ANN and Adaboost application for automatic detection of microcalcifications in breast cancer

AbstractObjectiveMicrocalcifications or MCs are considered to be the basic symptoms present in mammograms for breast cancer diagnosis. Therefore, the accurate detection of MCs is mandatory for the on-time diagnosis, effective treatment and reduction of mortality rates due to breast cancer. Mammogram analysis and interpretation is a challenging task, and there are many obstructions to the accurate detection of MCs such as small and non-uniform shape and size of the MCs clusters in addition to low contrast quality of MCs as compared to the rest of the tissue. These shortcomings of manual interpretation of MCs raise the need for an automatic detection system to assist radiologists in mammogram analysis. In this study, an automated system has been developed to minimize the manual inference and diagnose breast cancer with good precision. In this paper, we propose a two-fold detection algorithm. In the first stage, all suspicious regions from the mammogram are segmented out. In the next stage, these suspected regions are fed to a classifier which then detects whether the region was normal, benign or malignant. We compared the performance of a Neural Network classifier with Adaboost. ANN classifier shows more sensitivity and specificity but less accuracy as compared to Adaboost for tested images. Overall results show that the developed algorithm is able to achieve high accuracy and efficiency for the detection and diagnosis of breast cancer lesions for images from two different databases used, and also for mammograms obtained from a local hospital.ConclusionThe suggested algorithm was tested for DDSM, MIAS and local database and showed high level of overall accuracy (98.68%) and sensitivity (80.15%)

IL7R is associated with CNS infiltration and relapse in pediatric B-cell precursor acute lymphoblastic leukemia

No abstract available

Reconstruction of head-to-knee voxel model for Syrian adult male of average height and weight

Purpose: This study embodies the reconstruction of head to knee voxel model, named “SyrMan”, of an adult living Syrian male of average height and weight. This model contains main organs of one adult man representing the average of a group of adult males (25–50) years. SyrMan model was reconstructed to be used for Monte Carlo simulations to calculate dosimetric quantities for radiation protection and medical purposes. Method: The model was reconstructed from segmented CT images of a living volunteer who was 33 year-old, 172 cm in height, and 75 kg in weight. Masses of segmented organs were calculated and compared with previously published models. Results: Specific Absorbed Fractions (SAFs) were calculated and tabulated for each considered source organ. Comparison of SAF values was carried out with Zubal model where some significant differences were found due to differences in organ masses and in anatomy between both models. Conclusion: Comparisons with SAFs data of Zubal model accentuated the fact that the organ masses and the specific anatomy have a significant effect on SAFs. SyrMan model can be considered as the first model built in the Middle East region, and it is an important step toward the Syrian Reference Man

PI3K-Mediated Blimp-1 Activation Controls B Cell Selection and Homeostasis

Summary: Activation of phosphoinositide 3-kinase (PI3K) signaling plays a central role in regulating proliferation and survival of B cells. Here, we tested the hypothesis that B cell receptor (BCR)-mediated activation of PI3K induces the terminal differentiation factor Blimp-1 that interferes with proliferation and survival, thereby controlling the expansion of activated B cells. In fact, B-cell-specific inactivation of Pten, the negative regulator of PI3K signaling, leads to deregulated PI3K activity and elevated Blimp-1 expression. Combined deficiency for Pten and Blimp-1 results in abnormal expansion of B-1 B cells and splenomegaly. Interestingly, Blimp-1 also acts at early stages of B cell development to regulate B cell selection, as Blimp-1 deficiency results in an increased proportion of autoreactive B cells. Together, our data suggest that the combined requirement of deregulated PI3K signaling in addition to defective terminal differentiation represents the basis for proper selection and expansion of developing B cells. : Setz et al. show that BCR-mediated activation of PI3K induces the terminal differentiation factor Blimp-1 that interferes with cell cycling and survival, thereby preventing the expansion of activated B cells. Thus, the interplay between PI3K activity and regulation of terminal differentiation determines proper selection and expansion of developing B cells. Keywords: autoreactivity, proliferation, B cell development, selection, editing, clonal deletion differentiation, Pten, Blimp-

Pten controls B‐cell responsiveness and germinal center reaction by regulating the expression of IgD BCR

In contrast to other B-cell antigen receptor (BCR) classes, the function of IgD BCR on mature B cells remains largely elusive as mature B cells co-express IgM, which is sufficient for development, survival, and activation of B cells. Here, we show that IgD expression is regulated by the forkhead box transcription factor FoxO1, thereby shifting the responsiveness of mature B cells towards recognition of multivalent antigen. FoxO1 is repressed by phosphoinositide 3-kinase (PI3K) signaling and requires the lipid phosphatase Pten for its activation. Consequently, Pten-deficient B cells expressing knock-ins for BCR heavy and light chain genes are unable to upregulate IgD. Furthermore, in the presence of autoantigen, Pten-deficient B cells cannot eliminate the autoreactive BCR specificity by secondary light chain gene recombination. Instead, Pten-deficient B cells downregulate BCR expression and become unresponsive to further BCR-mediated stimulation. Notably, we observed a delayed germinal center (GC) reaction by IgD-deficient B cells after immunization with trinitrophenyl-ovalbumin (TNP-Ova), a commonly used antigen for T-cell-dependent antibody responses. Together, our data suggest that the activation of IgD expression by Pten/FoxO1 results in mature B cells that are selectively responsive to multivalent antigen and are capable of initiating rapid GC reactions and T-cell-dependent antibody responses.peerReviewe

Synergism between IL7R and CXCR4 drives BCR-ABL induced transformation in Philadelphia chromosome-positive acute lymphoblastic leukemia

Emergence of ABL1 kinase inhibitor resistant clones may cause disease relapse in Philadelphia chromosome-positive acute lymphoblastic leukemia. Here, the authors show interleukin 7 receptor (IL7R) signaling to contribute to this resistance mechanism, and that targeting the IL7R pathway may suppress incurable drug-resistant leukemia forms

The Small GTPase RHOA Links SLP65 Activation to PTEN Function in Pre B Cells and Is Essential for the Generation and Survival of Normal and Malignant B Cells

The generation, differentiation, survival and activation of B cells are coordinated by signals emerging from the B cell antigen receptor (BCR) or its precursor, the pre-BCR. The adaptor protein SLP65 (also known as BLNK) is an important signaling factor that controls pre-B cell differentiation by down-regulation of PI3K signaling. Here, we investigated the mechanism by which SLP65 interferes with PI3K signaling. We found that SLP65 induces the activity of the small GTPase RHOA, which activates PTEN, a negative regulator of PI3K signaling, by enabling its translocation to the plasma membrane. The essential role of RHOA is confirmed by the complete block in early B cell development in conditional RhoA-deficient mice. The RhoA-deficient progenitor B cells showed defects in activation of immunoglobulin gene rearrangement and fail to survive both in vitro and in vivo. Reconstituting the RhoA-deficient cells with RhoA or Foxo1, a transcription factor repressed by PI3K signaling and activated by PTEN, completely restores the survival defect. However, the defect in differentiation can only be restored by RhoA suggesting a unique role for RHOA in B cell generation and selection. In full agreement, conditional RhoA-deficient mice develop increased amounts of autoreactive antibodies with age. RHOA function is also required at later stage, as inactivation of RhoA in peripheral B cells or in a transformed mature B cell line resulted in cell loss. Together, these data show that RHOA is the key signaling factor for B cell development and function by providing a crucial SLP65-activated link between BCR signaling and activation of PTEN. Moreover, the identified essential role of RHOA for the survival of transformed B cells offers the opportunity for targeting B cell malignancies by blocking RHOA function