Rory's Extras from Tuesday =)

Sami-Jaine
Mind Map by , created over 6 years ago

BSc (Hons) Biology Mind Map on Rory's Extras from Tuesday =), created by Sami-Jaine on 05/07/2013.

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Sami-Jaine
Created by Sami-Jaine over 6 years ago
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Rory's Extras from Tuesday =)
1 Growth Regulation in normal cells v neoplastic cells
1.1 Growth factor dependency
1.1.1 many growth factors bind to receptors which initiates a series of biochemical changes within the cell which ultimately leads to cell dividion. Tumour cells are not as dependent on growth factors as normal cells
1.2 Density dependent inhibition of growth
1.2.1 Once dividing cells reach a finite density they stop proliferation. In contrast neoplastic cells so not cease proliferation
1.3 Anchorage dependence
1.3.1 most normal cells need contact with a substratum in the extracellular environment to reproduce. neoplastic cells are able to grow without attachment
1.4 Contact inhibition of movement
1.4.1 Normal cells when they come into contact with each other, one or both will change direction ensuring that the cells so not overlay each other. Neoplastic cells lack contact inhibition and often grow over or under each other
1.5 Adhesiveness
1.5.1 Tumour cells are often less sticky than normal cells and are less firmly attached to neighbouring cells or to the extracellular matrix
2 Genetic Basis of Malignancy
2.1 Oncogenes code for proteins which when present in abnormal form or amounts induce malignant growth by speeding up or switching on cell division
2.1.1 Tumour- suppressor genes have the opposite effect to oncogenes
2.2 One of the most common defects in human cancers involve the gene p53
3 Oncogenes and Cancer
3.1 Oncogenes cause notmal cells to grow out of control and become cancer cells. They are mutated forms of normal genes called proto-oncogenes
3.1.1 Protooncogenes normally control how often a cell divides and the degree to which it differentiates
3.1.1.1 When a proto-oncogenes mutates into an oncogene, it becomes permanently turned on when it ought not be
3.1.1.1.1 When this occurs, the cell divides too quickly, which can lead to cancer
3.1.1.1.1.1 Only one of the two allels of a protooncogene needs to be overactive in order to have an oncogenic effect
4 Initiation and Promotion

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5 Infections and Cancer
5.1 6. The virus itself or individual virus genes can often "transform" the growth of normal cells in cell culture
5.1.1 5. Every cancer of this type carriers the virus' genetic information (the viral genome) in every malignant cell
5.1.1.1 4. All patients with the type of cancer in question have previously been infected with the virus
5.1.1.1.1 3. Virus infection is just one link in a complex chain of events required for cancer development
5.1.1.1.1.1 2.. Cancer develops only in a small proportion of the individuals infected, usually many years after their initial virus infection
5.1.1.1.1.1.1 1. The viruses involved all establish persistent infections are often widespread in the normal human population
6 Histopathology Definitions
6.1 Quantitative changes: Too Small
6.1.1 Atrophy: Acquired shrinkage due to a decrease in the size or number of cells of a tissue, e.g. decrease in size of the ovaries after the menopause
6.2 Quantitative changes: Too Big
6.2.1 Hypertrophy: Increase in the size of an organ or tissue die to an increase in the size of individual cells, e.g. pregnant uterus
6.2.2 Hyperplasia: Increase in the size of an organ due to an increase in the number of cells, e.g. lactating breast. It can occur in the absence of stimuli, it may be controlled by apoptosis -> due to loss of regulation of the cell cycle
6.3 Qualitative Changes
6.3.1 Metaplasia: Replacement of one cell type in an organ by another. This implies changes in the differentiation programme and is usually a response to persistant injury. It is reversible so that the removal of the source of injury results in reversion to the original cell type. e.g. squamous metaplasia of laryngeal respiratory epithelium in a smoker. Chronic Irritation from smoking causes the normal columnar respiratory epithelium to be replace by the more resilient squamous epithelium
6.3.1.1 Epithelial cells lining the respiratory tract will undergo changes in appearance and function when exposed to noxious chemicals in the air
6.3.1.1.1 columnar cells are normally "joined" by goblet cells that secrete mucus that coats the epithelium, trapping dust and microbes. Cilia on the columnar cells move the mucus up to the back of the throat. However, Cig smoke also paralyses the cilia leading to mucus build up
6.3.2 Dysplasia: (revisable) changes in the cell type, size, shape and organisation, that do not revert to normal once the injury is removed. e.g. cervical dysplasia initiated by HPV infection persists alter eradication of the virus. Dysplasia is usually considered to be part of the spectrum of changes that lead to neoplasia - "precancerous"
6.3.3 Invasion: The capacity to infiltrate the surrounding tissues and organs is a character- istic of cancer
7 Tissue changes that occur in response to stimuli
7.1 our cells experience many different types of chemical and physical stimuli almost constantly
7.2 The cellular changes that occur in response to stimuli are an indication of both the susceptibility to signals and the adaptability that cells exhibit in response to theur environment
7.2.1 It is logical to expect that if a certain stimulus causes a cell to change in a particular way, then the cell should revert back to its original condition upon removal of the stimulus
7.2.1.1 A unique aspect of tumour cells is that they do not revert back to normal cells
8 Nomenclature
8.1 blood bits = lymphomas, leukemias, myelomas
8.1.1 Epithelium = carcinoma
8.1.1.1 Bone, muscle, cartilage = sarcoma
9 Hormones and Cancer
9.1 Hormones may explain differences in risk for some of the most commonly diagnosed female cancers and could be responsible for as many as 15% of cancers in the UK
9.2 Studies assessing serum levels of testosterone and other male sex hormones in men and risk of prostate cancer suggest a more than two-fold increase in risk in men with the highest testosterone
9.3 Risk of ovarian, endometrial and breast cancers increases with earlier age at menarche and later menopause, and reduces with each full-term pregnancy (the first full-term pregnancy providing more protection that successive ones)
9.4 Reproductive factors that influence breast cancer risk
9.4.1 early age at first menarche increases risk
9.4.1.1 younger first birth is reduces risk
9.4.1.1.1 increasing parity reduces risk
9.4.1.1.1.1 increased breastfeeding happens, the less the risk
9.4.1.1.1.1.1 late menopause increases risk
9.4.1.1.1.1.1.1 HRT increases risk by 66%; attributed to 3% of cancers
9.4.2 Oral contraceptives
9.4.3 Endocrine-disrupting chemicals (hormone mimics) found in pesticides may be risk to health (not just by cancers)
9.4.3.1 men may be at risk of testicular cancer if their mothers were exposed to EDCs
10 Central Tolerance
10.1 Clonal deletion (apoptotic cell death)
10.1.1 During maturation of lymphocytes in the thymus (t's) or bone marrow (b's) immature lymphocytes that recognise ubiquitous self-antigen with high affinity are deleted by negative selection
10.1.1.1 Double Negative (CD3/TcR- CD4-, 8-)
10.1.1.1.1 Large Double Positive CD3+, CD4+, 8+
10.1.1.1.1.1 Small Double Positive CD3+, CD4+, CD8+
10.1.1.1.1.1.1 98%
10.1.1.1.1.1.2 Single Positive CD3+, CD4+ (Helper)
10.1.1.1.1.1.3 Single Positive CD3+, CD8+ (Cytotoxic)
11 Peripheral Tolerence
11.1 Clonal anergy (inactivation)
11.1.1 functional inactivation without cell death: lack of co-stimulatory signal
11.1.1.1 Anergy = functional unresponsiveness -- 2 signals needed to activate t cells (1 from antigen, one from apc)...Ignorance = due to inaccessible or low concentration of self-antigen
12 Immune Surveillance Theory
12.1 Immune system continually surveys for the presence of abnormal cells
12.1.1 Cancer cells frequently arise
12.1.1.1 However, eliminated by the immune system
12.1.1.1.1 Tumours arise only if cancer cells are able to evade this immune surveillance
12.1.1.1.1.1 Evidence
12.1.1.1.1.1.1 Postmortom shows subclinical tumours
12.1.1.1.1.1.1.1 tumours contain lymphoid cell infiltrates
12.1.1.1.1.1.1.1.1 spontaneous regression of tumours can occur
12.1.1.1.1.1.1.1.1.1 tumours are more frequent when the immune system is weaker (very young/ old/ immunosuppressed)
12.1.1.1.1.1.1.1.2 surveillance is more effective against viruses not tumour cells
12.1.1.1.1.1.1.1.2.1 immunosuppression evidence seems impressive but the immune systems inability to fight the oncogenic virus seems more likely

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