Abstract The aim of this study was to assess the efficacy of hemostatic radiotherapy (HRT) in patients with advanced cancer. Eighteen patients with advanced cancer treated with HRT at the Fukuoka University and Kyushu Rosai Hospitals in Japan between July 2010 and February 2015 were retrospectively assessed. The hemostatic effect of tumor-related bleeding was assessed by the clinical course of bleeding, laboratory data, the endoscopic study, and the number of blood transfusion units (BTRUs) for one month before and after HRT. The median follow-up time was 2.6 months (range, 0.7 to 36.2 months). The median age of the patients was 77 years (range, 51 to 93). The primary diseases with tumor-related bleeding included gastric cancer, urinary bladder cancer, gynecological cancer, prostate cancer, non-small-cell lung cancer, and breast cancer. The median overall survival time was three months, and the one year survival rate was 22.9% of all patients. The HRT regimens ranged from 30 Gy in 10 fractions to 40 Gy in 20 fractions. In all patients, the anemia grade and the number of BTRUs decreased for 1 month after RT. The percentage of patients who were diagnosed as “successful” for hemostasis was 83% (15 of 18 patients). HRT is therefore strongly suggested as effective for the control of tumor-related bleeding in patients with advanced cancer. The optimal radiation doses and fractions are controversial; however, this treatment should be offered for patients with a poor life expectancy.
Keywords: retrospective study; hemostatic radiotherapy; conventional fractionation; advanced cancer

Abstract Introduction: Histopathologic subtyping according to the St. Gallen classification is predictive of response in women with breast cancer treated with neoadjuvant chemotherapy (NCT). Our aim was to confirm its predictive role when dose-dense (DD) chemotherapy is administered. Methods: A prospective study was performed in stage II-III breast cancer treated with four cycles of doxorubicin-cyclophosphamide every two weeks, followed by 4 cycles of docetaxel every 3weeks. Tumours were grouped into 4 subtypes. Simple and multivariate logistic regression analysis was performed to determine the association between pathologic complete response (pCR), according to the Miller & Payne classification and tumour subtype. In addition survival analysis was performed. Results: 71 patients were included. By phenotypic classification, 11.3% were Luminal A, 59.2% Luminal B, 8.5% pure HER2 and 21.1% TN. Following the administration of DD NCT, a pCR rate of 25.4% was achieved. There was a significant association between the pCR rate and the different immune phenotypes (p=0.05). The pCR rate was 46.7% for the TN patients and 19.6% for the others (p=0.046). At 30 months’ followup, the rate of disease-free survival (DFS) was 71.8% for the TN patients and 93.3% for all others. The difference was also significant for overall survival (p=0.006), with 100% of the non-TN patients alive vs 85.7% of the TN patients. Within the TN subtype, the patients who achieved pCR had a better DFS (p=0.04) and a better rate of overall survival. Conclusions: Tumour classification according to the St. Gallen phenotypes is useful in predicting response and survival in breast cancer patients treated with DD neoadjuvant chemotherapy.
Keywords: dose-dense; neoadjuvant; breast cancer; pathologic-response; phenotype; prognostic

Abstract Background: High grade glioma (HGG) is the most aggressive and lethal primary brain tumor. The treatment of patients with HGG still remains palliative with improvement in the quality of life and encompasses surgery, radiotherapy, and chemotherapy. The use of interferons (IFNs) in the treatment of HGG has been showed useful for these patients. Patients and methods: We report the use, outside of clinical trials, of recombinant IFNs-α and γ(CIGB-128) in 10 patients with glioma grade III-IV (1 anaplastic astrocytoma and 9 GBM). The aim of the study was to offer a treatment option to patients with malignant gliomas, primary (non-surgical) or progressive (Karnofsky performance status (KPS) >20), without other possible therapeutic options, and non-eligible for clinical trials. Patients received intralesional CIGB-128, 3 times per week, during one month, in doses from 3.5 MIU scalable up to 14.0 MIU. Safety was evaluated by the occurrence of adverse events. Others measurements were tumor responses measured by RECIST, KPS, muscular power (ASIA neurological assessment scale) and overall survival. Depending of treatment tolerability, clinical improvement and medical criteria, patients were maintained under treatment for 3 more months. Results: 70% of treated patients had KS<50. Seven patients had objective response (3 CR, 4 PR), one lesion progressed and 2 were not evaluable. The treatment prolonged the survival of patients to a mean of 34±14 months since diagnosis. The quality of life improved as measured by the increase in the KPS (66% of patients scaled the category) and improvement in muscular power in 50% of patients. CIGB-128 had an acceptable safety profile with fever as the most frequent adverse event, observed in 54.7%, followed by extrapyramidal symptoms and hypopotassemia in 14.2% of treated patients. All detected adverse events were reversible. There was no evidence of cumulative hematologic toxicity. Conclusions: CIGB-128 demonstrated signs of clinical improvement, with an acceptable safety profile and measurable improvement in quality of life in patients with non-operable or progressive highgradeglioma. The use of this drug should be explored further in clinical trials with a larger number of patients to confirm these encouraging results.
Keywords: intracranial treatment; glioblastoma multiform; primary brain tumor

Abstract Hereditary cancer that has monogenic inheritance affects every tenth patient, on average, who is diagnosed with cancer, and it has been suggested, based on twin studies, that approximately 30% of all cancer patients have a genetic predisposition to developing cancer. In this article, the author posited that familial syndromes become more organ specific with increasing age at tumor presentation to the point that very late in life, only a few organs are affected by tumors. The reason for this could be that the tumor originates from a more differentiated, organ-specific progenitor/stem cell later in life, while the progenitor/stem cell might be involved in organogenesis in different organs earlier in life. Examples are given for skin cancer, colon, endometrial and breast cancer. Patients with familial cancer who present with cancer at an older age have a more organ-restricted disease. This could be because the tumor has a more differentiated progenitor/stem cell origin. Examples are given for families with breast cancer, melanoma, non-melanoma skin cancer, endometrial and colon cancer.
Keywords: hereditary cancer; familial syndromes; stem cell origin of the tumor