Babak Rashidi et al. (2000) demonstrate that liver metastases from colon cancer are capable of remetastasizing to other sites ,1- however are there other tumors may follow this course ?
2- If metastatic cells re – metastasize , Do they Follow the approach that's similar to the primary tumor or that of metastatic site (as they originate primarily from metastatic site).
dear Omar
please, see another case report corresponding to a patient with lymphatic re-metastasis from hepatic metastasis in a patient with recto-sigmoid cancer.
http://www.ncbi.nlm.nih.gov/pubmed/11702258
one would intuitively think that once cancer cells have adapted a metastatic phenotype they would be equally 'fit' (if not fitter) as compared to the primary tumour cells to continue their metastases routes within the body of a patient.
additionally, maybe you are already aware of the self-seeding phenomenon proved by dr Norton's team, according to which metastasis is not a uni-directional process, since cells that have metastasized can travel back to the site of the primary tumor.
http://www.ncbi.nlm.nih.gov/pubmed/20064377
kind regards
Metastasis, being located in its new site of development, behave itself mostly like primary (in this site) tumor. It means it has the capacity to metastasize further. One must not forget that the theory of S.Paeget namely 'seed and soil' would also determine the place of the growing of these new metastasis of the metastasis.
Metastasis is an specimen of heterogenicicty and theory can have different behavior like again metastasis to other site
I think that metastases can be a source of metastasis in primary tumor and in other organs.
I'd say yes, secondary deposits may be the seeding site for another metastasis, but I don't know how in deep the subject was addressed, and if it will make a pivotal change in dealing with an actual clinical case, even more in the current days when biopsy of metastasis is becoming a more common practice, of course, it may have a basic sciences interest, at least
I presume that we are discussing re-metastasis from a metastatic site other than a lymph node.
In the past there was a Soil and Seed hypothesis which hypothesized that some tumour cells (the seed) have an affinity for growing in some particular distant site (the soil), or undue support from that soil. For example, malignant melanoma has predilection for brain and prostate malignancy for bones.
I remember reading long past an experiment where rats were injected with (?) melanoma cells. They developed metastasis at different sites. Tumour cells from the brain were isolated and reinjected into other rats. By doing this repeatedly, cells which only metastasized to the brain were developed suggesting thepossible truth of the Soil-seed hypothesis.
In a patient, whose tumour is multiclonal, it is possible that a metastasis develops in a particular site because that clone had affinity for that site or is supported by that soil. I would say that this patient has high chance for further metastasis to the same type of tissue, from the first metastasis; may be even more than rom the primary (in which this clone could have been eradicated by growth of other clones or by treatment.
ut it will be difficult to identify this other than by clonal studies and even then it is not easy.
The possible clinical relevance is that in such a patient similar sites should be screened more emphatically.
Narayanan
Sorry, I forgot to add that Daniil had mentioned the Soil-Seed hypothesis
Narayanan
Distant metastases shed tumor cells into the blood. There is no doubt that these CTCs can lead to other metastsses at different sites.
In epithelial Cancers, Epithelial - Mesenchymal - Transition (EMT) is the mechanistic basis for metastatic conversion of tumour cells. Once cancer cells metastasize to secondary sites, they institutionalise presence and colonisation through a reverse program (MET) which confer on the transited mesenchymal cells the ability to convert back to their epithelial derivatives (Mesenchymal-Epithelial-Transition: MET) hence the word “transition”. These cells are capable of further metastasis in a away that tend to maintain the original phenotype of the parent tumour cells thereby exhibiting molecular and morphological similarities. This has to a reasonable extent aided the prognosis of metastatic cancer cases such that “Patients with cancers of Unknown primary site (CUP) have poorer survival than patients with cancers of known primary site (CKP)”
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