![](/cdn/assets/images/search/clock.png)
We could not find any results for:
Make sure your spelling is correct or try broadening your search.
Share Name | Share Symbol | Market | Type | Share ISIN | Share Description |
---|---|---|---|---|---|
Scancell Holdings Plc | LSE:SCLP | London | Ordinary Share | GB00B63D3314 | ORD 0.1P |
Price Change | % Change | Share Price | Bid Price | Offer Price | High Price | Low Price | Open Price | Shares Traded | Last Trade | |
---|---|---|---|---|---|---|---|---|---|---|
0.00 | 0.00% | 11.125 | 10.75 | 11.50 | 11.125 | 11.125 | 11.13 | 194,022 | 08:00:00 |
Industry Sector | Turnover | Profit | EPS - Basic | PE Ratio | Market Cap |
---|---|---|---|---|---|
Pharmaceutical Preparations | 5.27M | -11.94M | -0.0129 | -8.62 | 103.17M |
Date | Subject | Author | Discuss |
---|---|---|---|
24/4/2023 13:25 | I imagine Big Pharma will be fighting over Covidity in the coming weeks with the new sub variant Arcturis running rampant. How many 100's of millions do you reckon it will be worth after all we know the current jabs don't stop transmission, don't stop you getting infected and don't prevent hospitalisations. Bearing in mind the 10's of billions spent so far Covidity has to be worth a few billion, can't believe the share price isn't exploding. | ![]() panama7 | |
24/4/2023 12:33 | From that link i gave circulating cells only survive 1 - 2.4 hrs Parasortix is at best a snap shot unless you are using the cells for other purposes but in Scancells case we are not. Scancell is looking for a snapshot of the damage done to the cancer by the vaccine rather than looking at what they already know ... so Parasortix is best looked at by the oncologist treating a "new patient" and that would be set against looking at a biopsy to establish from scancells point if the cancer is an "immune desert" or has inflammation from an existing immune response, this is the issue from our point of view we are looking at the immune system not the particular genetic make up of the cancer, because we already know what constitutes citrullination and homo citrullination which caused cells to become "circulating" and we are targeting that EMT ... Despite all of this help, CTCs persist in circulation for only 1–2.4 h according to in vivo experimental modeling and data from a small cohort of five patients (Meng et al., 2004). Most CTCs die in circulation as a result of shear stress and/or anoikis (Labelle and Hynes, 2012; Vanharanta and Massagué, 2013). Paradoxically, the half‐life of CTC clusters in circulation has been reported to be shorter than that of single CTCs, but this may be because large clusters get ‘cleared’ | ![]() inanaco | |
24/4/2023 10:25 | Thanks Mia. I was just thinking about how it could be of benefit in the Modi-1 and Modi-2 trials. | ![]() marcusl2 | |
24/4/2023 10:15 | Hi Marcus, as you say Parsortix is cleared for clinical use in MBC. Parsortix can however be used for all cancer types in non clinical activities such as CTC capture in drug trials, CTC capture in Laboratory Developed Tests LDT's offered from CLIA approved labs) etc. | ![]() miavoce | |
24/4/2023 09:56 | Am I correct in thinking that Parsortix is only cleared by the FDA for metastatic breast cancer ? | ![]() marcusl2 | |
23/4/2023 22:47 | anyway its a huge subject ............ but In addition, many epithelial tumours, such as breast, ovarian, gastrointestinal and prostate switch from expression of cytokeratin to vimentin during metastasis in a process known as epithelial mesenchymal transition (EMT). This change in phenotype enables the cell to become mobile and metastasize to new locations in the body. we have two Vimentin proteins on the case The second target protein is the metalloenzyme alpha-enolase (α-enolase), which is involved in the process of glycolysis. Many tumours tend to favour metabolism via glycolysis even in normal oxygen conditions (the “Warburg effect”) and generate energy by converting pyruvate into lactate. The α-enolase enzyme mediates the penultimate step in this metabolic process and is overexpressed in a variety of cancers. we have one enolase on the case .... coming soon another arm to assist ..... Modi2 | ![]() inanaco | |
23/4/2023 22:30 | I understand what it does Mia .... but ctdna gives you what moditope is killing which is great news for us ... once the cancer has been eliminated we then need to know if we have taken out micro mets ... i appreciate parsortix may find no circulating live cells after treatment but it cant find those already seeded until they appear on scan and that is 6mm and we already know that stem cancers cells come under the influence of Modi1 Maintenance of the pluripotent stem cell state is regulated by the post-translational modification of histones. The discovery that citrullination of the linker histone H1 is critical to this process represents a new role for the protein arginine deiminases (PADs) in development. this is why i keep saying separate the vaccine from what is in trial modi1 induces CD4 Killer T cell "proven" do they work ? so far ... yes because that is what the trial is about now ATB | ![]() inanaco | |
23/4/2023 17:55 | Hi Inanaco ctDNA only provides a partial view of the cancer i.e. analysis of DNA fragments from mostly dead cancer cells. Angle's Parsortix enables live cancer cells (both epithelial and mesenchymal) and cells undergoing E->M transition, and cell clusters, to be obtained from patient blood. These live cancer cells can be used for:- - DNA sequencing - RNA sequencing - Protein expression analysis - Cell culture By using live cancer cells a full picture of the cancer is available whereas ctDNA provides a very partial picture. Pharma's are now starting to adopt CTC analysis in their clinical trials (Angle now have five Pharma customers, and others in the imminent pipeline). The analysis is repeated at multiple time points in the trial. IMO the analysis of CTC's will become a standard part of cancer drug trials in due course because of the richness of information that it can provide. Having a complete analysis of the CTC's from patient blood could provide Scancell with valuable information, which they might otherwise not have, in relation to why some patients are responding and others are not. | ![]() miavoce | |
23/4/2023 16:55 | good news thou ... tickets for Division 1 are cheaper Loggie ... | ![]() inanaco | |
23/4/2023 16:53 | Miavoice .... You can try and bore me with the details ... ATB as i am interested | ![]() inanaco | |
23/4/2023 11:05 | What is your point Nigel ? | ![]() amaretto1 | |
23/4/2023 11:03 | What a absolutely naive stupid take on a situation......But Nigel has always had a huge self importance ego trip ! Clown | ![]() amaretto1 | |
23/4/2023 10:34 | (I wonder if Modi`s method of operation will work out like this.....?) Burble Further observation - modi-1 in clinic vs mouse models22 Feb 2023 10:58 A further observation from me. I was thinking at what we already know about Modi-1 data in the public sphere. AGM presentation - Look at page 11 - there is a bulletpoint which states 'tumour regression seen within 4 days of Modi-1 vaccination' If you think about mice models, it's generally suggested that 9 mouse days is the equivalent to a year as a human ( Or 1 mouse day is approximately 40 human days. I wonder whether many people following this share have conflated the two and thought that we would be seeing regression within 4 days. Yes in mouse models, but this is humans we are now talking about. So based on the Scancell data if this translated directly into humans, we should be looking at starting to see regression of tumours from about 160 days i.e. nearly 6 (5.2) months into the trial. Look at Figure 2Aii on the Modi-1 paper ( The circles indicate the day of immunisation and X indicates day of tumour analysis. For some of these mice, you see an immediate regression of tumour bulk. But for some (blue, pink, orange) you see stabilisation of their tumour without regression over about a 10 day period (i.e. approximately a year in human time) before which animals were sacrificed and tumours analysed. In the control, you see continued tumour growth. This is then shown again in the 2Aiii figure waterfall plot. We don't know how long this stabilisation continues because the mice are sacrificed early, but if that continued for longer, then you could be looking at a patient who has exhausted all current treatments, being given at least a year if not more to their lifespan even if Modi-1 doesn't remove tumour bulk. In the rechallenge work that was done also in this paper, this was performed in mice at 58 days. So in humans that would suggest a rechallenge equivalent in humans of 6 years after the initial dosing of Modi-1. Taking those together, what we saw in the mouse model data is being reflected in what we are seeing in the clinic. | ![]() marcusl2 | |
23/4/2023 09:43 | It may well be - that wasn't my point though. | ![]() nigelpm | |
23/4/2023 08:59 | Actually nigelpm the use of Parsortix in the Scancell trials would be a good thing as it is far better than the ctDNA analysis that Scancell are doing. I won't bore you with the details but I'm sure many with knowledge of Parsortix would agree. | ![]() miavoce | |
23/4/2023 00:40 | Thanks again Inan for yesterday - I thought that was all most helpful and I cautiously enjoyed your tentative conclusion. Happily no one has gone for the big quibble yet. News would be nice. ATB | ![]() torquayfan | |
22/4/2023 22:11 | Thought I'd seen it all. You've now got posters who hold stock in a different company (this case angle) trying to convince holders in a different company (scancell) that the different company should use their products. Wow. Desperate. | ![]() nigelpm | |
22/4/2023 21:48 | Are you invested in Scancell Panama7? | ![]() dominiccummings | |
22/4/2023 21:26 | TF, why on earth are you asking Inane, he has called everything wrong for 10+ years. He continually states that the Market is wrong, that Big Pharma is wrong and world class Scientists are wrong, have you not thought that it is actually wrong after all that 's what his history tells us. | ![]() panama7 | |
22/4/2023 10:59 | Scancell is using RECIST 1.1 and iRecist Also Elispot Researchers are trying to stop cancer by inducing tumor-specific cytotoxic T lymphocytes (CTLs) against dendritic cells loaded with tumor DNA. The response of these CTLs can be determined by ELISPOT assay Also ctDNA will be measured in blood. Circulating tumor DNA (ctDNA) is found in the bloodstream and refers to DNA that comes from cancerous cells and tumors Plus Immune cells will be profiled from available biopsy tissue | ![]() marcusl2 | |
22/4/2023 10:54 | It works .... Scancell now have the opportunity to get the best out of the CD4 killer t cell by looking at the environment ... nobody else has that opportunity its a case of ignore the market and keep buying | ![]() inanaco | |
22/4/2023 10:48 | Inan - from the detailed look at the 8 week progress that Johnnie posted, do you sense or do you have any cautious if early thoughts, in summary. Thanks again. | ![]() torquayfan | |
22/4/2023 09:36 | Detection of ctDNA can be helpful in the following cases: Detecting and diagnosing a tumor. Because tumor DNA has acquired multiple genetic changes (variants), leading to tumor development, ctDNA is not an exact match to the individual’s DNA. Finding DNA with genetic differences aids in tumor detection. Diagnosing the type of tumor using ctDNA can reduce the need for getting a sample of the tumor tissue (tumor biopsy), which can be challenging when a tumor is difficult to access, such as a tumor in the brain or lung. Guiding tumor-specific treatment. Analyzing the genome of tumor cells using ctDNA can help doctors determine which treatment will be most effective. Currently, however, approval from the U.S. Food and Drug Administration for ctDNA testing to personalize cancer treatment is limited. Monitoring treatment. A decrease in the quantity of ctDNA suggests the tumor is shrinking and treatment is successful. Monitoring periods with no symptoms (remission of cancer). A lack of ctDNA in the bloodstream indicates that the cancer has not returned. | ![]() inanaco |
It looks like you are not logged in. Click the button below to log in and keep track of your recent history.
Support: +44 (0) 203 8794 460 | support@advfn.com
By accessing the services available at ADVFN you are agreeing to be bound by ADVFN's Terms & Conditions