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The receptor expression between primary tumor and metastatic tissue may vary [ 9].
On the other hand, relatively small deposits of metastatic tissue may not lead to detectable differences in Treg phenotype when assessed in whole PBMC.
The discordance in alterations between primary and metastatic tissue may be of clinical relevance in the era of genomically directed precision cancer medicine.
This bears several limitations: (1) Metastatic tissue may not be available, (2) repeated sampling of metastatic tissue may not be feasible due to increased morbidity, and (3) metastatic breast cancer might be heterogeneous, implying that tissue from a single metastasis obtained at a single time point may not adequately reflect the tumor burden.
This discordance between paired primary and metastatic tissue may have clinical relevance in the era of genomic medicine since the genetic information gleaned from analysing primary tumors may not represent the relevant drivers in metastatic disease.
Within this context, determination of serum HER2 or evaluation of HER2 status in circulating tumor cells (CTCs) may be of clinical relevance because metastatic tissue may be difficult to obtain for analysis as a result of its localization.
Similar(54)
Interestingly we find a significantly higher expression level of CatS in primary tumour compared with lymph node metastatic tissue, which may imply a more important role for the enzyme in promoting tumour cell invasion and dissemination from the primary site.
Moreover, HER2-targeted treatment of PRIM-HER2-positive patients before biopsy of metastatic tissue or CTC sampling may interfere with HER2 testing.
However, these are currently determined using primary tumor tissue (e.g. HER2-status) or by means of sequential metastatic tissue biopsies because breast cancer phenotype may change during disease progression [ 1, 2].
Therefore, a differentially higher expression of MMCs in primary periampullary cancer, compared with metastatic lymph nodes or benign periampullary tissue may represent an adaptive mechanism to chronic cellular hypoxia.
Our findings suggest that a high serum hepcidin-25 level may indicate the progression of RCC, and that upregulation of hepcidin mRNA expression in tumor tissue may be related to increased metastatic potential.
Related(20)
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