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Ovid: Oxford Handbook of Medical Sciences

Editors: Wilkins, Robert; Cross, Simon; Megson, Ian; Meredith, David Title: Oxford Handbook of Medical Sciences, 1st Edition Copyright ©2006 Oxford University Press, 2006, except ‘Clinical aspects’ section of Chapter 2 (Copyright by Keith Frayn) > Table of Contents > Chapter 13 – Growth of tissues and organs Chapter 13 Growth of tissues and organs General Principles Atrophy Definition Decrease in the size of an organ or tissue as a result of decrease in size of the constituent cells and/or their number. Physiological atrophy

  • Remnant structures during development (e.g. thyroglossal duct)
  • Organs after a physiological stimulus to hyperplasia/hypertrophy has been removed (e.g. uterus after birth, skeletal muscles after retirement from weight training).

Pathological atrophy

  • Ischaemia (e.g. myocardium in chronic ischaemic heart disease)—the cells appear to decrease in size to reduce their metabolic needs in the face of ischaemia, to maintain survival, even if this is at the expense of some loss of function. Therapeutically, this can be important, since if the blood supply can be increased (e.g. by coronary artery bypass grafting), then the cells can increase in size again with a concomitant increase in function. (In the heart this is sometimes known as ‘hibernating’ myocardium)
  • Immobility—skeletal muscle rapidly atrophies if immobilized (p.347)
  • Denervation—denervated tissues undergo general atrophy which is most marked in muscle
  • General inadequate nutrition—if the body is starved of calories and protein, then protein is taken from skeletal muscle with consequent atrophy. This is starkly illustrated by pictures of malnourished people in famine conditions, but it should be remembered that this can occur in the immediate post-operative period in patients who do not have an adequate food intake but do have increasing nutrient needs
  • Removal of endocrine stimulus—tissues that respond to hormones, and endocrine glands themselves, undergo rapid atrophy if the trophic hormone specific to them is removed. This is a very important clinical consideration in patients receiving long-term systemic corticosteroid therapy. Such patients will have atrophic adrenal glands because the exogenous steroids will stop secretion of adrenocorticotrophic hormone (ACTH). Thus, if the body has a sudden need for additional corticosteroids (e.g. during the stress of a major operation), the atrophic adrenal glands are unable to respond. In these conditions, the medical staff have to play the role of the pituitary and prescribe increased doses of corticosteroids to cover the episode
  • Ageing—atrophy certainly occurs in many tissues with ageing, but it is not clear whether this is due to factors associated with ageing, such as decreased mobility, or an intrinsic ageing process.

Atrophy and apoptosis The pathological causes of atrophy can also stimulate apoptosis of cells if the stimulus is prolonged (p.71). This has the important implication that the tissue cannot return to its state prior to the stimulus, even if this is completely reversed. P.851
Hypertrophy Definition The increase in size of an organ or tissue due to an increase in the size of cells in that tissue. Requirements

  • Organ or tissue where cells cannot divide
  • Stimulus to cell division—usually increase in ‘work’ e.g.
    • Skeletal muscle: biceps in weightlifters, quadriceps in sprinters
    • Cardiac muscle: marathon runners, patients with aortic valve stenosis.

Complications of hypertrophy

  • Obstruction of adjacent tissue
  • Infarction of tissue if it outgrows its blood supply.

Pathological hypertrophy In some instances, hypertrophy occurs when no appropriate stimulus is present. This results in an organ which is oversized for the amount of ‘work’ it is required to do. The most illustrative example of this is hypertrophic obstructive cardiomyopathy (OHCM6 p.156) where the heart muscle, especially in the septum, hypertrophies to a massive extent despite no extra work being demanded of the heart. This leads to two potentially fatal complications (arrhythmia main cause of SCD):

  • Myocardial ischaemia and infarction—as the mass of muscle outgrows its blood supply.
  • Obstruction to blood flow out of the left ventricle—with reduced blood pressure and syncopal acts (which may be relieved by the apparently paradoxical treatment with beta-adrenergic receptor blocking drugs to reduce the strength of the cardiac contractions).

Hyperplasia Definition The increase in size of an organ or tissue due to an increase in the number of cells in that tissue. Requirements

  • Organ or tissue where cells can divide
  • Stimulus to cell division—usually increase in ‘work’ e.g.
    • Thyroid: thyroid-stimulating antibody in Grave’s disease (OHCM6 p.304)
    • Lymph node: reaction to viral infection e.g. infectious mononucleosis (OHCM6 p.570)
    • Prostate: unknown—?lifelong hormonal stimulus (benign prostatic hyperplasia) (OHCM6 p.496)
    • Skin (callous): repeated removal of upper layers of epidermis by abrasion/wear.

Complications of hyperplasia

  • Obstruction of adjacent tissue (e.g. urethra in prostate, trachea behind thyroid)
  • Infarction of tissue if it outgrows its blood supply.

Neoplasia Nomenclature of neoplasms General The naming of tumours is frustratingly inconsistent and, in the end, the only way to be sure about the names and significance of tumour names is to memorize them. As a start, the word ‘tumour’ simply means a swelling (which could include swelling after trauma such as burns or contusions), so ‘tumour’ is not the best word to use as a generic term for growths such as cancers. A better term for these is neoplasms (literally new growth). You also need to bear in mind the nomenclature that the general public use—usually ‘cancer’ to mean any malignant growth. If you use the word ‘cancer’ or ‘carcinoma’, then the average patient tends to assume that this will be the most virulent form and will kill them in a few months—at least until you have explained the detail. It is better to start with some less emotive term so that you can explain all the details about treatment and prognosis without the patient being in a blind panic about imminent mortality, especially when the tumour is a relatively innocuous one such as cutaneous basal cell carcinoma. General naming conventions (Table 13.1) There are some ‘rules’ which make some of the names of neoplasms easier to decipher:

  • All tumours tend to be denoted by the suffix-oma (e.g. carcinoma, lipoma). However, some reactive, non-neoplastic conditions also have this suffix (e.g. granuloma)
  • Benign tumours of mesenchymal (connective tissue) origin tend to end in-oma (e.g. lipoma = a benign tumour of fat, rhabdomyoma = a benign tumour of striated muscle)
  • Malignant tumours of mesenchymal origin tend to end in—sarcoma (e.g. sarcoma = generically a malignant tumour of mesenchymal origin, liposarcoma = a malignant tumour of fat, rhabdomyosarcoma = a malignant tumour of striated muscle)
  • All malignant tumours of epithelial origin are denoted carcinoma. These are further subdivided into the specific pattern of differentiation, which usually represents the epithelial cell type where the tumour arose (e.g. adenocarcinoma in the glandular-lined part of the gastrointestinal tract (stomach and more distally), squamous cell carcinoma on the skin and in the oesophagus, transitional cell carcinoma in the urinary tract)
  • Benign tumours of epithelial origin may have names specific to their site but, generically, have names again related to the epithelial cell type at that site (e.g. adenoma = benign epithelial tumour in a glandular lined organ (such as the colorectum), papilloma = polypoid benign epithelial tumour of either squamous or transitional cell origin).

Eponymous terms for neoplasms abound and are very frustrating (e.g. renal cell carcinoma (which is a sensible descriptive name) is also known as Gravitz’s tumour which gives no information about the origin or behaviour of the tumour). To complicate matters, this particular tumour may also be known as hypernephroma because, histologically, its appearance is similar to the adrenal gland (which lies above the kidney).

Table 13.1 Tumour naming conventions
Tissue Benign tumour Malignant tumour
Glandular epithelium Adenoma Adenocarcinoma
Squamous epithelium Squamous papilloma Squamous cell carcinoma
Transitional epithelium Transitional papilloma Transitional cell carcinoma
Melanocytes Naevus/lentigo Malignant melanoma
Striated muscle Rhabdomyoma Rhabdomyosarcoma
Smooth muscle Leiomyoma Leiomyosarcoma
Fat Lipoma Liposarcoma
Nerve sheath Neurofibroma Neurofibrosarcoma
Lymphocytes — Lymphoma*
Glial cells — Glioma*
*These two tumours are examples of the inconsistencies of neoplasm nomenclature, where the name seems to indicate a benign tumour but where the tumour is actually malignant. Melanoma would be another example, but it is usually prefaced by ‘malignant’ in most medical literature.

The morphology of neoplasia The pathway of progression from a normal tissue through to an invasive and metastasizing tumour is extremely complex and will be delineated by many changes, most of which will only be detectable at molecular level. However, there are a reasonably well-defined set of changes that can be seen morphologically, looking at sections under the light microscope, which help our understanding of the pathways of carcinogenesis. These morphological changes are most easily seen in epithelial surfaces, in small tissue biopsies or in individual cells that have been scraped from or fallen from (exfoliated) a surface. Metaplasia The change in a cell type from one full-differentiated pattern to another fully-differentiated pattern (e.g. bronchial epithelium from ciliated columnar to squamous epithelium in cigarette smokers) (p.72). This is not necessarily a premalignant change but often represents a response to a deleterious environmental factor, such as cigarette smoke, which may itself be carcinogenic. Dysplasia (Fig. 13.1) A term applied to epithelial surfaces when there is disorder of maturation of the cells. This is most clearly seen in an epithelial surface such as the squamous epithelium which covers the uterine cervix. The changes include:

  • Division of cells above the normally proliferating basal cell layer, as evidenced by higher mitotic figures in higher levels of the epithelium
  • Loss of polarity of the nuclei of the epithelial cells
  • Lack of differentiation of the epithelial cells (e.g. squamous cells failing to produce keratin).

Carcinoma in situ (Fig. 13.2) A term reserved for a severe degree of dysplasia in an epithelial surface where there is no discernible differentiation in cells between the base and top of the epithelium, but also no evidence of stromal invasion. As soon as cells breach the basement membrane at the base of the epithelium, then this term no longer applies and the lesion is an invasive carcinoma. Microinvasive carcinoma A pragmatic term which is used to describe tumours which have invaded through the basement membrane but only into the surrounding stroma to a small degree. This does not represent a distinct biological category but is used in selection of therapy for patients in relation to certain organ systems (e.g. microinvasive carcinoma of the uterine cervix can be treated by local resection rather than a formal hysterectomy and lymph node clearance). Invasive carcinoma Any tumour which has substantially invaded through the basement membrane of the epithelium. The important implication is that it can gain access to lymphovascular channels and metastasize to distant sites.

Fig. 13.1 Dysplasia. Fully-differentiated squamous epithelium on the left; dysplastic epithelium on the right, showing loss of nuclear polarity and no differentiation towards flattened keratinocytes at the top of the epithelium.
Fig. 13.2 Carcinoma in situ on the left, showing no difference in differentiation between the bottom and top of the epithelium. On the right, cells have invaded through the basement membrane so this is now invasive, rather than in situ, carcinoma.

Metastasis Definition Metastasis of a tumour is the spread of that tumour to a distant site in the body and its subsequent growth at that site. This is distinguished from extension into adjacent parts of the body by direct spread. To metastasize, tumour cells must travel to the distant site in either blood vessels or lymphatics, or by moving across a body cavity such as the pleura, peritoneum, or meninges. Most people who develop cancer, and subsequently die of it, do not die from the effects of the primary tumour (e.g. the breast cancer) because that has been completely removed by surgery when it was first diagnosed. They die of the effects of metastases in other parts of their bodies (e.g. replacement of the liver by metastatic tumour and death from liver failure). It is very important to know the mechanisms of metastasis because the most effective cancer therapies will be those that are directed against these. Processes in metastasis (Fig. 13.3)

  • Detachment from adjacent epithelial cells—epithelial cells are normally attached tightly to adjacent epithelial cells by cell adhesion molecules. Cancer cells lose these attachments and can detach from adjacent cells
  • Invasion through the basement membrane—until cancer cells have invaded through the basement membrane, a cancer is said to be in situ, with the implication that it does not have access to veins or lymphatics and so cannot metastasize. The basement membrane is a relatively impassable barrier made predominantly of collagen, so tumour cells must produce suitable enzymes (e.g. collagenases) to digest this. They also need some motility to pass through the damaged membrane
  • Invasion through connective tissue—once through the basement membrane, the cancer cells must move through connective tissue, again digesting structural fibres that hinder their progress using appropriate enzymes such as collagenases
  • Invasion into blood vessels/lymphatics—this again requires cell motility and enzymes to digest structural components in the vessel wall, though lymphatics have a very thin wall that is easily penetrated
  • Survival in the blood vessel or lymphatic—once in the vessel, cancer cells are exposed to the host immune system including lymphocytes, which may recognize them as ‘foreign’ and destroy them using mechanisms such as natural killer cells. To evade such defences, tumour cells may aggregate tightly together so that the central tumour cells are protected, or shed proteins that are recognized as ‘foreign’ from their surface so that immune cells bind to these rather than the cell surface of the tumour cells
  • Extravasation from the blood vessel or lymphatic—using the same mechanisms as intravasation
  • Growth at the distant site—most cells in the body require some growth factors to induce growth and then prevent apoptosis. Such growth factors are often derived from surrounding stromal cells, but cancer cells often develop the ability to produce their own growth P.857
    factors (autocrine production). A group of tumour cells can grow to a diameter of 1mm, but to increase in size beyond that, new blood vessels need to grow into the tumour because the central cells can no longer be supplied simply by diffusion from the outside of the tumour. To do this, cancer cells produce angiogenic factors which induce the growth of capillaries from the surrounding stromal tissue into the tumour.

With all these processes required for a cancer cell to successfully metastasize, it can be imagined that few cancer cells achieve this. However, a primary tumour may contain millions of cells, so the probability that a few will successfully metastasize is quite high. Therapeutic targets in the metastatic process Any of the steps described above can be targeted to try to block the metastatic process. At its earliest stage, it could be possible to cause cancer cells to produce the cell adhesion molecules that they have stopped producing and thus prevent detachment of some tumour cells. If the actions of tumour cell enzymes, such as collagenase, could be blocked at a local level, then this might prevent invasion through the basement membrane and connective tissue. At the moment, the most promising targets lie at the other end of the metastatic process where drugs that block the development of blood vessels have shown much promise in experimental models.

Fig. 13.3 The processes involved in metastasis. The numbers refer to the stages described in the text.

Molecular mechanisms of neoplasia There is no simple molecular mechanism for the development and progression of neoplasia—it not a simple mutation of one gene that produces cells which grow too fast and metastasize. Instead, cancer arises through multiple gene mutations and/or silencing mechanisms (such as hypermethylation) in a population of cells and may be modified by the surrounding environment of those cells. The genes which are mutated will vary between different types of cancer, but will also show considerable variation between individual tumours of the same type. There are some general principles that apply to this process:

  • Most mutations are not in the germ line but are acquired during an individual’s life—hence the steady increase in cancer incidence with increasing age
  • Although there may be a similarity in the pattern of gene mutations in the same type of cancer (e.g. mutation of the h-ras gene is common in colorectal cancer), each individual tumour has a unique pattern of genetic abnormalities
  • In the later stages of tumour progression (which may be the time when the tumour presents clinically), there is widespread abnormality of the genome which may include substantial aneuploidy due to breakdown of chromosomal structure. Thus, there will be many genomic abnormalities in samples from these tumours and this may not be representative of the important early pathogenetic genomic changes.

The molecular mechanisms of neoplasia will become much clearer over the next five years, and the overall picture will become more integrated and cohesive. Until this knowledge is available, the description of these mechanisms is necessarily less comprehensive. Proto-oncogenes Genes in which overactivity (e.g. by a gain of function mutation) leads to the development of cancer are called proto-oncogenes. This name gives the impression that they are sitting in the genome waiting to mutate and cause cancer rather than fulfil a useful function in a cell. This is unfortunate, since they are genes which, generally, have a critical role in the normal control of cell growth and differentiation. Ras genes as examples of proto-oncogenes

  • Ras genes are mutated in about 1 in 4 human cancers
  • Ras genes code for GTPase proteins which transmit signals from cell surface growth factor receptors
  • Mutation in Ras genes can produce a protein which is always active, even when there is no signal from growth factor receptors, which induces uncontrolled cell proliferation
  • Only one copy of a Ras gene needs to be mutated to have this effect. Thus, the mutation has a dominant effect.

Tumour suppressor genes Genes in which underactivity (e.g. by a deletion mutation) leads to the development of cancer are called tumour suppressor genes. Again, analogous with proto-oncogenes, this name tends to imply that the main role of these genes in cell function is to actively suppress tumours. However, they have important functions in normal cell biology. The retinoblastoma gene as an example of a tumour suppressor gene

  • Retinoblastoma is a rare tumour of the eye which can be inherited or sporadic; the gene was discovered from studies of inherited cases
  • The retinoblastoma gene codes for a protein which is involved in the control of the cell cycle
  • Mutation in both copies of the gene to produce non-functional or absent proteins will lead to lack of regulation of the cell cycle and uncontrolled proliferation
  • Individuals who inherit a mutant retinoblastoma gene only need to mutate the single normal copy of the gene to produce a tumour-producing phenotype
  • The retinoblastoma gene is said to have a recessive pattern of action with respect to tumour formation because both copies of the gene have to be mutated before there is an effect.

The ‘mutator’ phenotype Since the body is continually exposed to environmental carcinogens, and DNA replication during mitosis and meiosis produces many errors, it is actually surprising that cancer is not much more common and that individuals rarely develop more than one or two tumours in a lifetime. That this is so is testament to the efficiency of the cellular mechanisms which repair damage to DNA or prevent cells with DNA damage from replicating. If a cell acquires deficiencies in these protective mechanisms, then it will gain more and more damage to its DNA, which may cause loss of even more protective mechanisms. Cells which have an early loss of DNA damage detection and repair mechanisms are said to have a mutator (or replication error) phenotype because of their predisposition to acquire mutations. HNPCC as an example of a mutator phenotype

  • HNPCC = hereditary non-polyposis colorectal cancer
  • Due to a deficiency of one of a group of DNA mismatch repair proteins (e.g. MSH1, MLH1)
  • Individuals with HNPCC are born with one defective allele and the other allele is silenced by either mutation or hypermethylation
  • Colorectal cancers in HNPCC occur at an earlier age, have a mucinous pattern of differentiation, and occur more commonly in the right side of the colon than sporadic colorectal cancer
  • Tumours also occur at other sites including endometrium, ureter.

Commonly mutated genes in human cancers p53

  • Over 50% of human cancers have mutated p53 genes
  • Both copies of the gene contain deletion mutations in most breast, lung, and colon cancers
  • Most mutations are acquired during life
  • Individuals with a mutated p53 gene in their germ line have a 25x risk of developing cancer (Li-Fraumeni syndrome)
  • p53 protein is a nuclear protein which controls the transcription of other genes which mediate apoptosis and arrest of the cell cycle
  • p53↑ with DNA damage, thus preventing cells from replicating damaged DNA
  • If DNA damage is repaired, then cell allowed to continue in cell cycle
  • If DNA damage not repaired, then cell induced to apoptose
  • ∴ = tumour suppressor gene
  • Non-functional p53 proteins leads to progressive accumulation of DNA damage in successive generations of cells.


  • APC = adenomatous polyposis coli gene
  • 80% sporadic colorectal cancers show loss of both APC genes
  • Individuals born with one deleted APC gene develop hundreds of adenomas in the colorectum by the age of 20 years, and inevitably develop colorectal cancer
  • APC protein is located in the cytoplasm where, amongst other functions, it marks β-catenin for degradation ubiquitination
  • Deleted APC → ↑cytoplasmic β-catenin → ↑nuclear β-catenin → ↑transcription of genes which cause cellular proliferation
  • ∴ = tumour suppressor gene.

Chemotherapy and Radiobiology Cancer chemotherapy Definition The treatment of malignant disease with antiproliferative agents (aka cytotoxic chemotherapy). Until recently, there were no ‘magic bullets’ for cancer therapy. Most of these drugs cause non-specific DNA damage, either leading to cell death by apoptosis or preventing cell division. The majority of cellular biochemical processes are identical in normal and malignant cells, but malignant cells are characterized by uncontrolled proliferation, and may fail to recognize and repair DNA damage. In contrast, normal tissues exposed to chemotherapy demonstrate temporary loss of proliferating cells, with a variety of side-effects, but then recover through damage repair or replacement of cells from normal precursor or stem cells. Classes of chemotherapy agents by mechanism of action

  • DNA binding: direct alteration of DNA by alkylating agents (e.g. nitrogen mustard, cyclophosphamide) or platinum complexes (cisplatin, carboplatin)
  • Antimetabolites: block synthesis of purines and pyrimidines, essential for DNA synthesis (e.g. 5-fluorouracil, methotrexate)
  • Antimicrotubule: interferes with mitosis (e.g. vinca alkaloids, taxanes)
  • Topoisomerase: inhibition leads to DNA damage (anthracyclines e.g. doxorubicin; topo-I e.g. irinotecan; topo-II e.g. etoposide).

Chemotherapy side-effects Many such drugs affect organs which are dependent on cell renewal to maintain normal tissue integrity:

  • Bone marrow: neutropenia, infection, thrombocytopenia, anaemia
  • GI tract: nausea, vomiting, diarrhoea, mouth ulcers
  • Skin: hair loss
  • Gonads: infertility.

Others have more specific normal tissue effects:

  • Antimicrotubule: peripheral nerve damage
  • Anthracyclines: cardiomyopathy.

Chemotherapy dose and scheduling Generally, increasing doses result in increasing cell kill, both tumour and normal tissue. Chemotherapy is commonly delivered at the highest safe dose once every 3—4 weeks, in order to allow normal tissue recovery, in particular bone marrow. However, some drugs (e.g. 5-fluorouracil) are administered continuously, at low dose, with relatively reduced side-effects but increased tumour cell kill. Combination chemotherapy Successful eradication of some childhood leukaemias and adult lymphomas was achieved in the 1960s by combining three or more chemotherapy drugs. The principles behind combining these drugs are to use agents which are known to be active against the cancer, have different mechanisms of action, and different toxicity profiles, allowing safe delivery of P.863
each drug at full dose. However, even with such combined regimens, the majority of common cancers are not curable with chemotherapy alone. Role of chemotherapy in different cancers

  • Cure of advanced disease (e.g. lymphoma, leukaemia, testicular cancer)
  • Cure of microscopic residual disease after surgery (e.g. breast and colorectal cancer)
  • Palliative (non-curative) treatment of advanced disease (e.g. lung cancer).

Molecular targeted chemotherapy Recent advances in understanding of the molecular changes in cancer cells have led to the development of tumour-specific treatments (e.g. imatinib for chronic myeloid leukaemia). This drug was designed to target the mutated protein (BCR-Abl tyrosine kinase) which drives leukaemic cell growth. Such treatments are highly effective in controlling malignant disease but also have little impact on normal tissues which lack the mutated protein. P.864
Radiobiology Definition Study of the effects of ionizing radiation on normal and malignant cells. This is particularly important in the treatment of cancer with high-energy X-rays (radiotherapy). When an X-ray beam passes through living tissue, energy is absorbed, resulting in free radical generation and a variety of cellular effects, mainly due to DNA damage. This damage may be repaired, but if not repaired, may result in cell death or subsequent failure of cell division or cell survival with altered (mutated) DNA. Normal tissues The severity of damage to normal organs depends on the dose of radiation, measured in Gray (1Gy =1J/kg), and the volume of tissue treated. For each organ, a tolerance dose can be defined, below which full recovery will follow irradiation. Many tissues require continual cell renewal to maintain their integrity, and radiation exposure of these early responding tissues produces biological effects within 1–4 weeks. For example:

  • GI tract: mucosal ulceration (e.g. sore mouth, diarrhoea)
  • Skin: erythema and desquamation (similar to sunburn)
  • Bone marrow: myelosuppression (↓white cell count, platelets, then RBC)
  • Gonads: fall in sperm count, ovarian failure.

These acute effects recover within 2–6 weeks through normal cell proliferation—except loss of fertility, which may be irreversible even after low-dose radiotherapy. Other tissues exhibit late responses, expressing damage months or even years after radiation, and for these, damage may be irreversible e.g. lung fibrosis, spinal cord damage (myelitis). Fractionation The biological effects of a given dose of radiotherapy are markedly altered when the dose is administered in divided doses (fractions), with relatively greater sparing of normal tissue damage compared with cancer cells. Most curative radiotherapy uses multiple, daily, small fractions (around 2Gy/fraction) to a total dose of 60–70Gy. Small fraction size is particularly important in minimizing late radiotherapy damage to normal tissue. The overall treatment time for a course of radiotherapy may be adjusted by changing the dose per fraction and the number of fractions per day. For a given total dose of radiotherapy, shortening the treatment time increases the early effects on normal tissues but increases tumour cell kill. A short treatment time may be particularly important for fast-growing cancers. Oxygen effect Hypoxia causes relative resistance to radiation, and the abnormal vasculature supplying cancers can produce hypoxic areas within the cancer—a potential cause of failure to eradicate the cancer with radiotherapy. P.865
Radiosensitivity of cancers Malignant cells vary in their response to radiotherapy: Box 13.1 Radiosensitivity of cancers

Sensitive Intermediate Resistant
Hodgkin’s Breast Melanoma
Seminoma Lung Glioma

Carcinogenesis Normal somatic cells which survive radiation but sustain unrepaired DNA damage may, by chance, have DNA mutations which will eventually result in a malignant phenotype, producing a radiation-induced cancer. This process may take many years. Clinical use of radiotherapy

  • Curative treatment of macroscopic cancer (e.g. carcinoma larynx, cervix, prostate)
  • Curative treatment of microscopic cancer after surgery (e.g. carcinoma breast)
  • Palliative treatment of advanced cancer (e.g. carcinoma bronchus).

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