Archive for January 2nd, 2010

Immunity To Tumours

The second article of the day, the introduction is to this four page article is below. If this is what you were looking for please view the full article for free at The full article includes treatments, specific cell responses and the immune mechanisms.


A tumour is a swelling of part of the body caused by abnormal cell growth, this occurs when the normal cell division process becomes unregulated and cells proliferate uncontrolled. This results in cloned cells of the original defective cell, leading to a neoplasm – a new growth of tissue in the body that is abnormal. A tumour at a single site is known as a benign tumour, it becomes malignant (very virulent or infections and prone to reoccurrence after removal) when the tumour cells spreads to further sites within the body and begins to proliferate at these sites. Secondary malignant growths distant from the primary growth are known as metastases.

Not all tumours are cancerous, cancerous cells are damaged cells of the patients body that do not undergo apoptosis (programmed cell death), this means that their growth is no longer controlled and metabolism of the cells are altered.

Malignant tumours are named according to the tissue of origin:

  • Carcinoma – Arising in the epithelial tissue of skin or internal organs
  • Sarcoma – Arising in connective tissue or other non-epithelial tissue (mesenchymal cells)
  • Leukaemia – Arising in haematopoietic cells or blood forming organs such as bone marrow to produce abnormal leukocytes, these also suppress the production of normal blood cells
  • Germ Cell Tumours – Arising in reproductive tissues
  • Blastoma – Arising in embryonic tissues
  • Lymphoma – Arising in the lymph nodes

An early stage malignant tumour is called a premalignant tumour; premalignant tumours and benign tumours can often be treated with surgery alone. With malignant tumours this become much more difficult and other methods must be used in conjunction.



Luteolysis is the degradation of the corpus luteum (as opposed to luteinisation – the formation of the corpus luteum). Luteolysis occurs in the absence of pregnancy, at the end of the luteal phase. The process of luteolysis is initiated by oxytocin (secreted by the corpus luteum) and prostaglandin F2a in domestic animals.


Progesterone is produced by the corpus luteum, which inhibits the hypothalamus (the hypothalamus secretes GnRH, therefore progesterone inhibits GnRH secretion). The corpus luteum also secretes oxytocin.

Initially the oxytocin appears to have no effect, however after a short period of time (e.g. 12-15 days in the cow) oxytocin receptors begin to form. When these oxytocin receptors are stimulated by the oxytocin secreted by the corpus luteum, prostaglandin F2a synthesis and secretion by the endometrium is stimulated.

Prostaglandin inhibits the production of progesterone (which is inhibiting the GnRH secretion and thus preventing the emergence of new dominant follicles). If progesterone production is inhibited then the oestrous cycle is able to begin again.

Prostaglandin also stimulates further oxytocin release, stimulating more oxytocin receptors that cause further prostaglandin F2a release. This is known as a positive cascade system and is used to quickly progress a biological situation, here the situation would be the prevention of inhibition of progesterone (which is inhibiting GnRH secretion).

The reduction of plasma progesterone concentration means follicular growth can now continue and dominant follicles can now emerge. In pregnancy, there is no corpus luteum formation (luteinisation) so there is no luteolysis – therefore progesterone levels remain high.


  1. Corpus luteum produces progesterone and oxytocin – progesterone is inhibiting GnRH secretion
  2. Oxytocin receptors form
  3. Stimulated receptors cause prostaglandin F2a by endometrium
  4. Prostaglandin inhibits the secretion of progesterone and stimulates further oxytocin release
  5. Positive cascade system rapidly increases plasma prostaglandin concentration
  6. Progesterone levels are low again and GnRH secretion resumes
  7. Follicular development begins again, ready to repeat the oestrous cycle