FREE CHAPTER: The History And The Science (from ‘A Practical Guide to Claims Arising from Delays in Diagnosing Cancer’ by Bella Webb)



This chapter will look at the trend towards an increase in delayed cancer diagnosis claims and the rationale and statistics that underlie it. It will then go on to look at what we actually mean by cancer in medical terms. How does the disease operate and how is it diagnosed? A background understanding of both of these issues is essential to the management of any legal claim based upon an allegation of delayed diagnosis. If we as lawyers do not understand what cancer is and how it develops within the human body, we cannot hope to build and run an efficient and effective legal case. The application of the legal principles underlying breach of duty, causation and injury are always fact specific. This chapter will help us start to get to grips with some of the facts which permeate all cases of this type.

The History

Delayed cancer diagnosis claims are undoubtedly on the rise. Why? Cancer survival rates in the UK are a hot topic. The media have, in recent years, published articles which suggest that cancer survival in the UK is the worst anywhere in Europe. Moreover, Cancer Research UK published a report in September 2014 indicating that early diagnosis saves lives, and that late diagnosis of cancers in the UK can explain the poor survival rates in Britain compared with other countries. The same report also suggested that there was extremely wide variation in regional and local practice, accounting for nearly a threefold difference between the best and worst clinical commissioning groups.

On 30th January 2018, the CONCORD-3 report was published by the Lancet. CONCORD is the global programme for surveillance of cancer survival, led by the London School of Hygiene & Tropical Medicine. The steering committee is comprised of scientists and cancer patients from 13 countries, according to the Cancer Survival Group and LSHTM website. It updates the statistics for survival to 2014 and includes 18 cancers and groups of cancer that collectively represent 75% of the global cancer burden.

A review of the results shows (as confirmed by LSHTM) that whilst overall cancer survival has improved and continues to do so, with some cancers such as breast cancer (increased from 80 – 86%) and rectal cancer (from 55 to 63%) showing significant increases in five year survival; the UK still lags behind other comparable countries in respect of the survival statistics for several common cancers.

There is also worrying evidence reported by the BBC and other media outlets that:

(a) Delays in diagnosis are vastly different between the richest and the poorest. That reflects not only issues with access to care but also the propensity of the patient themselves to recognise symptoms of concern and attend their GP. It is said that income, age, gender and cancer type all play a part, and;

(b) Delays are more prevalent in certain regions – perhaps reflecting the socio-economic issues considered above.

League Tables and Audits

Such has been the concern about the UK’s approach to cancer diagnosis, that league tables for GPs were introduced during 2013, the first set of which appeared to find, according to articles in the media, including the Telegraph on 6th December 2013, that more than half are not referring such patients to specialists quickly enough. The national performance data – which covers all 8,000 GP practices in England – enables patients to look up their own surgery, and see how it performs against dozens of indicators about diagnosis and treatment of most of the common diseases and conditions.

It should however be noted that there is controversy about the interpretation that can properly be placed upon the results. Sean Duffy, national clinical director for cancer at NHS England, said, as reported on GP online on 9th December 2013, that the data was complex and not easy to interpret. For example, he noted that a large proportion of patients do not present to their GP with symptoms, such that cancers are only detected when the patient attends at A&E. He claimed that the statistics tell us more about how the system works as a whole. Similarly, GPC chairman Dr Chaand Nagpaul said that the tables were overly simplistic and did not show the complexity of diagnosing patients.

As recently as September 2016, a voluntary audit for GP practices was launched by a collaboration between the RCGP, Public Health England (PHE), Cancer Research UK and Macmillan. It collects data on how many cancers have been diagnosed, the types of cancers diagnosed, the number of tests and consultations GPs use and how many cancers are diagnosed late or early. The review looked first at data from 2014 and then aims to compare that to data from 2015 onwards to build a picture of how diagnosis has changed following the introduction of NICE’ latest guidance on diagnosing cancer, and then compared against the national average. The first set of results at the end of 2017 appeared to show rather better figures than those suggested elsewhere. Further, in 2016, NHS England made more than £200m available to Cancer Alliances from 2016-2018 in order to develop new models of care that will speed up diagnosis.

There have been other advances. New screening tests for bowel and cervical cancer are to be introduced during 2018 and 2019 (see NHS England’s website) and research continues into a universal blood test for cancer, known as the CancerSEEK test. According to an article by Alexander Castellino on 18th January 2018, published on, the test will aim to look for mutations in sixteen genes that regularly arise in cancer, as well as certain proteins that are commonly released. Further, a new cancer diagnosis standard, intended to ensure that patients learn within 28 days whether or not they have cancer, will be introduced in 2020. In preparation, a new Cancer Waiting Times System will be commenced in April 2018 so that teams of clinicians can ascertain how to collect data for the new standard. NHS England reports that five sites are already piloting the new 28-day standard across six cancer pathways – gynaecology, urology, head and neck, lung, lower and upper gastrointestinal.

As noted in the introduction, no doubt one of the primary reasons for the increase in litigation surrounding delayed cancer diagnosis is the fact that the patient body are now much more knowledgeable, media savvy and willing to question the views of medics than ever before. We are regularly exposed to news stories about poor diagnosis statistics, and about symptom awareness and self-care. That can only be a good thing in real terms but simultaneously gives rise to an increasing trend towards litigation and claim awareness.

The Science

It ought to go without saying, but the basis of any successful claim or defence in the field of clinical negligence, is an understanding of the medical building blocks of the injury or disease with which one is dealing. That is especially so of cancer. It is not enough simply to rely upon one’s expert or experts to tell us everything. Of course, they are vital (for which see later chapters) in establishing breach of duty and causation, and in assisting the legal team with the more intricate medical details. However, in order to get the best from one’s experts, and in order to test their credibility effectively, the lawyer must themselves have a background understanding of the condition in question.

There is a tendency to view “cancer” as a single disease. That is not the case, and different types of cancer have different rules, both medically and legally speaking. Plainly, this book is not the correct place to undertake a detailed exploration of what cancer is, and nor is the author appropriately qualified to do so. However, a brief summary of the medical building blocks is required. For further reading upon the topic, there are numerous medical texts and cancer websites available to assist the lawyer in this field.

It is important to remember that cancer is in fact a collection of multiple different but associated diseases. According to the National Cancer Institute ( website) and the Cancer Research website (, in all forms of the disease, a group of cells in the human body begin to divide uncontrollably and can spread into surrounding tissues. Cancer can start almost anywhere in the body. There are currently thought to be over 200 different types of cancer.

The NCI website and go on to tell us the following key facts:

(a) Cancer is a disease caused by changes to our genes, whether inherited or arising during our lifetime and for example, through environmental exposure to substances.

(b) Each individual’s cancer has a unique pattern of genetic change. As such, it is said that even within the same type of tumour there will be differences in cells with variable genetic alterations.

(c) In normal circumstances, cells grow and divide to form new cells as and only when the body requires them.

(d) When cancer develops that order breaks down and the development of extra abnormal uncontrolled cells can form growths called tumours.

(e) A tumour may contain millions of cancer cells.

(f) Most cancers form solid tumours but others, such as blood borne cancers do not.

(g) All of the tissues of the body have a membrane to keep that tissue’s unique cells inside its walls. Cancer has the ability to break through that membrane and invade other local tissues. The process by which it does so is not fully understood but it is thought that growth outwards occurs through one or more of the following:

  • Pressure from the growing tumour until it forces its way through the weakest party of the normal tissue and causing the normal tissue to die off when deprived of blood and oxygen;

  • The use of enzymes to break down cells;

  • Direct movement of cells. Cancer cells can generally move more easily than normal cells.

(h) Tumours that are cancerous can invade surrounding structures or some cells can break off and travel to (and start growing in) remote areas through the blood or lymph systems to form secondary tumours. These secondary tumours are called metastases and they will have the same type of cancer cells as the original cancer. So for example, if a patient/claimant starts off with bowel cancer which then spreads to the lung, the secondary cancer is a metastatic bowel cancer and not lung cancer, even though it is present within the lung cells and/or tissues. The process by which the cancer spreads to distant parts of the body is called metastasis.

(i) Benign tumours do not spread in the same way and do not usually have the same propensity to return (save perhaps for some brain tumours).

(j) Cancers are most often named for the tissues or the organs which are the focus of the disease’s formation. Cancer may also be described by the type of cell in which it is formed – ie: carcinoma, sarcoma, leukaemia, lymphoma etc:

A word about cancer spread. There is reference above to metastatic disease. One important point to keep in mind with cancer claims is that, as with a primary tumour, which takes time to grow and to form a tumour, so too do metastatic deposits. The name for areas of cancer spread that are, as yet, too small to be identified on a scan are micro metastases. For most cancers, Cancer Research UK remind us that there is, as yet in any event, no blood test to tell whether or not a cancer has spread, and as a result, the diagnosis of cancer spread (or its likelihood for our purposes as lawyers) is based upon a range of clinical factors, including:

(a) Experience from previous cases;

(b) If surgery has taken place to remove the primary tumour, an assessment of whether there are cancer cells in the blood vessels of the tumour;

(c) The grade of the cancer (the higher the more likely the spread), and;

(d) Analysis of the lymph nodes if removed surgically.

Whether or not there has been metastatic spread of the disease is critical in assessing treatment options and ultimately in determining survival prospects.

Some of the most obvious difficulties for the legal assessment of a delayed cancer claim will no doubt already be apparent from the quick summary of the scientific background above. In particular:

  • The sheer fact that each cancer and its development and growth is unique, working on an individual genetic pattern influenced by the patient’s own physiology, in combination with often multiple environmental factors, makes predictions about its rate of growth, and therefore its “likely” course but for any delay, incredibly difficult, and frequently open to controversy, and;

  • The potential for there to be micro metastases, not detectable by any form of scan, allows, in some cases dealing with higher grade or larger primary tumours, the potential for speculative argument about whether the disease would in fact have spread already at any earlier proposed diagnosis date, and therefore led to the same (poorer) outcome.

Those considerations, amongst others, will be highly relevant in the assessment of expert evidence on either side and in respect of causation, which will be considered in greater detail later in this book.

Grade and Stage


The grade and stage of the cancer are largely determinative of the treatment pathway recommended, as well as the survival prospects.

In terms of grading, the grade of the cancer will be relevant to an assessment of the likelihood that it has metastasised or might metastasise and as such, an understanding of both grade and stage are key to an effective assessment of causation in any delayed cancer diagnosis claim.

The grade of a tumour indicates how abnormal its cells and tissues are when compared with the norm. Whilst there are different types of grading systems, generally speaking there are three grades, with grade 1 indicative of a cancer which looks similar to normal cells and grows slowly, and grade three being the most abnormal and rapidly developing. The grade of a cancer does not change over time.

Stage and Staging Systems

The stage of a cancer is slightly different. Staging describes both size of tumour and the extent of its growth. Again, there are different types of staging system in place for different cancers – for example melanomas may be measured for their Breslow thickness, colorectal cancers have a Dukes stage and for prostate cancer the stage is a measure of the extent of growth or invasion and the Gleason grade is a measure of the aggressiveness of the cancer.

However, probably the most detailed and common staging system is the Tumour, Node, Metastasis (TNM) system, which was developed by the American Joint Committee on Cancer (AJCC) and the Union for International Cancer Control (UICC). Their website, https:// explains the system in detail. The size of the tumour is usually measured in centimetres and it is the size of the primary tumour which generally determines its T stage. T1 represents the smallest size and T2, T3 and T4 represent progressively larger tumours depending upon their spread to nearby tissues.

As described previously, at some stage in cancer development, some cancer cells may migrate from the primary tumour and spread to the lymph nodes. The nodes may swell and the size of the lymph nodes and / or extent of the spread is categorised by “N” in the TNM scale. N0 represents no lymph node spread with N1, 2 and 3 representing progressively more extensive spread. The T and N categories are different for each cancer type and the definitions of those categories make up a substantial component of oncology text books and are beyond this text.

The “M” classification stands for metastases or spread to other distant organs. M0 is applicable where there is no such spread and M1 where there is a spread beyond the regional lymph nodes.

Sometimes, those categories are further subdivided using letters and numbers. An “x” tends to mean that no measurement can be taken. In addition, the insertion of a “p” before the letters TNM stands for pathological stage, whereas “c” stands for clinical stage. It follows from that analysis that cancers are often staged twice – first on a clinical basis. That assessment is an estimate of the extent of the cancer and is based upon clinical examination, radiology and biopsies. If surgery is then undertaken, a pathologic stage can be assessed upon the results of surgery and a histopathological analysis of the tissues removed. Those stages are not always the same.

Doubling Times

In the context of a claim dealing with a delay in cancer diagnosis, there is no clear basis upon which to assess the likely size of a tumour (or its spread) in the absence of a previous coincidental x-ray or scan on which the tumour was visible but missed as an incidental finding. That is a rare thing. As such, if there is no radiology or other screening lurking in the historic medical records of the client/patient, the retrospective staging of the tumour will depend upon a combination of data on average tumour growth rates (and which vary between types of cancers) and factors specific to the patient and the tumour’s unique characteristics. We have already determined that each person’s cancer is a unique creature and it follows from that, that there will undoubtedly be controversy in presenting evidence of averages as probative of injury in any particular claim.

Oncologists talk about doubling times or volume doubling times (VDT) to describe the likely growth of a cancer. The medical journals are littered with articles considering the variable (and of course average/mean) VDTs for different types of cancer. The medico legal oncology expert will no doubt base a large part of their view as to the likely growth rate of the claimant’s cancer, and therefore the extent to which damage as a consequence of the alleged delay can be established, upon VDT literature.

The significance and management of the inevitable controversies surrounding VDTs will be considered in detail later on in this book, in the chapters dedicated to causation and expert evidence. However, a basic understanding of what is meant by doubling times and how they work is invaluable.

James J Stark, Professor of Medicine at the East Virginia Medical School, and author of the website, describes doubling times in basic terms. Essentially, solid tumours (and so not blood borne tumours) have, as do most other solid items, three dimensions. If one knows or can work out the length, width and height of the primary tumour, one can then work out the average volume. The most accurate VDTs are therefore determined by considering the volume at two or more different moments in time. Therein lies the primary difficulty described above, where the volume is known or ascertainable at only one point in time.

The doubling time is then essentially the time taken for the tumour to double in volume (not in length, width or height). The calculations themselves are complex and beyond the scope of this book and its author’s expertise, although there are online calculators available for use. It should also be borne in mind that metastases are generally faster growing than the primary tumour (Spratt et al J. Surg Oncol 61:68-83, 1996 by way of example).

The second difficulty with doubling times is the model upon which they are based. Some presuppose constant and predictable growth – such that if you have one cancer cell, it will double at every cell division, growing to two cells, then four, eight, sixteen and so on. However, research has shown that tumour growth is not constant or predictable over its life, but rather the growth rate slows with time. As such, the Gompertzian model of tumour growth developed by Laird AK in “Dynamics of tumour growth” Br J Cancer 1963; 18:490-502 assumes an exponentially decreasing growth rate over time and has become favoured in the assessment of cancer doubling times.

However, even the Gompertzian model has come under fire and there are other models out there to take account of the increasingly, but still incompletely understood means by which different tumours grow. The article by Philip Gerlee entitled “The Model Muddle: In Search of Tumour Growth Laws” published in April 2013 on gives an interesting insight into the variety of and differences in modelling that exist and are probably unheard of in most legal claims relating to cancer diagnoses.


What have we established then?

  • There is a rise in delayed cancer diagnosis litigation, due in part to a greater awareness of symptomatology and media coverage of the UK’s poor performance alongside other countries when it comes to cancer survival rates.

  • There is considerable variation in cancer survival rates depending upon region and socio-economic analysis.

  • There are ongoing changes being made by the government in an attempt to improve the UK’s survival rates and access to treatment. In particular, GP league tables started in 2013 and a voluntary audit commencing in September 2016 allow a review of how GP surgeries perform against national benchmarks, specifically in relation to the timing of referrals and diagnosis.

  • Cancer is not one disease but a series of related diseases, each with its own unique fingerprint, and varying according to the patient’s physiology and environmental factors.

  • Cancer has the ability to invade surrounding structures and to spread through the blood and lymphatic systems.

  • Whether cancer has spread is often only able to be determined by clinical assessment.

  • Tumours and their spread / metastatic deposits take time to grow. There may be a period when either are not visible or detectable by any form of scanning.

  • The treatment pathway and survival prospects are largely determined by the grade and stage of the cancer.

  • The grade of the cancer does not change over time and may assist with assessing how likely the cancer is to spread, return or have a good or poor prognosis.

  • There are various staging systems, of which the most used is the TNM system. There may be a difference between clinical and pathological staging.

  • Where there is no previous x-ray or scan which shows the tumour and which is often absent in a delayed diagnosis claim, the likely stage of the tumour at any earlier date will probably be based in part upon a review of doubling times.

  • The use of average doubling times is controversial (and will be considered further in relation to causation), and there is also controversy about the model for assessing VDTs.

  • Most VDT models assume a degree of exponential growth or reduced growth over the life of the tumour. It is not however thought that tumours grow in a stepwise fashion.