What exactly is cancer

Cancer arises because certain cells within a given tissue escape from normal growth controls, replicate more frequently, and migrate to sites distant from the parent tissue where further uncontrolled replication occurs. Such escape is facilitated by the accumulation of mutations within a cancerous cell as a result of the innate and environmental carcinogens to which cellular DNA is subjected. If errors generated in coding DNA are not repaired, these will be transmitted to the daughter strands as the cell divides. Clearly, mutations will arise more rapidly if external mutagenic stimuli are increased, or if the cell is defective in DNA repair systems.

This term refers to a gene which has been mutated to facilitate neoplastic growth. The normal function of such genes may be the synthesis of factors involved in growth control, the cell cycle or apoptosis. Oncogenes can be broadly divided into two groups, according to whether their oncogenic effect results from overactivity of a 'proto-oncogene' or the loss of a 'tumour suppressor function.

The majority of known oncogenes are components of signal transduction pathways in which mutations or the presence of increased copies of a gene result in overactivity, mimicking persistent growth factor stimulation. These include genes encoding receptors (e.g. erbB in breast carcinoma), cytoplasmic signalling moieties such as K-ras, and transcription factors such as c-myc (important in betrointestinal tumours and leukaemias). A recently described class encode mitotic spindle binding proteins; mutations in these genes promote premature exit from anaphase, leading to incorrect chromosome segregation to daughter cells, and anaploidy. In animals, a number of tumours are caused by retroviruses which carry activated oncogenes, but to date this has not been shown to be a common mechanism in human cancer. Nevertheless, several human cancers are undoubtedly caused by infectious agents. Important examples include human papillomavirus E7 (which inappropriately phosphorylates pRB), leading to cervical carcinoma; herpesvirus 8 (which encodes a cyclin that drives the host cell through the GI-S checkpoint); and Epstein-Barr virus, responsible for Burkitt's lymphoma and nasopharyngeal carcinoma.

Tumour suppressor genes tend to encode proteins whose normal function is to inhibit the cell cycle or to induce apoptosis to prevent transmission of uncorrectable DNA defects. Direct inhibitors of the cell cycle include pRB. Other tumour suppressor genes encode components of inhibitory growth factor-signalling pathways, particularly those of transforming growth factor (TGF)-B and its associated cytoplasmic signalling mole- cules such as Smad2 and Smad4 (which is the DPC4 'deleted in pancreatic carcinoma' gene). As noted in previous section, neurofibromin encodes a Ras inhibitor which is mutated in neurofibromatosis. APC, the gene mutated in familial adenomatous polyposis and 60% of sporadic colon adenomas and carcinomas, is thought to operate as an oncogene by rendering cells less susceptible to apoptosis. P53, a key tumour suppressor gene, normally uses both mechanisms to override other signals which would otherwise stimulate cell proliferation.The importance of p53 is illustrated by the fact that it is inactivated in over 50% of human tumours, including breast and colon carcinomas, and childhood leukaemias.

When an oncogene results from a mutation reducing the activity of a tumour suppressor, a single mutation usually is insufficient to generate oncogenic activity unless an additional mutation inactivates the second copy of the gene. This "two-hit' model of tumorigenesis, developed by Knudson. If, on the other hand, an oncogene results from overactivity of a proto-oncogene, a mutation in only one of the two copies may be sufficient to promote tumorigenesis. This is also true in an important exception to the two-hit rule, in the case of the tumour suppressor gene p53, since mutations in only one allele may be sufficient to result in a biological effect. This reflects the operation of the protein as a tetramer, so abnormalities in any one of the subunit may derange its function.

The cell's complex self-regulating machinery means that more than one mutation os often required to produce a malignant, metastasising tumour, such as a carcinoma, derived from epithelial cells. For example, if a cell mutates to produce a growth factor to which it already expressess the receptor (paracrine stimulation), that cell will replicate remore frequently but will still be subject to cell cycle checkpoints to promote DNA integrity in its progeny.If an additional mutation overriding a cell cycle checkpoint occurs, that cell and its progeny may go on to accumulate further mutations, some of which may allow it to replicate an unlimited number of times by synthesis of telomerase or, to separate from its matrix and cellular attachments without undergoing apoptosis. As deregulated growth continues, cancer cells become increasingly unable to differentiate, fail to respond to local signals as in the normal tissue, and cease to ensure appropriate chromosomal segregation predivision, generating the classical malignant pathological appearances of disorganised growth, variable levels of differentiation, and polyploidy. This sequence is illustrated for colon carcinomas.

Since DNA mutations occur so infrequently, only an occasional cell will go on to acquire a further mutation, but this will be transmitted to the progeny of that cell which, due to their faster replication rates, are likely to constitute an increasing fraction of the tumour. It is likely that morphological premalignant appearances of cancers per the underlying number of mutations, particularly as par logical evidence of increased malignancy can be seen an within premalignant lesions.

It is important to recognise that most of the mutations described above arise in a somatic cell and are not transmitted to the patient's offspring. Nevertheless, some human families are genetically prone to cancer. One group of cancer patients, exemplified by xeroderma pigmentosum (XP) and the hereditary non-polyposis colon cancer (HNPCC) families, have defects in DNA repair enzymes so that they accumulate mutations at a faster rate. More commonly, individuals in cancer-prone families inherita a mutation in a particular oncogene, essentially reducing the number of additional mutations a cell from that person requires to become neoplastic. The two-hit model explains why even in these cancer-prone families, tumours may require many years to develop. The inherited oncogene may be particularly relevant for a certain cell type, predisposing to a particular form of tumour (e.g. N-Ras and neurological tumours), or be able to deregulate growth in a variety of different cell types (e.g. p53 mutations in Li-Fraumeni families which are particularly prone to early-onset leukaemias, sarcomas, and breast and brain malignancies).

Haematological malignancies occur in cells which are already anchorage-independent and circulating. However, additional features are required for a solid tumour to grow and metastasise. The acquisition of additional mutations means that the secondary tumour cells may replicate faster than the primary, or be unable to differentiate as fully.

The blood supply to the enlarging mass of cells is initially rate-limiting, as evidenced by the ischaemic centres to solid tumours. Some tumours may acquire mutations to enhance the secretion of factors to stimulate neovascularisation (angiogenesis), but in many instances physiology suffices since hypoxia is a potent stimulus of the angiogenic factor VEGF (vascular endothelial cell growth factor).

Metastasis, the cardinal feature of most malignant tumours, requires a cancer cell to have the ability to detach from its surroundings without undergoing apoptosis. Certain mutations result in nuclei receiving signals as if they were anchored to local structures-for example, mutations in APC . In addition, metastasising cells must acquire the novel abilities to invade through local tissues to reach blood vessels, survive in the circulation, adhere to a blood vessel wall and migrate into the new tissue. Many of these features are facilitated by the synthesis of novel cellular adhesion molecules or tissue-degradative enzymes such as metalloproteinases. The adherence to the endothelium in the new site cannot simply reflect the fact that the cells adhere to the nearest capillary bed, since metastases display tissue specificity-for example, thyroid cancer to bone. Specific cellular adhesion mechanisms analogous to those used by inflammatory cells are thought to operate. In addition, to escape destruction by cells of the immune system, tumour cells may down-regulate cellsurface expression of recognition molecules or induce a general depression of immune responses.

Plants have proved to be an important source of anti-cancer drugs. Here we have investigated the cytotoxic action of an aqueous extract of Fagonia (cretica) indica , used widely as a herbal tea-based treatment for cancer.

Fagonia Cretica - As per illness, severity / stage of Carcinoma, varied mixing ratios with regards Leaf : Flower : Stem are used. The prime action of Organic Fagonia cretica shall be to initiate cell cycle arrest on the energy center of cancer DNA and thus enable remission in metastatic tendencies. Fagonia cretica induces cell cycle arrest and apoptosis via p53-dependent and independent mechanisms, with activation of the DNA damage response.

The action is initiated within 24-72 hours of intake and the lesser number of cancer cells, medicine are to enable into remission - sooner are the results achieved - and its this reason, we request for earliest intake so before cancer gets into progression mode, if we can start on with the protocol, results can be very encouraging. Its only in patients where metastasis is already confirmed or if there are high "free flow radicals" in the body channels, it does takes longer duration intake towards enabling a successful remission,but mother nature certainly rewards perseverance in the end.

Please do share with regards Age and illness details of patient in our email (AsmiConsultancyHerbals@gmail.com) so we can confirm the details on Medically recommended intake Dosage of Organic Fagonia cretica Tea. Because in an early case of Cancer, the mixing ratio with regards Organic Fagonia cretica is Leaf 40 : Flower 60 while in Stage 4 / Terminal illness, its Leaf 10 : Flower 90 and similarly as per illness severity / type of carcinoma, the mixing ratio of Leaf : Flower and daily intake dosage also varies.

We have Registered TradeMark of Organic Fagonia cretica Tea so all patients can be absolutely assured with regards the Authenticity of our Product and the accountability of our Herbal Formulations for cancer patients.