Pathogenesis of the megacolon is based on a continuous process of ganglion cell damage with participation of T lymphocytes expressing cluster of differentiation 8 and natural killer cell membrane antigens. B lymphocytes do not take part in the chronic inflammatory reaction.
We evaluated the failure pattern after definitive chemoradiotherapy in patients with stage III nonesmall-cell lung cancer harboring epidermal growth factor receptor mutations and/or anaplastic lymphoma kinase translocation. Although the epidermal growth factor receptor-mutant group showed a lower incidence of infield failure and higher incidence of out-of-field failure, the group with anaplastic lymphoma kinase translocation showed no characteristic in-field or out-of-field failure pattern. Introduction: This study was aimed at clarifying the failure pattern after definitive chemoradiotherapy in patients with stage III nonesmall-cell lung cancer (NSCLC) harboring epidermal growth factor receptor (EGFR) mutations and/or anaplastic lymphoma kinase (ALK) translocation. Methods and Materials: This retrospective study was a singleinstitution study conducted on patients with unresectable stage III non-squamous NSCLC treated by definitive chemoradiotherapy between January 2006 and March 2016. Only patients with information of EGFR mutations and/or ALK translocation were included. The prognosis and initial recurrence patterns were compared according to the presence/absence of EGFR mutation and/or ALK translocation. Results: A total of 173 patients (34 with activating EGFR mutations, 13 who were positive for ALK translocation) were enrolled, and the median follow-up duration was 36 months (range, 3-123 months). The 3-year overall survival rate was significantly higher in the EGFR-mutant group than in the wild-type EGFR group (75% vs. 46%; P ¼ .002). There was a tendency towards a better overall survival in the ALK-positive group than in the ALK-negative group (68% vs. 44%; P ¼ .085). No differences in the 3-year progression-free survival were observed according to the EGFR or ALK status. The EGFR-mutant group showed a significantly lower rate of in-field failure (P ¼ .027) and higher rate of out-of-field failure (P ¼ .029) as compared with the wild-type EGFR group. There was no significant difference in the rate of in-field failure or out-of-field failure between the ALK-positive and ALK-negative groups. Conclusions: Although the ALK-positive group showed no characteristic failure pattern, the EGFR-mutant group showed a lower rate of in-field failure and higher rate of out-of-field failure.
Since 1976, sera obtained serially from 10,218 pregnant women during the first, second, and third trimesters of gestation and cord sera were tested for CMV complement-fixing (CF) and immunofluorescent (IF) antibodies. CMV IgG-IF antibody was positive in 9,735/10,218 (95%) in the first trimester, and a significant rise of CF antibodies during pregnancy was found in 70/9,206 (0.76%) of the seropositive group and in 5/438 (1.14%) of the seronegative group. IgM antibody was found in 6/9,206 (0.06%) of seropositive women during the first trimester and in 7/70 (10.0%) of seropositive mothers with CF antibody rise and in 4/5 of seroconverted mothers of the seronegative group, suggesting that the incidence of primary infection with CMV during pregnancy was approximately 1% of susceptible women. All the mothers with immune response had infants with neither viruria nor IgM antibody in the cord blood, whereas seropositive mothers without an immune response had infants with viruria (7/1,826; 0.4%) or with IgM antibody in the cord blood (6/9,136; 0.06%). None of these 13 babies, shedding CMV or with IgM IF antibody, had physical or mental retardation. CMV IgG-IF antibody was present in almost 80% of infants between 7 and 12 months of age in 1988, suggesting that perinatal or postnatal CMV infection may occur in infants born to seropositive mothers in 70-80% of pregnancies.
Since 1958, we have studied experimental Chagas' disease (CD) by subcutaneous inoculation of 1,000 blood forms of Trypanosoma cruzi (Y strain) in Balb/C. mice. Evolution of parasitemia remained constant, beginning on the 5th and 6th day of the disease, increasing progressively, achieving a maximum on about the 30th day. After another month, only a few forms were present, and they disappeared from the circulation after the third month, as determined from direct examination of slides and the use of a Neubauer Counting Chamber. These events coincided with the appearance of amastigote nests in the tissues (especially the cardiac ones), starting the first week, and following the Gauss parasitemia curve, but they were not in parallel until the chronic stage. In 1997, we began to note the following changes: Parasites appeared in the circulation during the first week and disappeared starting on the 7th day, and there was a coincident absence of the amastigote nests in the tissues. A careful study verified that young forms in the evolutionary cycle of T. cruzi (epi + amastigotes) began to appear alongside the trypomastigotes in the circulation on the 5th and 7th post-inoculation day. At the same time, rounded, oval, and spindle shapes were seen circulating through the capillaries and sinusoids of the tissues, principally of the hematopoietic organs. Stasis occurs because the diameter of the circulating parasites is greater than the vessels, and this makes them more visible. Examination of the sternal bone marrow revealed young cells with elongated forms and others truncated in the shape of a "C" occupying the internal surface of the blood cells that had empty central portions (erythrocytes?). We hypothesize that there could be a loss of virulence or mutation of the Y strain of Trypanosoma cruzi.
Background/Aim: To investigate the usefulness of cell-free DNA (cfDNA) in patients with oligometastasis. Patients and Methods: This study included oligometastatic colorectal cancer (CRC) patients who underwent ablative irradiation using stereotactic body radiotherapy or proton beam therapy for metastatic lesions at a single institution. cfDNA was purified from the plasma of pretreated patients and gene mutations were analyzed by next-generation sequencing. Progression-free survival (PFS) was statistically compared according to gene mutation, clonality or allele frequency. Results: A total of 20 patients were analyzed. Mutations were detected in the following genes; TP53 (45%), APC (40%), KRAS (15%), PIK3CA (15%), NF1 (5%), BRCA1 (5%), ERBB2 (5%), FBXW7 (5%), KIT (10%), and HRAS (10%). Patients with multi-clonality of gene mutation showed tendency for poor PFS (p=0.07). Among 7 patients whose metastatic site was the lung, those with no cfDNA detected had significantly better PFS than those with cfDNA (p=0.02). Conclusion: cfDNA profiles could be predictive tools for early recurrence of oligometastatic CRC patients after ablative radiotherapy.
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