosoma polymerase chain reaction.
Pillay P, van Lieshout L, Taylor M, Sebitloane M, Zulu SG, Kleppa E, Roald B, Kjetland EF.
Cytojournal. 2016 Apr 20;13:10. doi: 10.4103/1742-6413.180784. eCollection 2016.