Galectin-3 immunoexpression was classified as 1 in 57.33% of tumors. The highest percentage of staining cells appeared in the most advanced cancer (p = 0.4899). Patients with recurrence had a great number of tumors with high score (p = 0.0465). In addition, high or moderate galectin-3 immunoexpression had been associated with an increased marginal risk for death (p = 0.0795). The immunoexpression of galectin-3 was strong or moderate in 42% of the colorectal tumors. Patients with strong or moderate immunoexpression of galectin-3 died or had recurrence more frequently. The risk of death was marginally reduced in patients with negative or low-grade galectin-3. Galectin-3 cytoplasmatic immunoexpression seems to be a prognostic factor in colorectal cancer because a higher risk of recurrence had been observed in tumors with a high score of galectin-3. However, a higher risk of death was not found on this group.

The role of differentiated trophoblast glycogen cells (GCs) in the ectoplacental cone (EPC) has not been elucidated yet. Recently, GC progenitors have been shown to be present from embryonic day 7.5 (E7.5), but glycogen is found in GC only from E10.5. Herein, we investigated the origin, localization and characterization of mouse GCs in EPC and their relationship with blood cells and trophoblast giant cells (TGCs) during placentation. Implantation sites (E5.5-E12.5) were processed for histological studies, histochemical detection (glycogen) and immunohistochemical staining (Ki67). Three-dimensional reconstruction of the EPC was obtained from suitably oriented embryos at E7.5. Our findings evidence that GCs are present and assembled in clusters from E6.5 to E12.5, and that they exhibit the classic vacuolated appearance and contain PAS-positive glycogen, which is amylase-sensitive and acetylation-resistant. In fact, only GCs were stained after acetylation, confirming unequivocally their presence in tissues. At E6.5, GCs showed numerous mitoses and vacuoles with scattered glycogen particles. At E7.5, GCs showed low numbers of mitoses and abundant vacuoles full of glycogen. During E7.5-E8.5, GCs were in close proximity to TGCs, and cells were intercalated by thin maternal blood spaces; placental GCs lost maternal blood contact during E9.5-E12.5. Our results indicate that GCs are originated and proliferate in the upper portion in the midregion of EPC at E6.5, and that at E7.5-E8.5 they show consistent glycogen deposits, which are likely metabolized to glucose. This compound may be directly transferred to circulating maternal blood, and used as a source of energy by GCs and TGCs during placentation.

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