risedronate of pathological responses, particularly in the case of use of oxaliplatin-based regimens . Pathologic complete response (pCR) is still reported as a rare situation,that addiction of BV to chemotherapy improves resectability [13] and the quality of pathological responses, particularly in the case of use of oxaliplatin-based regimens [14]. Pathologic complete response (pCR) is still reported as a rare situation.After neoadjuvant treatment of breast, esophageal or rectal cancer, the pCR is associated with significantly longer survival.PCR is also recognized as a new outcome endpoint in HCRM treated with preoperative chemotherapy, and an association with 76% of 5-year overall survival was reported.In recent years, some clinical predictive factors of pCR have been identified in patients with HCRM treated with preoperative chemotherapy followed by resection.

Objective responses assessed by CT scan are clearly related to the therapeutic outcome, although RECIST complete remission or posttreatment PET negativity is not predictive of Bergenin pCR.The limitation of standard radiologic assessment as a surrogate for pathological response is even more relevant for antiangiogenic treatments, which may delay disease progression mainly through stabilization. In fact, HCRM are generally characterized by heterogeneous density with thick and irregular margins; significant biologic responses to antiangiogenic treatment may not necessarily determine dimensional decrease and can conversely induce a radiologic shift into homogeneously hypodense lesions with a thin rim at the tumor-normal interface. Recently, these evidences have led to the definition of new morphologic criteria for HCRM treated with neoadjuvant bevacizumab-based regimens, demonstrating a significant correlation with pathologic response and, ultimately, with survival.Histologically, untreated HCRM shows purchase Bicalutamide large areas of viable tumor glands intermingled with zones of dirty necrosis.

Chemotherapy-induced regression of HCRM is characterized by sclero-hyaline fibrosis, foamy macrophages, small foci of necrosis and calcifications overgrowing the tumor cells. Residual tumor is usually present, predominantly at the periphery of nodules and mixed with normal liver parenchyma. Tumor regression grade ofHCRM is assessed semiquantitatively by the relative proportion of fibrous tumor replacement and residual order Bicalutamide neoplastic cells.Recently, residual tumor thickness at the tumor-normal interface was reported as new histological prognosticator of clinical outcome, with strong correlation with radiologic and pathologic degree of response.Moreover, significantly Fig. 5 Neoplastic glandular foci inside a backbone of necrosis and within the peripheral fibrotic rim, without invasion of normal liver parenchyma Med Oncol 123 smaller tumor thickness of resected HCRM was reported in the case of bevacizumab-based regimens. In this case, histological examination of HCRM showed the absence of those morphologic aspects that are typically observed after response to either standard chemotherapy or bevacizumab-based regimens.

On the contrary, we report the evidence of complete necrosis as a distinct pathological  lamina propria indicator of major response to preoperative mC and BV; this morphological aspect might be related to the peculiar biologic.