Our results suggested that the most dismal CRC harbors three definite vectors that may represent the strongest phenotype of putative systemic immune (CA19-9), distant metastasis (extent of liver metastases), and local progression (peritoneal dissemination).
This study showed a significant difference in tumour characteristics and treatment patterns in patients aged 80 and above. Even after adjustment for clinicopathological factors, the difference in survival persisted and age was considered a robust prognostic factor.
Aim
The optimal surgical management strategy for para-aortic lymph node (PALN) metastasis has not attracted as much attention as surgery for liver or lung metastasis. The purpose of this retrospective study was to evaluate the oncologic outcomes after synchronous resection of PALN metastasis in left-sided colon and rectal cancer.
Methods
Between January 1986 and August 2016, 29 patients with pathologically positive PALN metastases who underwent curative resection at our hospital were retrospectively reviewed. We examined clinicopathological characteristics, long-term oncologic outcomes, and factors related to favorable prognosis in these patients.
Results
The 3-year overall survival and recurrence-free survival (RFS) rates were 50.5% and 17.2%, respectively. In total, 6 (20.7%) patients experienced no recurrence in the 3 years after surgery, while postoperative complications were seen in 9 (31.0%) patients. The 3-year RFS rate was significantly better in the pM1a group than in the pM1b/pM1c group (26.3% and 0.0%, respectively, p = 0.032).
Conclusion
PALN dissection for patients without other organ metastases in left-sided colon or rectal cancer is a good indication as it is for liver and lung metastasis.
An LRHC for right-sided colon cancer has the advantage over an ORHC of better short-term outcomes, and both groups have similar long-term oncologic outcomes. An LRHC is thus an acceptable alternative to an ORHC for the treatment of this type cancer.
The activity of the retinoblastoma protein pRB is regulated by phosphorylation that is mediated by G 1 cyclinassociated cyclin-dependent kinases (CDKs). Since the pRB-related pocket proteins p107 and p130 share general structures and biological functions with pRB, their activity is also considered to be regulated by phosphorylation. In this work, we generated phosphorylationresistant p107 and p130 molecules by replacing potential cyclin-CDK phosphorylation sites with nonphosphorylatable alanine residues. These phosphorylation-resistant mutants retained the ability to bind E2F and cyclin. Upon introduction into p16INK4a -deficient U2-OS osteosarcoma cells, in which cyclin D-CDK4/6 is dysregulated, the phosphorylation-resistant mutants, but not wild-type p107 or p130, were capable of inhibiting cell proliferation. Furthermore, when ectopically expressed in pRB-deficient SAOS-2 osteosarcoma cells, the wild-type as well as the phosphorylation-resistant pRB family proteins were capable of inducing large flat cells. The flat cell-inducing activity of the wild-type proteins, but not that of the phosphorylation-resistant mutants, was abolished by coexpressing cyclin E. Our results indicate that the elevated cyclin D-or cyclin E-associated kinase leads to systemic inactivation of the pRB family proteins and suggest that dysregulation of the pRB kinase provokes an aberrant cell cycle in a broader range of cell types than those induced by genetic inactivation of the RB gene.
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