E-Cadherin

Dear shybird, Let me re-post your query. RESEARCH: E-Cadherin Gene is known a the tumor supressor gene. These are the proteins for which they code. Comment: the evidence for the role of E-cadherin as a tumor suppressor is due to increased risk of metastasis in its absence. E-cadherin testing is not standard of care, hence it would be best to discuss this with your doctor or the pathologist who had it done. E cadherin positivity could therefore mean two things: that E-cadherin is present which would mean it is not absent. The other definition would be: mutant E-cadherin is positive. I will not pretend to know which (as the testing is not recommended in the first place, except in differentiating lobular from ductal cancer), however, I will hazard that since the negative outcome is associated with decreased or absent E-cadherin, then E-cadherin positive means low risk (in the same manner that the Estrogen receptor positive means low risk). Also loss of E-cadherin is seen in lobular cancer – and you have ductal – meaning you do not have cadherin loss. Comment on E-cadherin risk: The information I have is for cases of hereditary breast and gastric cancer. A study done in 1999 did not show any increased risk (Int J Radiat Oncol Biol Phys. 1999 Aug 1;45(1):73-83.) this was actually a small population with less than a hundred cases. I am unaware of any large prospective study in which patients with E-cadherin were followed up to look at how many developed breast or gastric cancer. The converse has been reported: among those with established HEREDITARY breast or gastric cancer, there seems to be an increased incidence of mutations in CDH1 (which encodes the E Cadherin protein). I would be very interested if you can share your research source. They either have a DAMPENING or a REPRESSIVE effect on the regulation of the cell cycle, promote apoptosis, and sometimes do both. Comment: These metabolic pathways are not directly related to E-cadherin. There used to be a time when single pathways were deemed enough to understand development of cancer. It is now known that there are multiple pathways and interaction or cross-talk across these pathways. At most, there may be a relationship between E-cadherin and these proliferation/division or anti-death pathways. Cadherins are cell adhesion proteins. Normally, cells respect the space of other cells, they do not try to invade or impinge. This is called contact inhibition. A cancer cell has lost this inhibition. Hence, the absence of normal cadherins would mean, the cell keeps growing despite the presence of normal cells blocking its way. 1.) REPRESSION of genes are essential for the continuing of the cell cycle. If these genes are not EXPRESSED the cell cycle will not continue, effectively inhibiting cell division. a.) What does 'expressed' mean? b.) Are we trying to inhibit cell division? Comment: Genes encode proteins. Inhibitory proteins can stop the cell cycle (or cell division). Cell division would mean more cells. Cancer allows the cell cycle to continue and continue. The normal cell once it attains its function (such as the lining of a breast gland) will not need any further growth. Abnormal division should be stopped. There are certain cells that need to continue dividing – such as blood cells which are regularly replaced. 2.) Coupling the cell cycle to DNA damage: As long as there is damaged DNA in the cell, it should not divide. If the damage is repaired, the cell cycle can continue. a.) Is the purpose of chemo to repair damage to DNA? Comment: The purpose of chemo is to damage DNA, particularly the DNA that is actively being encoded. If the code is abberant and critical, the cell will undergo apoptosis or cell death. The idea is to inflict this critical damage. 3.) If the damage cannot be repaired, the cell should initiate apoptosis (programmed cell death) to remove the threat it poses for the greater good of the organism. a.) How will one know if cells have apoptosised? b.) This is wanted, correct? Comment: Apoptosis is desirable. This can only be documented in biopsies, which is not applicable to you (since you are post-surgery). Patients who have chemotherapy before surgery will have two specimens. The first specimen is the biopsy, the second is the specimen of the entire cancer. An analysis of the second specimen will show evidence if this occurred. This is not standard of care, but is done in research settings. 4.) Some proteins involved in cell adhesion prevent tumor cells from DISPERSING, block the loss of contact inhibition, and inhibit metastasis. These proteins are known as metastasis suppressors. a.) What does 'dispersing' mean? Comment: Dispersing means to invade or to metastasize. The cadherins maintain the integrity of the cell. Final comments: The reason I mentioned that E-cadherin is an area of active research is because all of these are still lacking applications. There is no drug specific for those who are E-cadherin positive or negative. A class of drugs meant to stop invasion is too toxic – so we don’t expect any breakthroughs in this respect any time soon. There is no drug combination known to improve outcomes for patients with this marker. Will knowing the status of E-cadherin make a difference in the management scheme? ER PR HER2 have specific guides. E-cadherin, no.

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