Member Info for Moab

Extraordinary! 46% rise on no news that I can see, and not a single post.

Let's be clear. This is a review article looking at previously published work. Nothing new here, move on please. I have not been able to access it, but if anyone can, please provide the full reference. I fear the SP sums up the reaction, rather than the much reiterated hype seen today

Plenty of buys at 438.5p - for ~3%

Yes, just what has been achieved? Can anyone point to progress over the last 5 years?

Nothing to see there, move along please................................

I have now watched this. AN starts with "The Work MAY turn out to be groundbreaking" (and then, again, may not.....) AN is into his default S&M* mode once more. I have made my comments on the flaky 47 patient sample on which he builds his tottering edifice previously. The response from big pharma will tell us just what they think, and while hoping for the best, I am not optimistic.

*Smoke and mirrors

Oh dear, EC, you are slightly out of your depth here. I repeat: The Molecular analysis Co's business is NOT analysing dead cancer cells obtained from a patients blood sample. If your source of info on something your post on day after day after day is a Google search, I am sorry for you.

Of course ctDNA comes from apoptosed tumour cells, BUT it is NOT the dead tumour cells that are analysed. There is a difference that seems to have eluded you.

Hope this helps.

E Carrot

You really must do more homework before you post. The Molecular analysis Co's business is NOT analysing dead cancer cells obtained from a patients blood sample. It uses circulating DNA fragments, hence the term ctDNA. Must try harder.

TGTD

Palatable! Best predictive error of 2024 - or was it?

Rocket

The in-house study reported last week was a set up, with no detail as to how patients were selected. In real life CTCs are not always present in blood, and almost certainly not until metastatic disease is present. There is no guarantee that CTCs will be found on which to review treatment decisions, which is why others are looking at cnDNA. I am sure that ultimately Parsortix will be a very powerful tool in the focused treatment of of various malignancies, but we are not there yet.

As with any Newland rns there is a generous dollop of hype to cover the missing info. A proper clinical study always begins with a section on Patients and Methods. This is missing. How were these patients selected? At what stage in the disease were they? I am guessing that they all had to have CTCs available at venesection because of likely metastatic disease. Only then was AGL able to compare the clinical value of Parsortix derived CTCs wth tumour derived DNA. AGL then comes up with the bleedingly obvious conclusion that Parsortix is of far more value, with appropriate downstream analysis, than ctDNA. A no brainer. Indeed, what clinically useful info does ctDNA provide over and above CTCs? I think the answer is NIL.

This seems to have been an inhouse study aimed at pointing out these differences for commercial consumption. It would not get past a half competent journal referee. BUT ctDNA is essentially a screening test to answer a single question: Could this patient have one of a number of cancers? Parsortix is NOT a screening test. Period. The two investigations have totally different purposes, and I can see no valid reason why they should have been run head to head apart from confirming the unsuitability of ctDNA for useful downstream analysis when compared with gold standard Parsortix.

Having said this, as a LTH I am only too happy to see the SP rise. The rns of 3 days ago describing the collaboration with the Jap. outfit is good news, but also indicates IMHO that at this stage Parsortix remains a clinical research tool rather than a tool with direct clinical application for all patients already diagnosed with a malignancy, but this will surely foĺlow.

EC

Try to explain what it is I do not understand. Your 10.12 post, apart from repeating bits of the RNS, fails to do so.

There are two issues here. the first is the SP, which was grotesquely low at ~10p, was looking for any excuse to rise. Well you have that now. The second is in the (missing) detail of this RNS. a) Is this published work? b) it seems that the selected patients were already known to have a one of the malignancies mentioned, and were reliably exhibiting CTCs in plasma. This would be a very highly selected population.

I think this work was simply designed to show up the limitations of ctDNA as a means of producing therapeutic information, as opposed to diagnostic information. It may be good at the former, but useless at the latter, where Parsortix clearly is essential.

EC

"What is totally obvious if you know the share well as I do."

I admire your arrogance. But what is equally clear is your ignorance of the underlying science.

This is not correct. cDNA has a role. it is completely different from the role of Parsortix and CTCs.

Think of this scenario: patient turns up with weight loss, or other rather non-specific symptoms. Doc takes blood and runs a cDNA screen which shows some cDNA tumour fragments. OK, now go find the primary. cDNA is a screening test pure and simple. CTCs then provide - if they are present in the blood, which is not a given - the excellent additional info on therapeutic options can be based.

In a way this RNS describes a study in which, for several cancers, cDNA and CTCs are put head to head. The answer is a no brainer

I am a LTH and like others have been through a hard time here. I am trying to be dispassionate about this RNS and what it really means. As I see it the nub of the RNS is: "Widely accepted actionable DNA variants (cancer mutations) were identified in CTCs that were not present in the ctDNA from the same blood draw in 70% of breast cancer patient samples, 70% of lung cancer patient samples and 60% of ovarian cancer patient samples."

But surely we knew that already; that live CTCs provide more info than circulating DNA fragments. I don't understand how analysing both cDNA and CTCs adds to the info provided by CTCs alone. It merely re-states the bleeding obvious, that CTCs provide infinitely more info than cDNA.

If there is an oncologist/cytologist on the board who has insight to put me right I would be grateful

Moab

WTF on 2 trades and no RNS? Presumably a typo somewhere.

Can PHE even afford to build a demo?

It is quite extraordinary that c0ck should be a naughty word in the LSE lexicon. Mrs Grundy and Mary Whitehouse would have approved.

Tom

On what do you base your strong belief? Hope you are right.