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Hepatocellular Carcinoma - Science topic

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Essentially, we have various HCC cell lines that we plan to do a migration assay using corning transwell 8.0 um pores w/ matrigel. Utilized a chemoattractant of 5% FBS/DMEM serum as the chemoattractant. Utilized some growth factor + inhibitor that was present in other wells for variation. We seeded 50,000 cells and they were visible in the insert following seeding. However, when I washed/scrubbed the insert following fixation (4% PFA, then 1% crystal violet soln). The issue comes when I observed the cell/inserts under the microscope for imaging. I noticed that there were only cells present around the edges of the insert..My assumption is during the scrubbing with the cotton swab, the cells were removed. In this assumption, I would then assume that the cells never migrated down through the pores. For the chemoattractant with the growth factor, we used a concentration of 50 ug/mL and on the last variable, we used an inhibitor following that pathway with a concentration of 1.0 uM. The cells were allowed to migrate for ~24 hrs. I suppose, we could increase invasion time to 36 hrs to see if that works, but not sure what else to troubleshoot, as scrubbing is necessary to remove non-invaded cells..
Thanks in advance for the assistance.
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The result you found could be due to several factors:
1- Have you optimised the "matrigel" concentration through which the cells invade?. Too much of that and none of your cells will pass, which may explain why you are seeing cells around the edges where the concentration of matrigel is usually less.
2- The medium you are using to attract the invading cells could possibly be the reason.
3- The duration of the experiment maybe too short for this type of cells, which may need a longer duration to invade. I suggest you review references about needed time for HCC to invade.
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Hello everyone!
We have fibroblasts isolated from hepatocellular carcinoma tissue samples. We are planning transcriptomics. However, I am not sure if it is doable since there are only 2500-3000 cells. Which method do you advise? Might Nanostring work?
Thanks in advance for your time and consideration.
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The above links include a single-cell RNA seq that may be helpful. Good luck.
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I'd like to determine microvessel dimensions in various tumor groups and am looking for an online database to draw pathology slides from.
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نعم ولكن تحتاج الى عملية بحث واسعة وكبيرة للحصول عليه
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I am interested in the study of mRNA vaccine for hepatocellular carcinoma. I have searched for a long time, but I can not find any articles? Can someone share me these articles?
Thank you very much.
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Yes of course
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In mice, chemical agents such as DEN and aflatoxin B1 can trigger liver cancer after several weeks. But can mice induce liver cancer with other chemical agents or methods in a short period of time?
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What is the best available treatment to get rid of (or limit the development of hepatocellular cancer in babies ( enfants about 1y)? Is the chemotherapy is dangerous for babies? Can a baby survive liver cancer if it is spread over many spots?
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Hepatocellular carcinoma is one of the deadly malignancies. It usually occurs in cirrhotic patients.
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With pleasure.
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I am looking for BL/6 mice to develop HCC model. or anyone already working on such model, i need guidance from that PI.
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no one i think ...still
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Would like to ask of any experience or evidence of anyone in Nuclear medicine or Interventional radiology regarding MAA lung shunting pre therapy for a case of SIRT therapy of Hepatocellular carcinoma?
1. If there is evidence of portal vein thrombosis, how accurate are the findings of MAA lung shunting percentage?
2. If there is no uptake on the MAA, at the site of liver lesions seen on CT, is there any value to do a FDG PET CT for this case, even though its a Hepatocellular carcinoma? Given that HCC has low FDG avidity unless it is an aggressive tumour?
Please share your experience. Thank you in advanced!
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The degree of the portal vein thrombosis is important since in cases with severe abnormality you cannot perform SIRT.
As you have mentioned, FDG is not a valuable tool for evaluation of most of HCC cases. FCH PET/CT would be a good choice where it is available.
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Can anyone provide information regarding the derivation of the Hepa1-6 murine hepatoma cell line, specifically, was this line originally derived from a male or female mouse? Thanks.
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the str profile on
says it is female
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Based on the similarities between Hepatitis B and Hepatocellular carcinoma, what's the probability that a drug developed to effectively rid the body of Hepatitis B could be effectively used to manage HCC caused by hepatitis B virus
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Clearance of serum HBV DNA and lowering HbsAg level by taking antiviral drug significantly reduce risk of developing HCC. Chiang et al had demonstrated a strong decline of HCC following antiviral treatment as the lifetime risk of developing HCC was as high as 21%.
By using antiviral drugs in those with hepatitis b induced HCC, overall survival rate of HBV-related HCC after curative and palliative therapies, are proven to be improved. This could be explained by antiviral drug which could reduce the viral load/HBsAg level, with improving liver function, reducing or delaying HCC recurrence. And this is already applied in some national treatment guidelines/consensus of hepatitis B induced HCC.
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Hi,
i am working on effects of gemcitabine in HepG2 cell line and i should use the IC50 of Gemcitabine in the experiments.i found different values in literature and the numbers are highly variable ranging from lower nanomolar to lower micromolar for the same cell line under same conditions.!!!!!!
but in my tests,which i use different dose of gemcitabine from 0.25 to 16 micro molar ,from dose up to 1 micro molar ,i got same viability percentage.(60 percent)for all of drug doses.and also when i look at my cells,their morphology change a little bit and cells become wider like they are in G1 phase of cell cycle and the apoptotic cells are not exist in my plates.i think that the drug arrest my cells proliferation.i cant get the IC50.
is it normal ???
what should i do?
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Dear Shadi,
I had the same problem with a drug which later on i realized that it wasn't soluble in the medium. And because of the insolubility, the IC50 of my tests changed dramtically. I suggest you to make sure of the drug solubility in the medium before adding it to the cells.
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I observed growth inhibition/cell arrest coupled with cell migration at the same time during treatment of drug X that activates MAPK signaling.
Why are cancer cells arrested before they could migrate?
Are these cells preparing themselves (preparation phase?: attain enough signals, morphological alternation etc. ?) so that they could migrate easily?
Reference to your input will be highly appreciated.
#metastasis #Cancer #Hepatoma #signaling
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Tumors are very heterogeneous genetically, phenotypically and metabolically. With clonal evolution you have more than one kind of cells that evidently behave differently.
If all the cells would be equal, chemotherapy would solve all cancers. It does not.
In your case you have two different kind of populations.
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Dear Colleagues:
the first table of the article describes the differences between cirrhotic and non cirrhotic hepatocellular carcinomas and notes that when the first is caused by alcoholic or viral insults to the organ, the later is, among other causes, derived of metabolic alterations. This statement, I consider should be revised because it has been widely studied the association of non-alcoholic fat liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) as cirrhosis causatives and their close link to metabolic origins.
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Metabolic syndrome is a constellation of problems including obesity, dyslipidemia, diabetes, and insulin resistance These diseases are associated with both increased risk for, and worsened outcomes of many types of cancer. In the liver, inflammatory and angiogenic changes due to underlying insulin resistance and fatty liver disease will likely lead to increased numbers of patients with HCC in the near future. Much work needs to be done to define more clearly the risks for development of HCC in those with underlying metabolic syndrome, the best methods of screening those at risk, and ultimately, the best treatments targeting the underlying mechanisms of pathogenesis.
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I just realized that my liver tissues may might have hepatocellular carcinoma (HCC) but I'm having difficulty finding any regions of potential HCC. Unfortunately I only have stained for cell nuclei and for transgene expression, which is unrelated unrelated to HCC.
Unfortunately I don't have any H&E images.
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Dear Matthew,
since DAPI is a nuclear dye, it is not sufficient to identify HCC cells. If you want to identify such cells in your sample you can co-localize DAPI with Squamous cell carcinoma antigen (SCCA).
Good luck with your research,
Davide
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Hi,
i am working on effects of gemcitabine in HepG2 cell line and i should use the IC50 of Gemcitabine in the experiments.i found different values in literature and the numbers are highly variable ranging from lower nanomolar to lower micromolar for the same cell line under same conditions.!!!!!!
the IC50 that i got from my experiments are different from loterature and also is variable in each test of mine.....
in each test i got different IC50 and the conditions are the same in all experiments.what should i do?
the source of gemcitabine that i use is powder and the solution of gemcitabine is unstable and each time i should make it...
do you have any suggestion to solve this problem?
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Mr Michael Theobald thanks for article that you suggest. and the expiry date on the drug package is for year 2020.
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We use DEN injection and high fat-choline deficient diet to induce the HCC model. The CPG-3 staining has no positive result.I also used ARG-1,but it's not a good marker as it can express in the normal liver tissue.
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The following article will be helpful-
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I am looking for a commercial supplier of Hep-G2/2.2.15 cells (Hep-G2 with stably integrated HBV viral genome). I cannot seem to locate them in any publicly accessible cell repository. Thanks.
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Ah. I did. They do not have. Any other suggestions?
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HepG2.2.15 is a hepatocellular carcinoma cell line which is transformed HBV.I want do some research about the influence of HBV for hepatocellular carcinoma .However,I don't have the cell line in my lab.If anyone would like to share the cell line with me,I will be eternally grateful.
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Does anybody from India
have the HepG2.2.15 cell line?
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I am working on hepatocellular carcinoma (HCC). Does anyone know if there are scRNAseq data of single cells isolated from whole adjacent liver/tumor tissues that published online? Thanks for help!
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The TCGA site mentions that they have characterized HCC into a dataset, but I couldn't find it with the link they provided. This may be a good starting point.
On the GEPIA site they have a differential expression analysis of HCC here: http://gepia.cancer-pku.cn/detail.php?clicktag=degenes###
Let me know if this helps or not. I can keep looking for other options if this doesn't meet your needs.
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I am working with Huh7 hepatoma cells. I have to starve the cells for my experimental purposes. If someone would share the experience of cell survival duration without FBS it would be highly appreciated.
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It depends on cell type. However you can go upto 36-48 hours in general.
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Primary cell isolation from human hepatocellular carcinoma
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Are there any clinical trials going on??
In Europe please
Regards
EPL
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If you check the ClinicalTrial.gov database you can find only 6 studies in this indication. Only 1 has been conducted in Europe and it is reported as "terminated". Below the link.
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I am trying to do transfection of SNU 449 hepatocellular carcinoma cells by GFP plasmids using Bio Rad micropulser electroporator ! according to its protocol it nables safe and reproducible transformation of bacteria, yeast, and other microorganisms.. I wonder if it will work for plasmids or crisper cas9 !!!
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Hi Nehal, unluckily the MicroPulser is an elecroporator designed for bacterial/yeast transformation, not eukaryotic cell transfection. So it would not work with your cells, it would probably fry them.
To do eukaryotic cells you would need something like the Gene Pulser XCell (to stay with BioRad), which can do bacteria, fungi, and eukaria depending on which components you buy with the base system.
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Cancer Immunotherapy:
Do You have anything to say?
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In our Anti-PD-L1 immune checkpoint inhibitor trial we are seeing 30% of patients with complete response, in oesophageal adenocarcinoma, We are still going to see heterogeneous responses, more work needs to be done to understand why.
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Most cancers are detected when they cause symptoms that lead to medical evaluation. Unfortunately, in too many cases this results in diagnosis of cancers that are locally invasive or already metastatic and hence no longer curable with surgical resection or radiation treatment. Medical therapies, which might be curative in the setting of minimal tumor burden, typically provide more limited benefit in more advanced cancers, given the emergence of drug resistance.
http://science.sciencemag.org/content/sci/359/6378/866.full.pdf
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Liquid biopsy detection is promising method to detect cancer at early stage. Following the progresses of developing the sensitive methods to detect the cancer-related DNA or proteins in the blood, early detection for cancer becomes realistic.
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What are the recent trends concerning Hepatocellular Carcinoma Prophylaxis & Treatment?
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I agree with Dr Luis Rodrigo that early detection is the best approach however new drugs are entering the scene Lenvatinib has a better progress free survival and higher response rate than sorafenib and we are waiting the results of nivolumab versus sorafenib
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New trends according to the high technology, diagnosis, prognosis, and treatment allocations.
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The new trends include to achieve an early diagnosis, to find more molecular signs related in HCC and to improve their therapies
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HepG2 cells are Hepatocellular Carcinoma (HCC) cells or hepatoblastoma cells?
Is this cell line really a misidentified cell line?
Regards
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thank you so much Max...i will have a look to it...
Best Regards
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Complications related to viral hepatitis, alcohol-related and non-alcoholic liver disease, are the main reason for seeking gastroenterologists and hepatologists advice. In addition, hepatocellular carcinoma often arise on the ground of hepatitis, representing the fifth most common cancer in men and the ninth in women. In 2015, the World Health Organization estimated that 325 million people were living with chronic hepatitis infections (hepatitis B or C) worldwide and that globally, 1.34 million people died of viral in 2015.
In front of this global health problem, gastroenterologists, hepatologists and hepato-biliary-pancreatic (HBP) surgeons, are daily involved in the clinical routine in taking difficult clinical decisions. As Sir William Osler quoted: “medicine is a science of uncertainty and an art of probability” and no doctor returns home from a busy day at the hospital without the nagging feeling that some of his/her diagnoses may turn out to be wrong, or some treatments may not lead to the expected cure. Probability is a recurring theme in medical practice and the ability of dealing with risk and uncertainty can be elicited through a special kind of intelligence. In 2012, The UK psychologist Dylan Evans defined it as “risk-intelligence” that is "a special kind of intelligence for thinking about risk and uncertainty", at the core of which is the ability to estimate probabilities accurately.  
Consequently, doctors are routinely asked to make predictions, and their predictions would lead to a consistent payoff when regarding a patient’s life. At the basis of “wise” medical decisions, physician’s experience surely plays a vital role. However, doctors can assume that their competency in a given area can be significantly higher than it really is. Such illusory superiority, is described as the Dunning – Kruger effect, a meta-cognitive bias leading to a discrepancy between the way people actually perform and the way they perceive their own performance level. The concept of “risk-intelligence” relies on the confidence that each subject has with their own knowledge, thus returning accurate probability estimates, and a “wise” doctor should be aware that he/she do not known, thus, returning high risk-intelligence.
To date, little is known about risk-intelligence and the Dunning – Kruger effect between doctors, and, especially, among hepatologists, a specialty strongly involved in important clinical decisions. With this aim we conducted a survey to test how risk-intelligence affects medical decision making in this particular clinical setting and whether the Dunning – Kruger bias can effectively affect these physicians.
If you are a gastroenterologist, hepatologist or HBP surgeon please help us in investigate this issue by completing the following survey:
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Thank!
(I hope you will find the correct answers in the appendix section of the manuscript we are writing!)
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I'm trying to interprete histological data of hepatocellular carcinoma sections. In some groups more necrosis and hemorrhage is present. Does this correlate with a worse stage HCC or is it a sign of tumor killing?
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This correlate with a worse stage HCC ; kindly see the Barcelona staging of HCC as well as AASLD guide for HCC treatment and response
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Actually sorafenib is less used in treatment of hepatocellular carcinoma for its drug resistance. However my research interest is focused on it. Now I am going to spread a new scientific project and evaluating whether it is good to continute the sorafenib research.
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I think still it is a field of research interest specially for elucidating the drug resistance mechanisms
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I've seen several patients that have their liver fibrosis reduced (determined by elastography) after treating hepatitis C with DAA and achieving 12 months of post-treatment undetectable viral load.
This is most obvious in patients that have a baseline result of F3 or F4. They frequently have their fibrosis reduced to values below 8-9 kPa, which would fall in the F1 or F2 category if they still had hepatitis C.
We've been screening these patients for HCC, and probably will do so for some more years (at least until we have more experience with the DAA), but does someone have a different perspective?
Thanks.
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I fully agree with Dr. Balaban opinion and we must follow these patients because after DAA treating the incidence of HCC is increased after the eradication of the HCV
Best regards
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HepG2 is considered as a model system for various cytotoxicity experiments according to many studies. Won't it produce wrong results if carcinoma cells have been used for such studies as such mutated cells will have altered metabolic behavior? I have to choose a chicken or porcine cell line which possibly could be used for testing aflatoxin B1 cytotoxicity. So likewise HepG2 which is a human hepatocellular carcinoma cell line, can I use chicken or pork hepatocellular carcinoma cell line?
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Even not perfect, cell lines are the best available and easiest tools to perform toxicity tests for humans. 
Without long and uncertain testings, using other species cells will anyway introduce additionnal variability due to species metabolic differences.
Some specific cells such as the human hepatic HepaRG cell line are quite good for toxicity experiments, due to metabolic properties close to normal hepatic cells, but their culture is quite long and delicate (since commercialy available). On an other hand, primary hepatocytes are perfect in short time testing.
Good luck
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hepatocellular carcinoma induced by by N- nitrosodiethyamine and tetrachloride in male Sprague Dawley rats. 
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Dear Salma,
One of the best confirmation is histopathological study next to some biomarkers of hepatocarcinoma please follow this link 
Best regards
Manal K Abdel-Rahman
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How hepatocellular carcinoma induced by NDEA and CCl4 in rats affect on protein and albumin metabolism.
Thank you for answers
Best regards
Aly R Abdel-Moemin
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Dear Dr Houda,
Thank you for positive answer and links provided. However, we actually focus on the metabolism of protein and albumin in HCC in animal model.
Best regards
Aly R Abdel-Moemin
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HepG2.2.15 is a hepatocellular carcinoma cell line which transformed by HBV. I need will use this cell line to my doctoral tesis  to evaluated the replication and stability of cccDNA, however I don't have the cell line in my lab. If anyone would like to share the cell line with me. I will be eternally grateful. Thank all..
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thank very much  Amos for you answer. 
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Hepatocellular carcinoma treatment is very difficult, but my dream is to achieve reprogramming of hepatocytes nucleus
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prevention: 1/ smoking cessation, 2/ treatment of  hepatitis due to C  virus  3/ avoid alcohol
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I will be using ELISA for detection of protein. 
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CD34 for breast cancer
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Reduced acylated ghrelin concentrations have been found in research at high altitude (e.g. http://www.ncbi.nlm.nih.gov/pubmed/22114179). Can anyone think of a mechanism behind the reduction? I believe total ghrelin levels remain unaltered at altitude, thus suggesting that it is the acylation that is being effected by low oxygen levels rather than the secretion of ghrelin. The acylation is an estrification reaction between ghrelin and a medium chain fatty acid, catalysed by ghrelin-O-acyl transferase. This posttranslational modification is necessary for ghrelin to bind to GHS-R to exert its biological actions. From my reading estrification is not directly reliant on molecular oxygen. Some have suggested that the acylation occurs in the liver and at altitude there may be a reduced blood flow to the liver. However, more recent work suggests that the acylation occurs in the stomach and on top of this other work suggests that there is not a reduced blood flow to the liver at altitude.
Can anyone think of a mechanism behind the reduced acylated ghrelin concentrations at high altitude (low oxygen environment)?
Thanks, 
Jamie
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A study published in the International Journal of Obesity found a strong association --no correlation proved of course-between altitude and obesity prevalence within the United States. Using data for over 400,000 people, researchers found Americans living closest to sea level were four to five times more likely to be obese, compared to people who live well above sea level in Colorado.
#2 This, info directly below,  provides an excellent review of GOAT, enzyme involved in ghrelin acetylation.
Stengel A, Wang L, Taché Y. Stress-related alterations of acyl and desacyl ghrelin circulating levels: mechanisms and functional implications. Peptides. 2011;32(11):2208-2217. doi:10.1016/j.peptides.2011.07.002.
#3 This article in Appetite June 2015 follows your line of thought http://www.sciencedirect.com/science/article/pii/S0195666315000665
#4 I have found this info in general hard to sort. You note: "I believe total ghrelin levels remain unaltered at altitude" but a few studies go against this so I am not holding my breath... LOL
The studies arguing a rise in ghrelin are older but --makes one wonder about what is really going on. Why is there this variation?
Ghrelin Rises
Conclusions: After 14 days of exposure to HA, we observed a significant ghrelin and GH increase without changes in GHBP, IGF1, IGF2, IGFBP3, ALS, and insulin. Higher GH seems to be needed for acute metabolic effects rather than IGF/IGFBP3 generation. Increased IGFBP1 and -2 may reflect effects from HA on IGF bioavailability.
European Journal of Endocrinology 166 969–976
# 5 This article is not completely translated and is on rats. High altitude made Ghrelin rise. Poor rats
Introduction: A high-altitude environment causes appetite loss in unacclimatised humans, leading to weight reduction. Ghrelin, cholecystokinin
(CCK), and glucagon like peptide-1 (GLP-1), are gut hormones involved in the regulation of food intake and energy metabolism. The liver is an important site of metabolic regulation, and together with the gut it plays a role in food intake regulation. This study intends to study the time dependent changes occurring in plasma gut hormones, PPARα, PPARδ, and PGC1α, in the stomach and liver during hypoxia.
Material and methods: Male Sprague Dawley rats were exposed to hypobaric hypoxia in a decompression chamber at 7620 m for different durations up to seven days.
Results: Hypoxia increased circulating ghrelin from the third day onwards while CCK and GLP-1 decreased immediately. An increase in ghrelin, ghrelin receptor protein levels, and GOAT mRNA levels in the stomach was observed. Stomach cholecystokinin receptor (CCKAR), PPARα, and PPARδ decreased. Liver CCKAR decreased during the first day of hypoxia and returned to normal levels from the third day onwards. PPARα and PGC1α expression increased while PPARδ protein levels reduced in the liver on third day.Conclusion: Hypoxia alters the expression of ghrelin and ghrelin receptor in the stomach, CCKAR in the liver, and PPAR and its cofactors,
which might be possible role players in the contribution of gut and liver to anorexia at high altitude. (Endokrynol Pol 2015; 66 (4): 334–341)
#6 In support of your point : (and may be whom you were reviewing?)
Influence of rest and exercise at a simulated altitude of 4,000 m on appetite, energy intake, and plasma concentrations of acylated ghrelin and peptide YY.
Wasse LK1, Sunderland C, King JA, Batterham RL, Stensel DJ.
#7 Drop in total Ghrelin at altitude
Nutr Neurosci. 2005 Jun;8(3):161-5.
Ghrelin and leptin levels of sojourners and acclimatized lowlanders at high altitude.
Shukla V1, Singh SN, Vats P, Singh VK, Singh SB, Banerjee PK.
#8 Rise in total Ghrelin at altitude
Eur J Endocrinol June 1, 2012 166 969-976
Adaptation of ghrelin and the GH/IGF axis to high altitude
Stefan Riedl, Michael Kluge1, Katharina Schweitzer2, Thomas Waldhör3 and Herwig Frisch
Sorry much is not on target to your central query. Always been puzzled by the varied results of total ghrelin at altitude.
Best, Marybeth Lambe MD FAAFP
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I need a protocol to induce hepatocellular carcinoma (HCC) effeciently in an animal (rat/mouse) model other than the methods involving Diethylnitrosamine. 
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Dear Dalia,
Take some centrally infected Betel Nuts and scratch the central black material. The Aspergillus Flavus, Aflatoxin B. The latter induces HCC.
Best,
Mannan 
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Recently, I met a patient with HCC recurrence, who received liver resection just 5 months ago, and followed with twice TACE treatment.
The primary single tumor is small, just 2cm diameter. APF is higher than 2000.
This is not the first time I met the patient like this. According to my experience, I feel that the recurrence is more easily detected in small HCC than big HCC. I searched many papers, but without relevant evidence.
Does someone have the idea about this issue?
Thanks for you answer in advance! 
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There is a known proverb that says that "Surgery is Prince, selection of cases is Queen and Biology is King" You can find your answer looking at this proverb.
However, in my opinion the most important fact is that when you have a large HCC and you proceed with surgery it means that it has not spread to other organs, not spread to lymphnodes and usually is a single tumor with no satellite lesions. This is your favorable biology right in front of you telling you that you can go with the operation and it may no recur. All other large tumors are not referred to you because the bad biology has already surfaced.
On the other hand, when you have a small tumor you have no idea if the biology is favorable or not because there was no enough time for the tumor to show distance metastases or lymphnodes and we expect cure in those cases and we are frequently deceived. In this context you are going to operate more small tumors with uncertain biology and whenever you face a really mean biology, it will strike back with full force like your case mentioned above.
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I will be using spinning disk and/or two photon intravital microscopes to capture images or videos of hepatocelluar carcinoma (HCC) and their interaction with immune cells. Are there any ways to differentially label HCC and hepatocytes using fluorochromes? Any ideas will be greatly appreciated. Thanks. 
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How about this one?
It states: "were no detectable positive reactions with other human tumor cell lines and solid tumour specimens. Showed negative reaction to all normal human adult tissues and fetal tissues tested."
To be sure I would e-mail them (or indeed other ab companies such as DAKO, Santa Cruz etc). Let them do your searching for you! They are the vendors... :)
Hope you find one and good luck with your research
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Controversial data are available in medical literature about the relation between autophagy and sorafenib effects in hepatocellular carcinoma. What is your opinion?
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Sorafenib has recently been reported to induce ferroptosis of hepatic cancer cells mediated by the disruption of systemXc- (antiporter of cystine and glutamate). Given that iron  metabolism is robust in the liver, the enhanced expression level of transferrin receptor is expected to susceptible to iron ion-induced redox stress leading to the elimination of hepatic cancer cells.      
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HCC Prediction is better than paliative treatment?
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There is actually not any good tumor marker for early detection of HCC. The US examination every 6 months is the usual clinical recommendation used for screening
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early prediction of HCC  is mandatory in high risk patients
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Dear Dr Amr
I suggest to read this paper
Tumour Biol. 2015 Nov;36(11):8399-404. doi: 10.1007/s13277-015-3607-8. Epub 2015 May 28.
Serum DLK1 is a potential prognostic biomarker in patients with hepatocellular carcinoma.
Li H1, Cui ML1, Chen TY2, Xie HY3, Cui Y4, Tu H1, Chen FH1, Ge C1, Li JJ5.
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In General: propagation of Primary cell culture without using Growth factors.
Please provide with practical details.
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You have not stated why do you need to culture the primary cells without any GFs?
Go through the following link, and optimize it for your cell culture condition/need
F-12 Nutrient Mixture - Mammalian Cell Culture
Dulbecco's Modified Eagle Medium (DMEM) : Nutrient Mixture F12 (Ham's)
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Hi,
I plan to do some gene silencing in HepG2 cell line. However, to draw a profound comparison between normal and cancerous liver (in this case, hepatocellular carcinoma) phenotypes, a normal liver cell line is needed. So, would you suggest a healthy liver cell line? Are there any factors to be taken into account to find an appropriate healthy liver cell line?
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HCC is a vascular tumor with enhanced angiogenesis
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as a predictor for HCC
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It seems that PD-1 is also responsible for virus, I am confused about the potential cure.
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These antibodies should be effective, because tumor cells are likely to express viral antigens, making them immunogenic (recognized by the immune system as non-self).
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The role of autophagy in cancer metastasis seems to be complex. During early stages autophagy can play an inhibitory effect on metastasis. However, during advanced stages, autophagy acts as metastatasis promoter.
A recent review (Su et al, 2015) summarizes some of these aspects (see link). I am working in hepatocellular carcinoma, but my experience analyzing the relationship between autophagy and metastasis is limited.
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Sorry Jose, I have never  analyzed the role of autophagy in cancer metástasis.
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Hi All,
I am planning to use 2 gRNAs and wt-CRISPR to KO my target protein from the cell lines I pick (ex. Hepatocellular carcinoma cell lines). I want to clone both gRNAs into vectors and transfect the purified plasmid. However, I am not sure what is the best way to transfect those huge vectors into target cells.
Are there any good transfection reagents for this purpose? I would like to avoid electroporation if possible.
Thank in advance for any suggestions!!
Best,
Lyra
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Which are the main molecular mechanisms related with resistance to sorafenib in hepatocellular carcinoma?
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Dear Jose,
The following recent publication covers the answer to your question.
 
 Dig Dis. 2015 Oct;33(6):771-9. doi: 10.1159/000439102. Epub 2015 Oct 21.
Molecular Mechanism and Prediction of Sorafenib Chemoresistance in Human Hepatocellular Carcinoma.
Nishida N1, Kitano M, Sakurai T, Kudo M.
Author information
 
Abstract
Hepatocellular carcinoma (HCC) is the second leading cause of cancer death worldwide, and prognosis remains unsatisfactory when the disease is diagnosed at an advanced stage. Many molecular targeted agents are being developed for the treatment of advanced HCC; however, the only promising drug to have been developed is sorafenib, which acts as a multi-kinase inhibitor. Unfortunately, a subgroup of HCC is resistant to sorafenib, and the majority of these HCC patients show disease progression even after an initial satisfactory response. To date, a number of studies have examined the underlying mechanisms involved in the response to sorafenib, and trials have been performed to overcome the acquisition of drug resistance. The anti-tumor activity of sorafenib is largely attributed to the blockade of the signals from growth factors, such as vascular endothelial growth factor receptor and platelet-derived growth factor receptor, and the downstream RAF/mitogen-activated protein/extracellular signal-regulated kinase (ERK) kinase (MEK)/ERK cascade. The activation of an escape pathway from RAF/MEK/ERK possibly results in chemoresistance. In addition, there are several features of HCCs indicating sorafenib resistance, such as epithelial-mesenchymal transition and positive stem cell markers. Here, we review the recent reports and focus on the mechanism and prediction of chemoresistance to sorafenib in HCC.
Hoping this will be helpful,
Rafik
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1 month postoperatively there s no sign of recurrence on the lung-abdominal CT Scan. The patient had fever for 10 days, he received Levofloxacin for a small collection near the liver transection line, which is in regression now. 
Otherwise, there are no other clinical signs or symptoms of recurrence, 
What should we do further, or what could cause this high rise in AFP blood lvl?
Thank you.
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How was the bilirubin plasma level of the patient at the time of AFP increae? Very high level of AFP can be observed during drug induced hepatitis. Levoxacin can induce hepatitis, mainly cholestatic (low cytolisis with low ALT level) and the timing usually is  2-3 weeks after the administrtation.
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Dear All.
I want to do ImmunoHistoChemistry(IHC) for chemically induced liver cancer. Can you tell me What are all the markers specific for Hepatocellular carcinoma.
Thank you
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Hi Srinivas
take a look at these papers, and also considers their reliability. It is good to know a marker, but it must also be reliable.
Good Research
DFC
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Contrast agent for CEUS: SonoVue
1,5 Tesla MRI
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Yes of course there are some. Here below is one ref but you could find others easily.
Solid focal liver lesions indeterminate by contrast-enhanced CT or MR imaging: the added diagnostic value of contrast-enhanced ultrasound.
Quaia E.
Abdom Imaging. 2012 Aug;37(4):580-90.
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I am working on discover biomarkers for Fibrolamellar hepatocellular carcinoma using next generation sequence estimating copy number variation, i need data calculate Log 2 ratio for WGS .I can not fined it on NCBI .
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CONTROL DRUG FOR HEPG2 CELL LINE  
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You can use the solvent of real drug. 
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Is anyone familiar with hepatocellular carcinoma cancer inducers for rat.
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THANK YOU SIR
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I have been looking for weeks on how to make a solution for these cells. I ordered this exact product:
it came in two small microtubes with no instructions on how to reconstitute these cells.
Any help?
Thank you.
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Hi Jacob,
S9 rat liver is an extract, these are not cells. This respresents the supernantant (S) of a 9000 x g centrifugation of a rat liver homogenate. The receipy how to make the solution to be used in the Ames test is described in the Mortelmans and Zeiger paper 2000 (http://www.ncbi.nlm.nih.gov/pubmed/11113466).
Best,
Michel Kranendonk
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We've already tried EpCAM, ASGPR, CK-18 and Albumin. They were all positive in healthy blood making them useless. AFP showed great results but we need a second one to increase specifity.
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There was a study published in Cancer Cell 2009 from Heikenwalder group showing lymphotoxins (LTa, LTb, LTR) in mouse model and human HCC. In my experience in another mouse model, it seems they are highly associated in the development of HCC. Unless you search for mutations, it would be worth to compare the marker expression with data in healthy subjects. I hope this help you. To answer your question more properly, I need more information about your study subject. 
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Dear All, 
Does any of you work with HepG2 cells? if so could you provide me with a couple of vials? My lab will pay for the shipment. Thank you in advance. Best regards
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You can get it from ATCC.
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How to get the most data from a paraffin embedded liver biopt (10 mg tissue) by using advanced sequencing techniques?
I have a liver biopt of a HCC patient which I want to screen for the expression of liver carcinoma related proteins and the genetic makeup. It is 10 mg of tissue embedded in paraffin for making microscopic slides. I want to extract proteins, DNA, mRNA for genotyping and expression analysis by HTP sequencing/proteomics. The sample is unique, so I want to be sure that the procedure gives maximum results (data will be linked to MRI, CT scans and extended blood chemistry, which are available). I consider to put all data in a publicly accessable repository, so any hints for financing this operation would also be useful.
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Dear Bruno,
thanks for your suggestions. Have you checked my publications on this topic?
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I injected the h-AMSC-luciferase (10 6 ) into the mouse model of hepatocellular carcinoma in situ by tail vein. At the beginning, the h-AMSC can be detected in the lung by the small animal imaging systerm (2 hours after injection), but after 30 hours nothing could be detected! I wanted to know whether the h-AMSC could homing to the tumor that inplanted in the liver. Is anyone had been did this experment? Or give me some suggestion!
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Thank you for doctor bipasha and Daniel. I still have some questions, first, after 30th hour I can't detect any fluorescence in the body, just the in the vein tail where I injected the AMSC had little signal be detected. So is it mean that AMSC is still alive, but it disperse to the every part of the body, then it caused  the signal is so weak that it can't be detected? And some weeks later they will homing to the tumor and be detected?The second, I had executed the mouse and found the tumor was inplanted in liver and caused some necrosis in the liver, is it enough to recruit the AMSC to the liver?
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i am planning to dissolve methonolic extract in deionised water but in articles people have mentioned to dissolve their extracts in carboxy methyl cellulose 2%, DMSO 2% and PEG 2%. but i tried to dissolve my extract in deionised water and its taking time to dissovle completely but its dissolving.so can i use deionised water for hepatocarcinoma invivo SD rat model?? and for invivo SD rats how much mL of deionised dissolved extract can i give orally??
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Dear Shankar,
Complete dissolution of extract depends on its chemical components. As it is plant extract, there must be some hydrophilic and some lipophilic compounds. If the extract contains more lipophilic constituents, then some part will dissolve in water and most of the part will remain as it is and vice versa. 
And as your sample is water soluble, you should use water, although it takes more time to dissolve. Because other solvent have the possibility to show at least some pharmacological activity where water don't have any possibility to have any activity.
Besides, for animal experiments, our main concern is to administer the drug sample only. So you should administer as lower as possible but the volume should be same for control and treatment groups. For rats the highest volume can administer depends on its body weight (10 ml/kg).
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I would like to characterize cells isolated from a murine model of hepatocellular carcinoma and I am wondering which methods (if any) are used for collecting an heterogenous cell population from solid biopsies.
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I have hands on experience in isolating tumor cells from Nod scid murine HCC tumor. You can follow the instruction of "Tumor processing for isolation of single cells" in the paper.
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Dear all
I need your advice, I'm working on genomic DNA from hepatocellular carcinoma patient. I make screening for specific single nucleotide polymorphism using PCR rflp . I use the restriction enzyme (Hpy99I) for cutting my DNA after PCR but it cut only 3 samples out of 50 sample. When I have read about this enzyme, I found that it can be blocked by methylated DNA. I want to know how can I make sure that It is not blocked by methylation
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I assume that you have isolated genomic DNA, and have produced PCR product using this DNA. A PCR product will not methylated, even if the genomic DNA is methylated, because you do not have any methylases in your PCR reaction mixture. If you use Hpy99I on genomic DNA, it will not cut the site where CpG methylation occurs. However, in your case, the reason why your PCR product is not digested by Hpy99I is possibly because of a mutation in the restriction site in the genomic DNA. When you amplify this region by PCR, the mutation carries over and the restriction enzyme cannot recognize it.
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Whether the tumor specific markers, such as AFP,  mostly express on the cell membrane or secret into the blood?  Is the expression level of AFP persisting or declining in human primary hepatocellular carcinoma cells?
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thanks for Saravana R K Murthy.
Dose the expression of AFP keep the same level or decline along with the cell passage on human primary HCC?
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I tried 2500,5000 and 6000 cells on 0.8% but it didnt work.
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Hello Oluseyi and Vandana,
I am facing similar problems with colocrectal cancer cells (DLD-1). I plated them at various densities (5000, 10,000 and 12,500) per well (6 well plate) in the same soft agar concentrations as Oluseyi mentioned. I checked the literature and various groups have used a maximum of 5000 cells of DLD-1 in a 6-well plate (This also indicates that DLD-1 cells do form colonies in soft agar). I have followed the protocol to the t including the tedious process of maintaining the right temperature of the agar and the media. I would really like to get your suggestions/inputs as to what might be going wrong here.
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Anyone linked the hepatocellular carcinoma with cmv?
We had a patient that came in initially with the neuro immune dysfunctional syndrome, later pre-scheduled appointment for the pet-scan revealed the patient inflicted with the hepatocellular carcinoma. We already had the viral serology reflect the high numbers on cmv rooted infection.
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Dear Dr. Garcea,
Thank you very much for your input. I did vist the article suggested by Dr. Schnieder and it is very helpful. I am open to any clinical study collaboration surrounding CMV.
If you know anybody interested in it, please refer. 
Thank You.
Sincerely,
Dr. Sheikh
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Hepatoma Research has published its first manuscript in Ahead of print section. Welcome to read, comment, and cite.
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Agreed, in particular with the point that transplantation should be first choice for resectable HCC in the context of liver cirrhosis which was convincingly demonstrated by the Bismuth article above. A more recent meta-analysis by Zhou et al (Transplanation Proceedings 2013) suggested similar short-term outcomes but perhaps decreased long-term survival with SLT.
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I have both trypsin and collagenase, but I donot know how to perform it well, could anyone share your experience?
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thanks a lot.
due to the limited experimental conditions, the HCC cells obtained from the operating room only can be isolated by trypsin or collagenase, so my concern is how to use these enzymes to isolate the tumor cells.
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What will be the consequences out of this?
Extract by Florent Mouliere / Montpellier and Nitzan Rosenfeld / Cambridge:
Circulating tumor DNA (ctDNA) is now widely investigated as a biomarker in translational and clinical research. However, despite the growing field of clinical applications, the biology of ctDNA remains unclear. In trying to learn about the origins of ctDNA, nature provides us with very few clues. One of the important accessible parameters is the size of those DNA fragments. In addition, a well-informed model of these sizes and biases can help design more efficient and accurate diagnostic methods. In PNAS, Jiang et al. take an important step in that direction.
Significance
We used massively parallel sequencing to study the size profiles of plasma DNA samples at single-base resolution and in a genome-wide manner. We used chromosome arm-level z-score analysis (CAZA) to identify tumor-derived plasma DNA for studying their specific size profiles. We showed that populations of aberrantly short and long DNA molecules existed in the plasma of patients with hepatocellular carcinoma. The short ones preferentially carried the tumor-associated copy number aberrations. We further showed that there were elevated amounts of mitochondrial DNA in the plasma of hepatocellular carcinoma patients. Such molecules were much shorter than the nuclear DNA in plasma. These findings have shed light on fundamental biological characteristics of plasma DNA and related diagnostic applications for cancer.
Abstract
The analysis of tumor-derived circulating cell-free DNA opens up new possibilities for performing liquid biopsies for the assessment of solid tumors. Although its clinical potential has been increasingly recognized, many aspects of the biological characteristics of tumor-derived cell-free DNA remain unclear. With respect to the size profile of such plasma DNA molecules, a number of studies reported the finding of increased integrity of tumor-derived plasma DNA, whereas others found evidence to suggest that plasma DNA molecules released by tumors might be shorter. Here, we performed a detailed analysis of the size profiles of plasma DNA in 90 patients with hepatocellular carcinoma, 67 with chronic hepatitis B, 36 with hepatitis B-associated cirrhosis, and 32 healthy controls. We used massively parallel sequencing to achieve plasma DNA size measurement at single-base resolution and in a genome-wide manner. Tumor-derived plasma DNA molecules were further identified with the use of chromosome arm-level z-score analysis (CAZA), which facilitated the studying of their specific size profiles. We showed that populations of aberrantly short and long DNA molecules existed in the plasma of patients with hepatocellular carcinoma. The short ones preferentially carried the tumor-associated copy number aberrations. We further showed that there were elevated amounts of plasma mitochondrial DNA in the plasma of hepatocellular carcinoma patients. Such molecules were much shorter than the nuclear DNA in plasma. These results have improved our understanding of the size profile of tumor-derived circulating cell-free DNA and might further enhance our ability to use plasma DNA as a molecular diagnostic tool.
Jiang P et al.: Lengthening and shortening of plasma DNA in hepatocellular carcinoma patients. Proc Natl Acad Sci U S A. 2015 Feb 2. pii: 201500076.
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well pointed out.
We also have this discussion at the web group of theTheodor-Billroth-Academy on LInkedin and Reinhold Kiehl, Hossein Rahmati Roudsari and Jan Voskuil made very important points and I try summarizing those:
-tumor markers as CEA or CA19-9 should be used for follow-up-never for making the diagnosis, as the overall accuracy is too small. Further tumor markers are expressed proteins on surface membranes and we learned from epithelial cysts that such can mimick a cancer, e.g.in spleen cysts very high CA-19-9 had been observed without any association of any cancer, nor during follow-up
Therefore, we by now do not know 
- the influence and value and accuracy of detectable DNA
-when the best time is measuring it and how the values are influenced
-how storing would be best and how the interobserver variability might be
-when free DNA is measurable, how do such values differ after treatment
-are they proven being related to the observed cancer or assumed to be
-microRNA#s had been observed in ling cancer patients assuming having impact on spread and even cancer development but again: assumed!
-to my knowledge no standard protocol is accepted or suggested determining free DNA so far
Additionally Ijaz Jamall added a valuable insights deepening he comment from Hossein Rahmati Roudsari and Jan Voskuil (copy and pasted):
Ijaz Jamall: "I agree with Dr. Rousdari and Jan: one key factor to consider in measuring anything in the blood is its half-life and how to "normalize" the thing being measured - per ml blood or serum, per g protein, etc. because essentially we are measuring a concentration as opposed to a mass and dilution and binding kinetics or changes in hydration or albumin content can make huge a difference. In fact, diurnal variation can itself make a huge difference"
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what is the current consensus
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Dear Thomas,
despite the theorethical advantages of sorafenib in improving tumor response after locoregional therapies for HCC, definitive data is still lacking. With regard to selective internal radiation (radioembolization) a recently published RCT by the Chicago group (Kulik L et al, Journal of Hepatology 2014) conducted in the pre-tranplant setting failed to find a significant increase in tumor response with the combined regimen (sorafenib+TARE). Our group in Milan has presented at AASLD meeting in 2013 a small retrospective report comparing 15 patients treated with sorafenib+TARE vs 30 treated with TARE alone and, again, no differences were observed. Therefore, to the best of the actual knowledge and with the few available data, sorafenib does not seem to exert a radiosensitizing effect. Other agent with better described DNA-damaging effect, such as capecitabin, should be tested in combination to internal or external radiation in HCC patients.
Kind regards.......
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Anybody know any Camptothecin-resistant liver cancer cell line?
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yes i had an experiment about camptothecin resistance on HeLa, MCF7, CaCo and BJ.
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In hepatocellular carcinoma, there are many things that change such as increasing of tumor cells and decreasing of its own cells so what happened to its functions ? For example, detoxification, gluconeogenesis etc. 
Thank you so much
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thank you
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Within a small time span I want to induce cancer in mouse liver so that I can check the anti-cancer activity of my compounds which are already in vitro evaluated. Importantly, our lab is not suitable to work with nude/SCID mice so I want to work with any normal mouse. So kindly give me your valuable suggestions to proceed.
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2-Nitropropane (2-NP) is suggested to be a human carcinogen, a genotoxicant and hepatocarcinogen in rodents
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We know that R0 resection is clearly desirable in preventing local recurrences, but in the setting of large resections, e.g. extended or trisegmentectomy, with potential R1 resection due to positive margins, has anyone had experience with IORT to supplement margins?  The use of IORT in rectal cancer and breast cancer have been demonstrated, but little reports for primary intrahepatic cholangiocarcinoma or HCC.  
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Maybe a  better question to ask is: do you use Stereotactic body radiotherapy (SBRT) aka Cyberknife, for treatment of any liver tumors?  There has been a wealth of experience from Asia that SBRT is as effective and less toxicity than TACE or RFA.
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I am trying to perform a reprogramming method for somatic cells. The article which I am based uses HEK293gp cell line (which I did not find good explanations on internet). I have HEK293ft cell line frozen, so I would like to know if both can be used for this purpose.
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Hi Luiz Fernando! HEK293GP is used for retrovirus production, and constitutively expresses gag and pol proteins for retrovirus packaging. To produce retrovirus, you transfect the cells only with the transfer vector, and the envelope vector, like pCMV-VSVG. HEK293FT is used for lentivirus production, and expresses SV40 large T. To produce lentiviruses, you transfect these cells with lentiviral transfer vector, a helper plasmid expressing gag/pol/rev and an envelope vector.
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I'm working on plant crude extracts. I want to check their anticancer activity for hepatocellular carcinoma.
Please give suggestions for cell lines and bio-assays for standardization.
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thank you sir