A Virtual Wiretap Channel for Secure MessageTransmission

In the Wyner wiretap channel, a sender is connected to a receiver and an eavesdropper through two noisy channels. It has been shown that if the noise in the eavesdropper channel is higher than the receiver\u27s channel, information theoretically secure communication from Alice to Bob, without requiring a shared key, is possible. The approach is particularly attractive noting the rise of quantum computers and possibility of the complete collapse of today\u27s’ cryptographic infrastructure. If the eavesdropper’s channel is noise free, however, no secrecy can be obtained. The iJam protocol, proposed by Gollakota and Katabi, is an interactive protocol over noise free channels that uses friendly jamming the receiver to establish an information theoretically secure shared key between the sender and the receiver. The protocol relies on the Basic iJam Transmission Protocol (BiT protocol) that uses properties of OFDM (Orthogonal Frequency-Division Multiplexing) to create uncertainty for Eve (hence noisy view) in receiving the sent information, and use this uncertainty to construct a secure key agreement protocol. The protocol has been implemented and evaluated using extensive experiments that examine the best eavesdropper’s reception strategy. In this paper, we develop an abstract model for BiT protocol as a wiretap channel and refer to it as a virtual wiretap channel. We estimate parameters of this virtual wiretap channel, derive the secrecy capacity of this channel and design a secure message transmission protocol with provable semantic security using the channel. Our analysis and protocol give a physical layer security protocol, with provable security, that is implementable in practice (BiT protocol has already been implemented)

Molecular Genetic Characterization of Acute Lymphoblastic Leukemia with a Poor Prognosis

Acute lymphoblastic leukemia (ALL) affects individuals at all ages, with peak incidences in children 50 years. ALL is broadly categorized into B-cell precursor (BCP) and T-cell ALL with specific clinical features associated with outcome. In contrast to pediatric ALL, which has a favorable prognosis, adult ALL is associated with a much poorer outcome with less than 40% overall survival rates, decreasing with higher age. The presence of specific acquired genetic abnormalities is important for diagnosis, prognostication, and treatment stratification. ALL can be further categorized into subgroups defined by structural or ploidy abnormalities. One such subgroup, hypodiploid ALL (79 chromosomes, showing a possible hypodiploid origin due to the extensive loss of heterozygosity identified in such cases. That all three cases harbored TP53 mutations emphasized similarities to low hypodiploid ALL. In conclusion, screening for specific genetic abnormalities routinely in the clinic may improve prognostication and treatment stratification in cases with a poor prognosis

Near-haploid and low hypodiploid acute lymphoblastic leukemia - two distinct subtypes but consistently poor prognosis

Hypodiploidy <40 chromosomes is an uncommon genetic feature of acute lymphoblastic leukemia (ALL) in both children and adults. It has long been clear by cytogenetic analyses, and recently confirmed by mutational profiling, that these cases may be further subdivided into two subtypes: near-haploid ALL with 24-30 chromosomes and low hypodiploid ALL with 31-39 chromosomes. Both groups are associated with a very poor prognosis and these patients are among those who could benefit most from novel treatments

Novel gene targets detected by genomic profiling in a consecutive series of 126 adults with acute lymphoblastic leukemia

In contrast to acute lymphoblastic leukemia in children, adult cases of this disease are associated with a very poor prognosis. In order to ascertain whether the frequencies and patterns of submicroscopic changes, identifiable with single nucleotide polymorphism array analysis, differ between childhood and adult acute lymphoblastic leukemia, we performed single nucleotide polymorphism array analyses of 126 adult cases, the largest series to date, including 18 paired diagnostic and relapse samples. Apart from identifying characteristic microdeletions of the CDKN2A, EBF1, ETV6, IKZF1, PAX5 and RB1 genes, the present study uncovered novel, focal deletions of the BCAT1, BTLA, NR3C1, PIK3AP1 and SERP2 genes in 2-6% of the adult cases. IKZF1 deletions were associated with B-cell precursor acute lymphoblastic leukemia (P=0.036), BCR-ABL1-positive acute lymphoblastic leukemia (P<0.001), and higher white blood cell counts (P=0.005). In addition, recurrent deletions of RASSF3 and TOX were seen in relapse samples. Comparing paired diagnostic/relapse samples revealed identical changes at diagnosis and relapse in 27%, clonal evolution in 22%, and relapses evolving from ancestral clones in 50%, akin to what has previously been reported in pediatric acute lymphoblastic leukemia and indicating that the mechanisms of relapse may be similar in adult and childhood cases. These findings provide novel insights into the leukemogenesis of adult acute lymphoblastic leukemia, showing similarities to childhood disease in the pattern of deletions and the clonal relationship between diagnostic and relapse samples, but with the adult cases harboring additional aberrations that have not been described in pediatric acute lymphoblastic leukemia

Genetic and epigenetic characterization of hypodiploid acute lymphoblastic leukemia

Purpose: To investigate the genetic and epigenetic landscape of hypodiploid (&amp;lt;45 chromosomes) acute lymphoblastic leukemia (ALL). Methods: Single nucleotide polymorphism array, whole exome sequencing, RNA sequencing, and methylation array analyses were performed on eleven hypodiploid ALL cases. Results: In line with previous studies, mutations in IKZF3 and FLT3 were detected in near-haploid (25-30 chromosomes) cases. Low hypodiploidy (31-39 chromosomes) was associated with somatic TP53 mutations. Notably, mutations of this gene were also found in 3/3 high hypodiploid (40-44 chromosomes) cases, suggesting that the mutational patterns are similar in low hypodiploid and high hypodiploid ALL. The high hypodiploid ALLs frequently displayed substantial cell-to-cell variability in chromosomal content, indicative of chromosomal instability; a rare phenomenon in ALL. Gene expression analysis showed that genes on heterodisomic chromosomes were more highly expressed in hypodiploid cases. Cases clustered according to hypodiploid subtype in the unsupervised methylation analyses, but there was no association between chromosomal copy number and methylation levels. A comparison between samples obtained at diagnosis and relapse showed that the relapse did not arise from the major diagnostic clone in 3/4 cases. Conclusion: Taken together, our data support the conclusion that near-haploid and low hypodiploid ALL are different with regard to mutational profiles and also suggest that ALL cases with high hypodiploidy may harbor chromosomal instability.Funding Agencies|Swedish Cancer Society; Swedish Childhood Cancer Foundation; Ellen Bachrachs foundation; Swedish Research Council</p