David McNally v Gentoo Group Limited [2026] EWHC 750 (KB)

[2026] EWHC 750 (KB)Case No KB-2024-003515
IN THE HIGH COURT OF JUSTICE
KING'S BENCH DIVISION
Venue Royal Courts of Justice, Strand, London, WC2A 2LLDate 31/03/2026
Before
DAVID PITTAWAY KC
Between
David McNallyClaimantGentoo Group LimitedDefendant
Ivan Bowley (instructed by Slater and Gordon UK Limited) for ClaimantA.John Williams (instructed by Kennedys Law LLP) for DefendantHearing Hearing dates: 17, 18, and 19 February 2026
Approved JudgmentThis judgment was handed down remotely at 10.30am on Tuesday 31 March 2026 by circulation to the parties or their representatives by e-mail and by release to the National Archives..............................DAVID PITTAWAY KC

DAVID PITTAWAY KC (SITTING AS A DEPUTY HIGH COURT JUDGE):

[1]In this case breach of duty is admitted and quantum has been agreed at £250,000 subject to the deduction of statutory benefits. The sole issue is causation, more properly diagnosis.[2]The claimant was a painter and decorator who worked for the local authority in Sunderland for the whole of his working life. The details of his employment are set out in his witness statement. He was exposed to asbestos throughout. He was also a heavy smoker. He is now 66 years old. He was diagnosed in 2023 with mesothelioma, after attending his general practitioner complaining of shortness of breath. Initially, the treating hospital considered he was suffering from lung cancer but later, after further consideration, they revised their diagnosis to mesothelioma. He was treated with immunotherapy which has had a positive outcome but as there is no cure for mesothelioma, there will come a time when his condition deteriorates, and the illness will become terminal.[3]Mr and Mrs McNally attended the hearing.[4]The issue on diagnosis is whether Mr McNally has proved, on the balance of probabilities, that the disease from which he is suffering is mesothelioma. It is agreed that if I find that Mr McNally is suffering from mesothelioma, then he will recover damages of £250,000. If he has not, then the claim will be dismissed. The options are binary, either Mr McNally is suffering from mesothelioma or lung cancer. Other cancers have been considered by the experts and excluded.[5]Dr Moore-Gillon, the distinguished respiratory physician, states in his report that this is the most difficult case that he has had to consider in his long career as an expert on mesothelioma. He concluded that he was not satisfied that the medical evidence proved that Mr McNally was suffering from mesothelioma. Professor Attanoos, histopathologist, considers that Mr McNally is suffering from lung cancer. Dr Rudd, an equally eminent respiratory physician, considers that Mr McNally is suffering from mesothelioma. Professor Nicholson, histopathologist, also considers that this is a case of mesothelioma. The respiratory physicians agree that the outcome of this case will depend upon which histopathologist’s evidence I accept.[6]The case turns on the test results in histopathology and molecular analysis. The histology relies upon tissue taken at Freeman Hospital, Newcastle-upon-Tyne, which was subject to testing successively in Newcastle, Royal Brompton Hospital, London, and University College Hospital, Cardiff. Using Table 1 from the Guidelines for Pathologic Diagnosis of Mesothelioma 2023 Update (published November 2024) Mr Williams, on behalf of the defendant, has prepared a useful table, which sets out the results of the panels tested for mesothelioma and adenocarcinoma at the various hospitals in this case.[7]The respiratory physicians are agreed that the radiology cannot determine the differential diagnosis alone. If it could, then it would favour mesothelioma. Professor Nicholson’s initial opinion was that the radiology of a pleural effusion was supportive of a diagnosis of mesothelioma. Professor Attanoos agrees with that opinion.[8]Professor Attanoos requested a Claudin-4 test which if positive, can distinguish adenocarcinoma from mesothelioma with a 99% specificity. The result of the test was positive. The test first became available in 2006. That test was not carried out by the Freeman or the Brompton hospitals. Professor Nicholson said that it was not available at the Brompton although he had been asking the hospital managers for some time to make it available. He initially considered that the results from the histopathology marginally favoured lung cancer, however, he considered that the samples should be subjected to molecular analysis. The facilities for that analysis are available at his hospital, the Brompton and Cardiff. Based upon the tests undertaken at the Freeman and the Brompton, and additional tests Professor Nicholson considered could assist in the differential diagnosis, he ordered a molecular analysis. Molecular analysis was not undertaken at the Freeman. It was available in Cardiff but Professor Attanoos did not consider that it was necessary. He was satisfied, based upon the testing that he had seen, and the result of the Claudin-4 test, that molecular analysis was not required. The results of the molecular analysis at the Brompton tilted Professor Nicholson’s opinion to mesothelioma.[9]The task I have is to reconcile the results of the immunohistochemistry and molecular analysis to arrive at a conclusion.[10]From the literature which has been provided, I can see that it is well-recognised that cases of primary lung cancer can closely mimic cases of malignant pleural mesothelioma clinically. I observe that in one paper, where Professor Attanoos was the lead author, it said in 2003 that Calretinin is the most reliable specific marker for malignant mesotheliomas. It cautions that tumour misdiagnosis may have medicolegal implications in asbestos-related claims. Ae Ri An et al have published a paper (2020) in which they said:
“the tumour growth pattern makes it difficult to differentiate PLC [lung cancer] from MM [mesothelioma] based on radiologic findings and histologic confirmation is needed. IHC [immunohistochemistry] provides an adequate sensitivity and specificity for distinguishing PLC from MM.”
It goes on to refer to the absence of reports of genetic alterations in PLC. Dagogo-Jack et al have published a paper (2022) in which they recorded that the following genes were altered in MPM [malignant pleural mesothelioma]: CDNK2A 49%. BAP1 44%, MTAP 34% and NF2 33%. Table 1 broke the cases down into epithelioid and nonepithelioid cases of mesothelioma. The research confirmed that the mesothelioma somatic mutational landscape is largely defined by inactivation of tumour suppressor genes. Epithelioid mesothelioma is one of three types of mesothelioma. I am not concerned with the other two.[11]Before I turn to the evidence, there is an issue between the pathologists as to how I should treat the molecular analysis. Professor Attanoos’s position is that the Guidelines for Pathologic Diagnosis of Mesothelioma 2023 Update (published November 2024) set out the appropriate testing to be undertaken for a diagnosis of mesothelioma.[12]In the RCP Standards and Datasets for Reporting Cancer, (March 2024), two of the four authors were Professor Nicholson and Professor Attanoos. The foreword said that those guidelines were developed for the most common circumstances and recognised that they:
“cannot anticipate every pathological specimen type and clinical scenario. Occasional variation from the practice recommended in this guideline may therefore be required to report a specimen in a way that maximises benefit to the patient.”
[13]Later in the paper, under Considerations for Microscopy the guidelines state that:
“The distinction between EM [Epithelioid mesothelioma] and MAC [lung cancer] cannot be made with confidence on morphological grounds alone and immunohistochemistry is mandatory. Currently, no single antigen indicative of mesothelial or adenocarcinoma differentiation is sufficiently sensitive or specific, so a panel is recommended.”
It also refers to referral to regional or national experts in complex and difficult cases.[14]The Guidelines for Pathologic Diagnosis of Mesothelioma (November 2024), where again Professor Nicholson and Professor Attanoos are named as authors, relate primarily to immunohistochemistry but also refer to molecular assays. The evolving role of diagnostic molecular assays is addressed, where it states:
“regardless of site, a diagnosis of mesothelioma should always be based on compatible morphologic and immunohistochemical results obtained from an adequate tissue sample. … a history of asbestos exposure should not be taken into consideration by the pathologist when confirming or excluding mesothelioma. Molecular studies might be necessary in a minority of cases.”
[15]The Guidelines state that: “Since none of these markers are perfectly sensitive or specific, it is recommended that, in addition to broad spectrum cytokeratin, 2 mesothelial and 2 epithelial markers be included in a first line immunopanel to establish mesothelial lineage. If the results are concordant, the diagnosis can be considered established. If discordant, the immunopanel can be expanded for a second round of staining …”.[16]The Guidelines go onto state that: “in the authors experience, Claudin-4 is sufficiently reliable to serve as the sole epithelial marker in most differentials. It states: “Tables 1 and 2 list markers that are useful in distinguishing epithelioid pleural mesothelioma from adenocarcinoma and squamous cell carcinoma of the lung ….”.[17]In a section on Molecular Sequencing In Routine Diagnosis And Management, it refers to the potential for tumour profiling to provide diagnostic, prognostic and therapeutic information in a single assay. It states that: “at present routine genomic sequencing of mesotheliomas is performed only in select referral or academic centres and it is not currently recommended for routine clinical use. Immunohistochemical studies remain the ancillary assay of choice, with targeted molecular studies … in select cases”.[18]The Guidelines conclude that:
“Molecular studies … are useful in challenging cases with nondiagnostic morphologic and immunophenotypic findings. Importantly the pathologist must always correlate morphology and ancillary findings with clinical, radiographic and operative findings”
. They finish by referring to the rapid evolution in the field of mesothelioma diagnosis.[19]There are also two further papers which consider the relationship between NF2 and BAP1. I refer to the Fanaroff paper (2025), where it states that:
“Immunohistochemistry is widely available for the detection of the most frequent molecular alterations in DPM including BAP1, MTAP, NF2 and TP53 and may be used in resource limited settings where molecular testing is not available.”
. The paper concludes that:
“the findings of this study suggest that histologic features and molecular findings can be complementary in providing prognostic information for patients with pleural mesothelioma.”
[20]The histopathologists agree that molecular analysis is part of a developing science, however, the difference between them is that Professor Attanoos does not accept that there is sufficient provenance for a more general application for use in diagnosis. They are agreed that the facilities to carry out molecular analysis would only be found in large tertiary hospitals and regional centres.[21]It seems me to me that the molecular analysis in this case should be treated as adding to the sum of knowledge which is available for the purposes of the differential diagnosis. It is not suggested that there is any inaccuracy with the results of the molecular analysis carried out in this case. Professor Nicholson draws the distinction between the histology which tested for proteins and the molecular analysis examining the genes, which, in fact cause the cancer. In my view, once that analysis has been undertaken, it would be artificial to disregard the results. It has, however, to be given proper weight as part of the collective information that has been obtained.[22]The molecular analysis showed that NF2 was inactive, which it is in 40% of mesothelioma cases. The pathologists are agreed that based on the molecular analysis alone, the probable diagnosis is mesothelioma. There is, however, a stark difference between the NF2 and Claudin-4 test results. Claudin-4 has a 99% specificity and is positive for lung cancer. Each being the highwater mark of the parties’ respective cases. It is, therefore, necessary to examine the tests which were undertaken. The other histopathology and molecular results are not conclusive.[23]So where does that leave the issue?[24]The table, helpfully prepared by Mr Williams, shows the results for epithelioid mesothelioma (EM) and lung adenocarcinoma (LAC) or (NSCLC): “Epithelioid Mesothelioma”(1) Calretinin. It is positive in 95% of epithelioid mesotheliomas, (EM) staining is often strong and diffuse and must be both nuclear and cytoplasmic, 5 to 10% of lung adenocarcinoma (LAC) or (NSCLC) are positive, usually focal.(2) Cytokeratin 5 or 5/6. It is positive in 91% of EM, 5-20% of LACs are positive, usually focal.(3) WT1 positive (nuclear) in 88% EM; LAC virtually always negative,(4) D2-40 positive (membranous) in 93% of EM, 3% of LACs virtually always negative. Lung adenocarcinoma (1) Claudin-4, positive (punctuate or continuous membrane staining) in 99% of LAC, usually strong and diffuse, mesotheliomas virtually always negative. (2) CEA (positive in 84% of LAC; < 5% of EM positive, typically focal). (2) TTF1 (positive (nuclear) in 82% of LACs; mesotheliomas negative. (3) Napsin A (positive in 83% of LACs; mesotheliomas virtually always negative. (4) MOC 31 (positive in 96%; 8% of EMs (or one recent study 35% positive, usually focal.(5) BER EP4 (positive in 96% LACs; 15% of EMs (or one recent study 35% positive.(6) Cytoplasmic Mucin (PAS-D) Positive in LACs; generally negative in mesotheliomas.(7) BAP1 (inactivated in 60% of mesotheliomas) MTAP. Molecular (1) CDKN2 A/B (inactivated in 40-70-% of mesotheliomas; also seen but less common in NSCC). (2) BAP1 (inactivated in 69% pleural mesotheliomas). (3) NF2 (inactivated in 40% mesothelioma cases) disagreement as to NSCC case. Lung adenocarcinoma

Molecular

[25]In summary, the immunohistology produced positive results in Claudin-4 testing at Cardiff, which was not undertaken at Brompton. The CEA, TTF-1, Napsin A tests were negative at all hospitals, The MOC-31 test was positive at Cardiff. The BER-EP4 tests were positive at all hospitals. The Cytoplasmic Mucin test was positive at Freeman. The BAP 1 and MTAP were non-mutated at Cardiff and not inactivated at Brompton. It follows that, if Mr McNally’s disease is epithelioid mesothelioma, he would fall within a very small percentage of cases, where the result of the Claudin-4 was positive. The results of the tests in MOC31, BER EP4, Cytoplasmic Mucin, BAP1 and MTAP would also support that he has lung cancer.[26]The support for epithelioid mesothelioma comes in immunohistology from the Calretinin test. The result of the tests at the Freeman Hospital were cytoplasmic + nuclear (occasional cells) weak staining, at Brompton and Cardiff, isolated cell positivity. And the Cytokeratin tests where the results were positive at the Freeman Hospital, (occasional cells), and uncertain at Brompton and Cardiff. The WT-1 and D2-40 test was negative.[27]The molecular testing showed that NF2 was mutated, CDKN2A/B and TP53 were also mutated. The other molecular tests, ALK, KRAS, and MET were not mutated.[28]I now turn to the expert evidence.[29]Dr Rudd was initially asked to report on Mr McNally’s illness due to mesothelioma and its relation to asbestos exposure in the course of his employment. He is generally recognised as one of the leading consultants in respiratory medicine and medical oncology. At that stage, after considering the material provided to him, he did not consider that Mr McNally’s diagnosis by the Freeman Hospital was likely to be contentious. He did not examine Mr McNally.[30]Dr Rudd set out in his report that Mr McNally had spent his entire working life with the same employer which went through a series of entity changes. He started in 1976 with Sunderland Council as a painter and decorator and worked in that capacity for the next 39 years. He had several TUPE transfers, initially to Sunderland Housing Group in 2001 and later the defendant from 2007. He retired due to ill-health in 2015. His role did not change when his employment moved to Sunderland Housing Group and later to Gentoo. He worked on public buildings and domestic premises including houses and flats. He was exposed to asbestos in many ways. He detailed the work that Mr McNally undertook in residential property where he encountered asbestos, working with soffit boards, in garages, kitchens and bathrooms, lagged pipes, and bin stores, lined with asbestos boards. He noted that before 2001 there was little or no asbestos awareness training and there was no protective equipment other than paper dust masks.[31]Throughout his adult life, Mr McNally has been a regular smoker, at times smoking 20 or more cigarettes per day. He also suffered from prostate cancer in 2012, which was successfully treated. He was a heavy drinker. He has a history of chronic obstructive pulmonary disease (COPD) before his present illness. He has had other medical complications which it is not necessary to set out here. Following his diagnosis, Mr McNally has been treated successfully with immunotherapy albeit that is not a cure for mesothelioma.[32]After investigations in July and August 2023, Mr McNally’s case was reviewed at an MDT on 15 September 2023 in the Respiratory Clinic at Sunderland Royal Hospital where it was concluded that he had either a mesothelioma or lung cancer. Molecular tests were suggested. These were subsequently reported not to have identified any mutations predictive of response to various agents used for treating metastatic carcinoma [lung cancer].[33]On 12 October 2023 he was seen in the oncology clinic at Freeman Hospital by Dr Jones, consultant oncologist. He noted that histology had shown an epithelioid malignancy with an unusual immunohistochemical profile with a differential diagnosis of epithelioid mesothelioma or metastatic carcinoma. There was no evidence of a primary lung cancer or a primary outside the thorax. The tumour had been shown to have high PD-L1 expression at 95%. His recent CT scan showed diffuse pleural nodularity in the right hemithorax which had increased since July. He was breathless on exertion. Dr Jones considered that the radiological pattern was in keeping with epithelioid mesothelioma.[34]On 19 October 2023 Mr McNally’s case was discussed at a lung multi-disciplinary team (MDT) meeting at which it was agreed that the probable diagnosis was mesothelioma, and he should go ahead with treatment for that condition. They noted that the appearances of the radiology were characteristic of mesothelioma and unlikely to be due to any other cause.[35]Dr Rudd, in his report of 11 March 2024, said:
“Mr McNally has malignant mesothelioma of the pleura of epithelioid type. The diagnosis was not completely definitive on the basis of immunocytochemical stains but the radiological appearances are characteristic of mesothelioma and there is no evidence of a primary tumour elsewhere. I do not consider there is any significant doubt about the diagnosis of mesothelioma.”
[36]Dr Rudd considered that based on Mr McNally’s witness statement his employment materially increased the risk that he would develop mesothelioma before 2013. He considered that symptoms of mesothelioma started in the latter part of June 2023.[37]Dr Rudd prepared further comments on 16 October 2025. By that time had read the reports by Professor Nicholson, consultant pathologist, dated 29 May 2025 and 28 August 2025, an email dated 17 December 2024 and report dated 4 June 2025 from Professor Attanoos, and the joint statement by Professor Nicholson and Professor Attanoos of 7 October 2025.[38]Dr Rudd considered that the presence of a pleural based tumour extending circumferentially around the lung in the absence of evidence of a primary tumour elsewhere strongly favours a diagnosis of mesothelioma. As explained by Dr Jones to Mr McNally the multi-disciplinary team responsible for his care considered the clinical and radiological features as well as the pathological findings and agreed a diagnosis of mesothelioma. He has received immunotherapy which is standard treatment for mesothelioma and his mesothelioma has responded to it. Dr Rudd remained of the view that the most likely diagnosis is mesothelioma.[39]In a letter dated February 2026, Dr Rudd was asked to comment on 2023 CT scans which he had not seen previously. A CT scan dated 19 July 2023 showed a large right pleural effusion which makes assessment of the hilum difficult. In his opinion it shows no convincing evidence of a soft tissue hilar mass lesion. It does show irregular right pleural thickening anteriorly in the mid zone with slight irregular thickening of the mediastinal pleura anteriorly. His view is that these appearances are consistent with mesothelioma. A CT scan dated 27 December 2023 shows circumferential pleural thickening in the right hemithorax. It does not show a right hilar soft tissue mass lesion. Following review of these images, he had not changed his conclusion that, on the balance of probabilities, Mr McNally has malignant mesothelioma.[40]In cross-examination Dr Rudd maintained his opinion that this was a case of mesothelioma. As set out above, he did accept that the literature refers to lung cancer mimicking mesothelioma. He agreed that such cases are very uncommon. He said he sees one or two such cases each year out of two to three hundred.[41]Dr Moore-Gillon covers much the same ground as Dr Rudd in the earlier part of his report. He does, however, draw attention to the very detailed cytology report, following therapeutic pleural aspiration, which was arranged and performed on 21 July 2023, including immunocytochemical testing. In particular, the cytologist’s opinion was that the appearances “are therefore best regarded as raising the possibility of malignancy of uncertain type. The features seen in the specimen are not considered diagnostic.” He records that these results were not available when Mr McNally’s case was discussed in the MDT on 27 July 2023.[42]It is to be noted that on 28 April 2025 the CT appearances were again stable, and on 8 May 2025 Mr McNally was seen by Dr Jones, who wrote:
“The clinical presentation, biopsy and radiology was reviewed in our multidisciplinary team with experts in all forms of thoracic malignancy, and in view of the fact that this is a purely pleural-based malignancy, the team agreed a diagnosis of mesothelioma.”
[43]Dr Moore-Gillon states in his report:
“I have seen a recent CT scan from 28 04 25 which shows volume loss in the right hemithorax superiorly and irregular pleural thickening laterally, and inferiorly there is mild pleural thickening on the right with some larger pleural nodules. On the lung windows there is extensive emphysema with widespread bullae. There are no obvious intrapulmonary lesions. This imaging favours mesothelioma rather than lung cancer.”
[44]After reviewing the expert evidence, he states that Mr McNally undoubtedly has a tumour involving the pleura. He draws attention to the uncertainty as to whether this is a mesothelioma or a lung cancer involving the pleura. He observes that in formulating a diagnosis all available information must be considered. This includes an individual’s preexisting risk factors, their clinical presentation, the results of imaging and other investigations and the pathological appearances. He draws attention to the phraseology used by Professor Nicholson to suggest that he has considered the imaging appearances when reaching his view of the significance of the molecular tests. Professor Nicholson subsequently rejected this analysis in his answers to CPR Part 35 questions.[45]Dr Moore-Gillon concludes his report by stating that:
“After the most careful thought, I cannot reach the view that this is, on balance, mesothelioma. I advise the Court, though, that this is one of the most finely balanced cases I can recollect, and that a conclusion that this is mesothelioma rather than lung cancer is well within a range of reasonable expert opinion.”
[46]There is further correspondence from Dr Moore Gillon regarding the CT scans and radiography he subsequently has seen. It is noteworthy that in his letter of 30 January 2026, he records that he had seen:
“a further CT scan dated 28 09 23, which had also not previously been seen by Dr Rudd. The appearances are of extensive malignancy with irregular nodular pleural thickening and volume loss in the right hemi thorax. There is involvement of the fissures. The appearances are very suggestive of mesothelioma, but pleural spread from a peripheral lung cancer arising close to the pericardium would be an alternative explanation.”
[47]He agrees that:
“these appearances are more suggestive of mesothelioma than any other diagnosis, but these appearances cannot themselves preclude an alternative diagnosis. As pointed out at page 19 of my first report, it is very well recognised that lung cancers arising in the periphery of the lung can have the imaging appearances of malignant mesothelioma.”
[48]In cross-examination Dr Moore-Gillon elegantly maintained his opinion that this was a finely balanced case where he was not satisfied that it was case of mesothelioma. He essentially deferred his opinion to that of the histopathologists. As to the sum of knowledge available to me, he added that in urban centres where asbestos was imported, there was a higher incidence of mesothelioma. He did resile from the opinion expressed in his report that Professor Nicholson’s opinion had double counted the clinical setting.[49]I should mention that the joint statement from Dr Rudd and Dr Moore-Gillon essentially deferred the diagnosis to the pathologists. Dr Rudd considers that:
“on the basis of Professor Nicholson’s opinion that the pathological findings alone favour mesothelioma even disregarding the clinical setting which also favours mesothelioma, on the balance of probabilities, the tumour is a mesothelioma in Dr Rudd’s opinion. Dr Moore-Gillon considers that Prof Attanoos regards molecular testing “as not yet being a fully validated approach to the diagnostic process in matters like this, and Prof Attanoos appears to continue to be robust in his view that this is a lung cancer.”
His view is that:
“the diagnosis in this case must be determined by the Court’s preference for the opinion of either Prof Nicholson or Prof Attanoos. Had both these experts been unable to reach a view either way then I would have regarded the pathological findings as being neutral and indeed been swayed by the imaging towards a diagnosis of mesothelioma.”
[50]Professor Nicholson considered 53 stained slides and two blocks, labelled PR034288/23, and three cytology slides, labelled CN1945Y/23. The former showed sections with pleura diffusely infiltrated by a malignant epithelioid tumour with variably sized islands of predominantly moderately pleomorphic epithelioid cells.[51]He concluded that there was a malignant epithelioid tumour in the pleura with a differential diagnosis of metastatic non-small cell carcinoma (NSCLC) [lung cancer] and epithelioid mesothelioma. As set out above, and in Professor Attanoos’s correspondence, the ideal is to have either two positive “mesothelial” markers and two negative “epithelial” markers to diagnose epithelioid mesothelioma, or two positive “epithelial” markers and two negative “mesothelial” markers to diagnose NSCLC [lung cancer].[52]At that time, he marginally favoured this tumour being metastatic non-small cell carcinoma rather than epithelioid mesothelioma. He raised the possibility that additional molecular testing via next generation sequencing to look at a broader spectrum of molecular abnormalities which might help alter the balance of probabilities when reviewed in a multidisciplinary setting.[53]His supplementary report followed genetic testing, which found that:
“Pathogenic/likely pathogenic variants were detected in the CDKN2A, NF2 and TP53 genes. Additional results: No mutations were detected in the regions analysed within the ALK, BAP1, BRAF, KRAS, MET, ERBB2 and RB1 genes”
. His view was that:
“The genomic landscape of mesothelioma is predominantly characterized by tumour suppressor alterations, with the most frequently occurring including BAP1, CDKN2A, NF2 and TP53 (1). NF2 alterations are frequently seen in mesothelioma and are not a feature of lung cancer, to my knowledge. CDKN2A alterations can be seen in non-small lung carcinoma but are not as commonly seen as in mesothelioma. MET amplification and P53 alterations can be seen in both mesothelioma and non-small cell lung carcinoma.”
[54]In answer to CPR Part 35 Questions based on the diagnostic immunohistochemistry, Professor Nicholson favoured the tumour being metastatic non-small cell carcinoma [lung cancer], however, based on the mutational profile, he favoured a diagnosis of epithelioid mesothelioma. His opinion is that the tumour is an epithelioid mesothelioma.[55]In cross-examination Professor Nicholson also maintained his opinion that this was a case of mesothelioma. He was questioned about his experience giving evidence in court proceedings, which he explained was limited to giving evidence in the coroners’ courts. He has not previously given evidence in a case of mesothelioma. He was asked whether he had applied the 2024 Guidelines to the immunohistology data. His view was that he had done so. He said that the information in the Guidelines about molecular data is limited. His oral evidence was that testing has evolved significantly over the past three years.[56]His view is that the results of the NF2 test is more commonly seen in mesothelioma and carries greater weight than the immunohistology data. He did make one concession when he corrected the assertion in his report that mutations in the NF2 test is not seen in lung cancer cases. After reading further literature, he accepted that mutations in the NF2 test is seen in 2 to 5% of lung cancer cases. He also accepted that BAP1 is a commonly mutated gene in mesothelioma but was not mutated in the test in this case, and that 40% of BAP1 cases do not carry the gene. TP53 showed genetic abnormality, which he said is found in both diseases, 15% in mesothelioma and 50% in lung cancer. When confronted with the result of the Claudin-4 test, he believes that the molecular data carried greater weight. He had experienced Claudin-4 being positive in cases of mesothelioma in two other cases. He was questioned about whether he had complied with his expert’s duty in his report where he stated that molecular testing might help alter the balance of probabilities. He said that he put the wording down to his inexperience in writing medico-legal reports. He accepted that before molecular testing the scales were tilted towards lung cancer. His view is that when everything is put together it points to mesothelioma.[57]Professor Attanoos in his first report, dated 4 June 2025, concluded that Mr McNally has contracted metastatic non-small cell carcinoma and not pleural epithelioid mesothelioma. He had initially provided an email to the defendant’s solicitors, where he had set out similar preliminary views.[58]I have set out the relevant parts of his report. “Mr McNally has contracted a malignant epithelial tumour involving the pleura, the application of a wide panel of immunohistochemistry and including histochemical analysis has allowed for a robust diagnosis of metastatic non-small cell carcinoma. The immunophenotype and histochemistry does not support a diagnosis of pleural mesothelioma epithelioid type. It is recognised that immunohistochemistry has an important role in the differential diagnosis between many tumours, and in this setting, between pleural epithelioid mesothelioma and metastatic non-small cell carcinoma. A broad panel of markers have been studied. Cytokeratin AE1/3, CK7 and GATA-3 (positive in Mr McNally’s tumour) may be positive in mesothelioma or carcinoma so are non-discriminatory overall. “The combined positive ‘epithelial/carcinoma’ marker expression of Claudin-4 (a highly sensitive and specific marker for carcinoma – see Husain 2024 Table 1- ‘Positive (punctate or continuous membranous staining) in 99% of lung adenocarcinomas, usually strong and diffuse; mesotheliomas virtually always negative’), together with the diffuse high intensity expression of ‘positive carcinoma’ markers -MOC-31, Ber EP4, and CD15/Leu-M1, appears more definitive, in my opinion to support metastatic non-small cell carcinoma than the opposing staining pattern - The ‘positive mesothelial’ marker expression of thrombomodulin (a second line mesothelial marker as there is overlap expression in carcinomas), with isolated CK5/6 and calretinin together with negative staining in Mr McNally’s tumour for first-line mesothelial markers WT1, and D2-40, does not support epithelioid mesothelioma. “In addition, the PASD neutral mucin-present in Mr McNally’s tumour strongly favours adenocarcinoma. The site-specific carcinoma markers are broadly non-informative – negative for lung (Napsin A; TTF1), Prostate (PSA, PSAP), Thyroid (TTF1, PAX-8), colon (CK20), Kidney, Thymus (PAX8, CD117). GATA-3 (positive in Mr McNally’s tumour) may be positive in a wide variety of epithelial tumour sites and other non-epithelial tissues so has limited utility. Regards molecular testing - The majority of epithelioid mesotheliomas (although not non-small cell carcinomas) would be mutated in the combined testing of BAP-1 and MTAP (CDKN2A/B) – there is no observed mutated status in Mr McNally’s tumour.[59]In his second report dated 15 September 2025, he was asked to comment on the molecular genetic testing organised by Professor Nicholson. He does not accept that the testing is diagnostic. His thesis is that genetic testing is:
“an evolving area of discovery, and it is not sufficiently proven in the same manner as conventional diagnostics which rely on tumour morphology, immunohistochemistry and wide immunohistochemical panels.”
He states that he is: “not aware of any report or treatise on mesothelioma diagnosis which supports the position that greater weight should be placed on molecular studies when conventional pathology favours an alternate diagnosis of carcinoma. His view is to rely on the established diagnostic approach, centred in conventional diagnostics. He concedes that molecular genetics will play a greater role in the future in tumour diagnostic, prognostics and disease causation.[60]In cross-examination Professor Attanoos maintained his opinion that this was a case of lung cancer. He relied primarily on the result of the Claudin-4 test. He also relied upon the results of BAP1 and MTAP tests being non-mutated. Given those results, he did not consider that molecular testing would have altered his final conclusion. The tests had to be read with other markers studies in this case, set out above, which he believed strongly supported lung cancer. He repeated his reservations about the provenance of molecular testing and its use for diagnosis at the present time.[61]I should mention that the joint statement from Professor Nicholson and Professor Attanoos recognises that this a complex case with no conclusive answer, and they agree it is a matter of how much weight is placed on the individual pieces of evidence by the individual assessing the data. Both pathologists agree the various modalities investigated in this case have yielded somewhat differing balance of probabilities in relation to the differential diagnosis. They also agree that conventional diagnostics, as stated above, favour NSCLC [lung cancer] and both pathologists agree the molecular analysis, in isolation, favours mesothelioma.[62]The joint statement sets out the issue I have to decide in these terms:
“Professor Nicholson places greater reliance on the tumour mutational profile. He is of the opinion that the molecular analysis changes the balance of probability, as NF2 mutations (~30% versus ~2%) (https://www.cbioportal.org, PMID: 35704798, 39788204, 34580349) and, to a lesser extend CDKN2A mutations, are more frequently seen in mesothelioma than NSCLC. In the context of a primarily pleural presentation of disease, Professor Nicholson is of the opinion that the molecular profile favours mesothelioma on the balance of probabilities.” “Professor Attanoos places greater reliance on conventional diagnostic modalities which have been fully validated. He recognises the evolving role of molecular analysis in diagnostics although considers that presently for mesothelioma, as a diagnostic tool, it is insufficiently validated and does not overturn a diagnosis concluded using conventional diagnostic methods as listed above. He remains in favour that Mr McNally has contracted NSCLC and not pleural epithelioid mesothelioma, on the balance of probabilities.”
[63]I have considered carefully all the expert evidence which has been presented to the court. I was impressed by all four experts and fully accept that they are all seeking to assist the court. Dr Rudd and Dr Moore-Gillon have considerable experience in mesothelioma cases and recognise the complexities of this particular case, as indeed do both Professor Nicholson and Professor Attanoos.[64]In my view, there is a difference between Dr Rudd and Dr Moore-Gillon as to how they have expressed their opinions.[65]Dr Rudd is satisfied that Mr McNally is suffering from mesothelioma. Indeed, at the outset when he prepared his first report, he did not consider that the diagnosis was likely to be disputed. A diagnosis of mesothelioma had already been reached by Dr Jones, the treating oncologist, and the other members of the MDT in October 2023. Dr Rudd accepts, however, that the radiology, which points to mesothelioma is not conclusive, and can only be seen as part of the material available. He, ultimately, defers to the opinion of Professor Nicholson, whilst maintaining his own opinion that this is a case of mesothelioma.[66]Dr Moore-Gillon’s opinion is more nuanced in favour of lung cancer. He recognises the finely balanced nature of this case. Albeit that he comes down on the side of lung cancer, the impression from both his report and oral evidence is that he does not believe that the case for mesothelioma has been proved, which is, of course, a decision I have to come to. He rightly withdrew his analysis that Professor Nicholson had double counted the clinical setting in reaching his conclusion on the results of the molecular testing.[67]I was impressed by the evidence given by Professor Nicholson, who was less familiar with giving evidence than Professor Attanoos. His evidence was refreshingly candid, thoughtful, and considered in its delivery. I reject the suggestion made to him in cross-examination that he was departing from his duties as an expert and seeking to promote Mr McNally’s case. I find that when he suggested molecular testing, he was seeking to explore the possibilities of resolving the diagnosis. I am troubled by Professor Attanoos’ view that it was not necessary to go on to consider molecular testing when the results of the immunohistology were available. There may be comfort in that conclusion in clearcut cases, however, all the experts are agreed that this is not such a case. They recognise the difficulty in diagnosis.[68]I am not satisfied that Professor Attanoos engaged sufficiently with the results of the molecular testing, once obtained. I do not accept his criticism that molecular testing in mesothelioma cases is not sufficiently validated to be relied upon. Where it has been obtained, and there is no criticism of the results themselves, then, it forms part of the material, which is before me in reaching an opinion as to whether Mr McNally is suffering from mesothelioma or lung cancer. I accept Professor Nicholson’s evidence that the role of molecular testing has evolved rapidly in the past three years since the guidelines were written in 2023.[69]Nevertheless, I must reconcile the result of the molecular testing with that of the Claudin 4 test. I have concluded that Mr McNally is one of those very rare individuals who come within a very small percentage of cases where the positive result is not indicative of lung cancer. In reaching that decision I have considered the totality of the immunohistology and molecular results, particularly NF2, and to a lesser extent CDKN2A/B and TP53, which are both less conclusive. It seems to me the results in the tests in Calretinin and Cytokeratin are not sufficiently certain to be relied upon. It also seems to me that the radiology, pointing towards mesothelioma, is a relevant consideration. Finally, I do not place significant weight on the opinion of Dr Jones and the treating consultants, that this is a case of mesothelioma, it is, however, another piece in this complex jigsaw that fits with a diagnosis of mesothelioma.[70]Accordingly, I have concluded, on the balance of probabilities, that Mr McNally is suffering from mesothelioma and, in those circumstances, the claim succeeds. I ask that counsel draw up an appropriate order that is submitted to the associate for my approval.