MOESM1 of Whole exome sequencing and single nucleotide polymorphism array analyses to identify germline alterations in genes associated with testosterone metabolism in a patient with androgen insensitivity syndrome and early-onset colorectal cancer

Additional file 1: Table S1. Variants of tumor genes detected by Sanger sequencing in the proband

MOESM6 of Whole exome sequencing and single nucleotide polymorphism array analyses to identify germline alterations in genes associated with testosterone metabolism in a patient with androgen insensitivity syndrome and early-onset colorectal cancer

Additional file 6: Table S6. Chromosomal rearrangements of cancer function-related genes detected in the proband through single nucleotide polymorphism

Flow-chart of patients population.

<p>Flow-chart of patients population.</p

ALK FISH examples.

<p>Gain of ALK GCN (including both low and high genomic gain) was defined as a mean of 3 to 5 fusion signals in ≥10% of cells (Figure on right). Disomic cells are shown in Figure on left.</p

Additional file 2: of PD-L1 assessment in pediatric rhabdomyosarcoma: a pilot study

Figure S1 PD-L1 expression pre and post therapy. Changes in PD-L1 expression are revealed in pre- and post-treatment RMS tissue from the same patients: RMS24, RMS18, RMS22 (A,C and E), all at diagnosis and with no prior treatment, show absence or a mild expression of PD-L1 in the immune component; RMS25, RMS19, RMS23 (B,D and F), all following several lines of treatments, mainly chemotherapy, display a moderate expression in the immune contexture outside and infiltrating the tumor burden. (PPTX 6110 kb

Overall survival analysis.

<p>Kaplan-Meier curves for overall survival according to ALK status: increase of gene copy number vs. disomic status.</p

Supplementary Material for: The Clinicopathologic Heterogeneity of Grade 3 Gastroenteropancreatic Neuroendocrine Neoplasms: Morphological Differentiation and Proliferation Identify Different Prognostic Categories

<b><i>Background/Aims:</i></b> Gastroenteropancreatic (GEP) neuroendocrine carcinomas (NECs) are defined as neuroendocrine neoplasms (NENs) with a Ki-67 index >20% according to the 2010 WHO classification. Some reports suggest that this category is heterogeneous. We retrospectively studied a series of 136 patients affected by grade 3 GEP-NECs with the aim to clarify the prognostic role of tumor morphological differentiation, proliferation, defect in mismatch repair proteins (MMRd), CD117 expression, and site of origin. The primary endpoint was the correlation between these parameters and the overall survival (OS). <b><i>Methods:</i></b> Univariate and multivariable Cox proportional hazards regression analyses were used to assess the prognostic significance of various clinical and histopathologic features. <b><i>Results:</i></b> With a median follow-up of 81 months, the median OS was 12.9 months. At multivariate analysis, morphological differentiation, Ki-67 index, MMRd, stage, and CD117 expression were independent prognostic markers in NECs. Three different prognostic categories of NECs were identified according to the degree of morphologic differentiation (well vs. poorly differentiated) and Ki-67 index (<55% vs. ≥55%). On this basis, median OS was 43.6 months in well-differentiated neoplasms with a Ki-67 index 20-55% (named type A), 24.5 months in poorly differentiated neoplasms with a Ki-67 index 20-55% (type B), and 5.3 months (p < 0.0001) in poorly differentiated neoplasms with a Ki-67 index ≥55% (type C). <b><i>Conclusions:</i></b> The present study suggests that GEP-NECs represent a heterogeneous group of neoplasms which can be better classified in different prognostic categories using both tumor morphology and Ki-67 index

Additional file 2: of MIF/CD74 axis is a target for novel therapies in colon carcinomatosis

Figure 1. Phase contrast microscope images of C1 and C2 organoids. Figure 2. Ingenuity Pathway Analysis of C2 secretome. Figure 3. Western blot analysis of C2 organoids after 4-IPP treatments. (PDF 282 kb

MOESM3 of GNAS mutations as prognostic biomarker in patients with relapsed peritoneal pseudomyxoma receiving metronomic capecitabine and bevacizumab: a clinical and translational study

Additional file 3: Figure S2. Comparison of Kaplan-Meier curves for progression-free survival according to GNAS mutational status in both the prospective (metronomic capecitabine and bevacizumab) and the retrospective cohort (FOLFOX-4)

MOESM2 of GNAS mutations as prognostic biomarker in patients with relapsed peritoneal pseudomyxoma receiving metronomic capecitabine and bevacizumab: a clinical and translational study

Additional file 2: Figure S1. Comparison of Kaplan-Meier curves for progression-free survival according to GNAS mutational status in the retrospective cohort (FOLFOX-4)