Right atrial systole

Myeloid:
Megakaryoblast - Megakaryocyte - Platelets
Proerythroblast - Reticulocyte - Erythrocyte
Myeoblast - Baso/Neutro/Eosino phils
Monoblast - Monocyte

Lymphoid:
Natural Killer
Small - B & T cells

Addition, substitution, duplication, insertion, inversion, deletion

Carried out by keratinocytes in the presence of UV light. Further conversion to active hormone needed in liver and kidney

breast cancer.
lung cancer.
prostate cancer.
bowel cancer

Pons

Lymphoma affects lymphocytes. The abnormal cells develop in the lymph nodes or organs of the lymphatic system.
Leukaemia affects white blood cells, including lymphocytes in bone marrow or blood stream.
Myeloma affects a particular type of white blood cell called a plasma cell. The abnormal cells develop in the bone marrow.

P53
P16ink/CDK4
RB1
APC
MSH2, MLH1
TP53
ATM
CDKN2A
ATM
BRCA1, BRCA2/ TP53 and PTEN

E. coli, C. Diff, S. Pneumonia, S. aureus

Chemotherapy can be given:

by injection or a drip directly into a vein (intravenous chemotherapy)
by mouth as tablets or capsules (oral chemotherapy)
by injection into a muscle (intramuscular) or under the skin (subcutaneous)
by injection into the fluid around the spine and brain (intrathecal chemotherapy)
directly into a body cavity (intracavitary), for example the bladder
directly to the skin as a cream for some skin cancers.

The mucosal barrier protects the stomach from self-digestion. It includes a thick coating of bicarbonate-rich mucus; the mucus is physically protective, and bicarbonate neutralizes gastric acid. Epithelial cells meet at tight junctions, which block gastric juice from penetrating the underlying tissue layers, and stem cells quickly replace sloughed off epithelial mucosal cells.

In acute leukaemias, the bone marrow cells cannot mature the way they should.
In chronic leukaemia, the cells mature partly but not completely.

• Oncogenes: genes whose presence can trigger the development of cancer. A single mutation event creates an oncogene.
• Tumour suppressor genes: genes whose loss or inactivation can trigger the development of cancer. A mutation event causes the inactivation of the tumour suppressor gene. This doesn’t have an effect as there are 2 copies of genes. Only when there is a second mutation event affecting the other gene does the tumour suppressor gene become inactivated.

Hematogenous, Lymphatic, Transcoelomic

Its mechanism of action is to target the Bcr-ABL tyrosine kinase. This mutated kinase is formed by the Philadelphia chromosome abnormality in chronic myeloid leukaemia (CML), leading to the constitutive activation of the kinase. The effect of imatinib is to inhibit the cell proliferation driven by Bcr-Al positive cells, whilst at the same time inducing apoptosis. Imatinib also inhibits the receptor tyrosine kinases for platelet derived growth factor and stem cell factor.

The left brachiocephalic vein, the aortic arch and the proximal parts of the brachiocephalic trunk and left common carotid artery, and the fibrous pericardium.

The main difference between lymphocytic leukaemias and lymphomas is that in leukaemia, the cancer cell is mainly in the bone marrow and blood, while in lymphoma it tends to be in lymph nodes and other tissues

The Philadelphia chromosome is found in the leukaemia cells of almost all patients with CML. The swapping of DNA between the chromosomes leads to the formation of a new gene (an oncogene) called BCR-ABL. This gene then produces the BCR-ABL protein, which is the type of protein called a tyrosine kinase. This protein causes CML cells to grow and divide out of control.

The most common symptom is fever, although malaria may present initially with general malaise, headache, vomiting, or diarrhoea.

Gastrointestinal symptoms (pain, diarrhoea, nausea), fatigue, headaches and sometimes rashes.

The epiglottis is a region of the larynx that is important during the swallowing of food or drink. As a person swallows, the pharynx moves upward and the epiglottis closes over the trachea, preventing food or drink from entering the trachea. If a person’s epiglottis were injured, this mechanism would be impaired. As a result, the person may have problems with food or drink entering the trachea, and possibly, the lungs. Over time, this may cause infections such as pneumonia to set in.

CML cause splenomegaly because it is very active in removing WBC’s from the blood, leading to a shortage of RBCs and platelets. An enlarged spleen causes early satiety and decreased appetite by pressing on the stomach, hypermetabolic state of fever, chronic fatigue, weight loss, excessive sweating, and left upper quadrant (LUQ) “gripping” pain due to spleen infarction.

If there is a mutation in the p53 protein due to methylation of C at CpG (in gene promoter regions) it silences the gene. When the DNA in a cell becomes damaged by agents such as toxic chemicals, radiation, or ultraviolet (UV) rays from sunlight, this protein plays a critical role in determining whether the DNA will be repaired or the damaged cell will self-destruct (undergo apoptosis). If the DNA can be repaired, p53 activates other genes to fix the damage. If the DNA cannot be repaired, this protein prevents the cell from dividing and signals it to undergo apoptosis. By stopping cells with mutated or damaged DNA from dividing, p53 helps prevent the development of tumours.

Cannot arrest the cell cycle if there is a fault in the DNA. Leads to uncontrolled cell proliferation, leading to neoplasia.

1) Cyclin dependent kinases – always present but the majority of the time are inactive. Activated by specific cyclins
2) Cyclins – specific cyclins are made at specific times

Used to convey messages of ligands into changes of biological activity of target cells. Signalling pathways that control cell growth and division, cell death, cell fate, and cell motility. Mutations that convert cellular proto-oncogenes to oncogenes can cause hyperactivation of these signalling pathways, whereas inactivation of tumour suppressors eliminates critical negative regulators of signalling. Tyrosine kinases are transmembrane-structured enzyme protein receptors with tyrosine kinase activity in the inner segment of the cell. The extracellular domain binds to the growth factor ligand and then activates the intracellular domain of the enzyme active region.