Only variable reactivity has been seen with CK7,
CK8, CK18, and CK19.
Concurrently, in vivo exposure to EE, 25, and 250 [micro]g BPA/kg-BW significantly suppressed luminal progenitor markers (determined by alignment with
CK8) (Figure 3B).
The immunohistochemical stains gave positive results for cytokeratin 7 (CK7), cytokeratin 8 (
CK8), estrogen receptor (ER) (strong, 99%), progesterone receptor (PR) (strong, 99%) (Figure 5), Smad4 (DPC4), GAtA binding protein 3 (GATA-3), gross cystic disease fluid protein 15 (GCDFP-15), and mammaglobin (Figure 6).
Immunohistochemistry showed that those carcinoma cells were specifically positive for not only CK7 (Figure 1(f)) but also CK18 (Figure 1(f)) and c-kit (potential stem cells marker) [3, 5], whereas they were negative for
CK8, Hepatocyte, and CD56.
The observed groundwater levels are from some wells including CK7 and
CK8. And the measured solute concentrations are from well
CK8.
In the poorly-differentiated case of SCC, CK1 and CK10 were not expressed, but simple epithelial keratins (
CK8, 18, and 19) were expressed.
Only four of the Food and Drug Administration (FDA)-approved markers (CA 15-3, CA 27.29, HER- 2/neu, and circulating tumor cells analysis of EpCAM, CD45,
CK8, 18, 19) can be measured and assessed longitudinally.
The lining epithelia exhibited a negative expression pattern for
CK8 and CK18.
The tumor cells were positive for HMB45, SMA, Melan-A (A103), vimentin and negative for CD117, CK7,
CK8, CD10, and RCC.
AE1/AE3, Cam5.2) and low-molecular weight cytokeratins (CK7,
CK8, CK19).
The stains showed diffuse +AFP, Glipan, and
CK8; +Heppar in the solid areas; +CK17 and 19 in the glandular areas; -chromogranin, CD20, ER, PR, and GCDFP15; +luminal/focal polygonal CEA (Figures 2(a) and 2(b)).