We are made of cells – a lot of them. They cooperate to make tissues, and those tissue make up organs. The cells take on different characteristics (it’s called DIFFERENTIATION), according to what they’re required to do (eg they may become nerve cells, or gut lining cells, or bones, or skeletal muscles etc). Generally, they behave. Indeed, there is a theory that normal cells die unless they are constantly told not to.

All cells (except red blood cells) have a nucleus and in that nucleus is a complete copy of the individual’s GENOME – that is, about 30,000 genes – which can be found in the DNA (DEOXYRIBONUCLEIC ACID). Not all of them are turned on, however. The genes that are turned on determine what the cell does and what it looks like (ie how it differentiates); in other word, different genes are active in nerve cells to those active in muscle cells.

By ‘behave’ I mean they die when they are told to (programmed cell death or APOPTOSIS), or they divide when they are told to, or they do their everyday job. When a cell divides, it has to replicate its DNA.

Cancer cells have changes in their DNA so that they ignore the messages that all other cells obey. They divide when they’re not supposed to, and don’t die when they should. This behaviour leads to a lump. The cells that don’t do as their told gradually pick up more genetic abnormalites because when a cell divides it is at its most vulnerable to mistakes in DNA replication. Thus cancers get worse and worse as they age. Malignant lumps infiltrate the surrounding tissues., perhaps getting around nerves or into thin-walled vessels

Bits of the tumour may break off (METASTASISE) and grow elsewhere; cancers of the surface cells usually go to lymph nodes, but they make also go to the liver, to the lungs, to the bones or to the brain. In fact they may go anywhere. Cancers of the cells that make up muscles, fat, fibrous tissue etc tend not to head for lymph nodes; I don’t know why.

There are many different kinds of cancer because there are many different kinds of cell. In face, at a genetic level, each cancer is unique, hence in future, genetic analysis of the tumour may lead to optimisation of treatment. That’s the hope, anyway.


There are 3 common types of cancer, although there are many types of rare skin cancer. The 3 common types – BASAL CELL CARCINOMA (BCC), SQUAMOUS CELL CARCINOMA (SCC) and MALIGNANT MELANOMA (MM) – are all very different in behaviour and who they usually affect.

BCC and SCC usually affect older people. They are often associated with sun exposure, although BCCs may occur in areas of the skin where there is prolonged immune suppression, such as the lower legs when there is long-term venous eczema.

BCCs spread locally but very, very rarely do they spread beyond the point where they arise (they don’t METASTASISE as the medical jargon has it). That doesn’t mean they’re not dangerous, because they are inexorable. They grow and grow to incredible size if not treated, SO GET THEM SEEN EARLY. They may invade bone, and blood vessels, and eat away at the body. There are some shocking examples of what they can do in medical museums. There are different types of BCC – low risk types (superficial and nodular) and high risk types (because their edges are difficult to identify clinically – morphoeic and micronodular). Superficial BCCs can be treated by cream, other types by surgery or radiotherapy, both of which have both advantage and disadvantages.

SCCs can spread from the original site (but also invade locally as BCCs do) and so are more dangerous. They usually spread to local LYMPH GLANDS or NODES; in the case of the leg, those are in the groin, arm (armpit, aka AXILLA), head (neck). It is more common for people to die from SCC although it is still rare in the UK.

MM can affect the young as well as the old, and are much more worrying. They can be very difficult for pathologists to identify (the pathologists often say that MM can look like anything. They don’t have to be very advanced to spread; far-flung deposits can show up years after the original lesion has been treated and all-but-forgotten. They made spread to the liver, lungs or anywhere (another old saw of doctors is to ‘beware the patient with the false eye and the big liver) because an MM of the eye (yes, it can occur in the eye) treated by its removal may result in liver deposits years later.

Cervical Cancer

In the UK, there are just over 3,000 cases of cervical cancer diagnosed each year, of which it is estimated that over 99% (that’s not a typo) are preventable, although over 800 people die from it each and every year. The highest incidence is in those aged between 25 and 29 (and that ain’t a typo either) so, in other words, it is a disease of the young. It is associated with smoking and other factors, but it is caused by the Human Papillomavirus (HPV).

Men carry the virus and pass it on to their sexual partners.

HPV is everywhere. There are over a hundred different types and they’re numbered. They cause things as benign as skin warts but they also cause cancers, such as penile cancers (yes, there is such a thing), anal cancer (nasty) and cervical cancer. Some types are troublesome, but benign. Some types, though, cause the cancers. Types 16 and 18 cause cervical cancer.

Cervical screening aims to spot the changes that lead up to cancer, because HPV works slowly, over a course of years, but it isn’t easy. This much is known. The changes that lead to cervical cancer begin in the TRANSFORMATION ZONE (TZ) of the cervix. where the nature of the covering of the cervix abruptly changes from SQUAMOUS (multilayered) to GLANDULAR (single cell layer). They are known as CERVICAL INTRAEPITHELIAL NEOPLASIA, which for the sake of simplicity is known as CIN (pronounced ‘sin’ and I know not if that is a deliberate choice of pronunciation). CIN1 is mild, CIN2 and CIN3 are high grade. Progression to cancer (which is invasive and potentially spreads) is not inevitable, but you don’t want high grade CIN.

The cervical screening test is embarrassing and uncomfortable. The person taking the sample tries to scrape off cells from the TZ. They are then put into a machine that washes the cells and spreads them on a slide. A human being then has to scan that slide and look for cells that mean CIN is present. If they see them, a punch biopsy may be taken to confirm the diagnosis of precancerous changes; the punch biopsy will be looked at by a medically-qualified pathologist.

If high grade CIN is diagnosed, the usual treatment is LOOP EXCISION OF THE TZ (LETZ), which aims to cut out the abnormal area and can be done in out-patients; it is again uncomfortable and embarrassing. In the great majority, that will cure the patient and they won’t develop cancer.

HPV vaccination has been introduced, the aim being to stop HPV 16 and 18 causing the cancer. HPV testing is also undertaken on samples. Soon, everything will change, and it will be for the better. Fewer cases, fewer cervical smears, fewer deaths. But only if that letter calling patients to be tested is not ignored.

Cervical cancer is a horrible way to die.