A single session of intralesional steroid injections showed promising results for the prevention of stricture after ESD for esophageal cancer.

Although we usually report 5-year cancer survival using population-based cancer registry data, nowadays many cancer patients survive longer and need to be followed-up for more than 5 years. Long-term cancer survival figures are scarce in Japan. Here we report 10-year cancer survival and conditional survival using an established statistical approach. We received data on 1 387 489 cancer cases from six prefectural population-based cancer registries in Japan, diagnosed between 1993 and 2009 and followed-up for at least 5 years. We estimated the 10-year relative survival of patients who were followed-up between 2002 and 2006 using period analysis. Using this 10-year survival, we also calculated the conditional 5-year survival for cancer survivors who lived for some years after diagnosis. We reported 10-year survival and conditional survival of 23 types of cancer for 15–99-year-old patients and four types of cancer for children (0–14 years old) and adolescent and young adults (15–29 years old) patients by sex. Variation in 10-year cancer survival by site was wide, from 5% for pancreatic cancer to 95% for female thyroid cancer. Approximately 70–80% of children and adolescent and young adult cancer patients survived for more than 10 years. Conditional 5-year survival for most cancer sites increased according to years, whereas those for liver cancer and multiple myeloma did not increase. We reported 10-year cancer survival and conditional survival using population-based cancer registries in Japan. It is important for patients and clinicians to report these relevant figures using population-based data.

Cancer survivors are at excess risk of developing second primary cancers, but the precise level of risk in Japanese patients is not known. To investigate the risk of survivors developing second primary cancers, we conducted a retrospective cohort study using data from the Osaka Cancer Registry. The study subjects comprised all reported patients aged 0-79 years who were first diagnosed with cancer between 1985 and 2004 in Osaka and who survived for at least 3 months, followed-up through to December 2005. A metachronous second primary cancer was defined as any invasive second cancer that was diagnosed between 3 months and 10 years after the first cancer diagnosis. The main outcome measures were incidence rates per 100 000 person-years, cumulative risk and standardized incidence ratios (SIR) of second primary cancer. Metachronous second primary cancers developed in 13 385 of 355 966 survivors (3.8%) after a median follow-up of 2.5 years. Sex-specific incidence rates of metachronous second primary cancer per 100 000 person-years increased with age, and were higher among men than women (except for the 0-49 years age group), but these rates did not differ over the study period. The 10-year cumulative risk was estimated as 13.0% for those who first developed cancer at 60-69 years of age (16.2% for men, 8.6% for women). The SIR among those with first cancer diagnosed at 0-39 and 40-49 years of age were 2.13 and 1.52, respectively, in both sexes, whereas the SIR among cancers of the mouth/pharynx, esophagus and larynx were much higher than one as for site relationships. We showed that cancer survivors in Osaka, Japan, were at higher risk of second primary cancers compared with the general population. Our findings indicate that second primary cancers should be considered as a commonly encountered major medical problem. Further investigations are required to advance our understanding to enable the development of effective measures against multiple primary cancers. (Cancer Sci 2012; 103: 1111-1120 A pproximately 50% of men and 40% of women will develop a cancer during their lifetime,(1) and half of all cancer patients in Japan will survive for at least 5 years.(2)Because of the longer survival times for several forms of cancer and the aging of the population, it is estimated that 5-10% of all cancer patients develop a further, independent primary cancer. (3,4) A better understanding of multiple primary cancers should yield greater insights into the shared etiological factors and basic mechanisms of carcinogenesis and could thus provide a more sound basis for the management of cancer patients, including the development of protective measures. In a previous study using data from the Osaka Cancer Registry (2000 Census population; 8.8 million), one of the largest population-based cancer registries in the world, we reported that 2.0% of cancer patients developed metachronous second primary cancer between 1966 and 1986. (4) We also calculated the 10-year cumulative risk for metachronous second primaries to be approximately 10% ...

Plexins are receptors for the axonal guidance molecules known as semaphorins, and the semaphorin 4D (Sema4D) receptor plexin-B1 induces repulsive responses by functioning as an R-Ras GTPase-activating protein (GAP). Here we characterized the downstream signalling of plexin-B1-mediated R-Ras GAP activity, inducing growth cone collapse. Sema4D suppressed R-Ras activity in hippocampal neurons, in parallel with dephosphorylation of Akt and activation of glycogen synthase kinase (GSK)-3b. Ectopic expression of the constitutively active mutant of Akt or treatment with GSK-3 inhibitors suppressed the Sema4D-induced growth cone collapse. Constitutive activation of phosphatidylinositol-3-OH kinase (PI(3)K), an upstream kinase of Akt and GSK-3b, also blocked the growth cone collapse. The R-Ras GAP activity was necessary for plexin-B1-induced dephosphorylation of Akt and activation of GSK-3b and was also required for phosphorylation of a downstream kinase of GSK-3b, collapsin response mediator protein-2. Plexin-A1 also induced dephosphorylation of Akt and GSK-3b through its R-Ras GAP activity. We conclude that plexin-B1 inactivates PI(3)K and dephosphorylates Akt and GSK-3b through R-Ras GAP activity, inducing growth cone collapse.

The incidence of HCC in Osaka started to decrease by 2000, mainly because of decreased HCV-related HCC.