The Internet of Things (IoT) opens opportunities for wearable devices, home appliances, and software to share and communicate information on the Internet. Given that the shared data contains a large amount of private information, preserving information security on the shared data is an important issue that cannot be neglected. In this paper, we begin with general information security background of IoT and continue on with information security related challenges that IoT will encountered. Finally, we will also point out research directions that could be the future work for the solutions to the security challenges that IoT encounters.

Rhabdoid tumors are aggressive pediatric malignancies for which, currently, there are no effective or standard treatment strategies. Rhabdoid tumors arise because of the loss of the tumor suppressor gene INI1. We have previously demonstrated that INI1 represses Cyclin D1 transcription in rhabdoid cells by directly recruiting histone deacetylase 1 complex to its promoter, leading to G 0-G1 arrest. Expression of Cyclin D1 overcomes cell cycle arrest mediated by INI1 and Cyclin D1 overexpression in human rhabdoid tumors is a common phenomenon. However, it is not clear whether Cyclin D1 is a critical downstream target of INI1 in vivo and whether the derepression of this gene is essential for rhabdoid tumorigenesis. To determine the requirement of Cyclin D1 for genesis of rhabdoid tumors in vivo, we developed Ini1 heterozygous mice by targeted disruption. We found that the tumors developed in these Ini1؉͞؊ mice are rhabdoid, defective for Ini1 protein, and like the human tumors, express Cyclin D1. We crossed Ini1؉͞؊ mice to Cyclin D1؊͞؊ mice and found that Ini1؉͞؊ mice with Cyclin D1 deficiency did not develop any spontaneous tumors, in contrast to the parental Ini1؉͞؊ mice. These results strongly support the hypothesis that Cyclin D1 is a key mediator in the genesis of rhabdoid tumors. Our results provide an in vivo proof of concept that drugs that target Cyclin D1 expression or activity could be potentially effective as novel therapeutic agents for rhabdoid tumors.INI1͞hSNF5 ͉ cell cycle ͉ atypical teratoid ͉ tumorigenesis R habdoid tumors, including malignant rhabdoid tumors of the kidneys (MRT) and atypical teratoid and rhabdoid tumors (AT͞RT) of the brain and soft tissues, are highly aggressive pediatric malignancies (1-3). Prognosis for infants with these tumors is poor and Ϸ80% of the children die within 1 yr of diagnosis despite intensive treatment. Chemotherapy is effective only transiently in some AT͞RT patients and the use of radiotherapy is limited in children under 3 yr of age because of subsequent neurological damage and because surgical resection is challenging (3). In the past several years, there has been significant progress in the cytogenetic and molecular genetic studies, which indicated that the majority of MRT and AT͞RT tumors harbor recurrent biallelic alterations in the INI1͞hSNF5 gene, located in chromosome 22q11.2 (4-6). Several studies support the model that INI1 is a tumor suppressor. Children who harbor germ-line constitutive mutation in one allele of INI1 develop MRT or AT͞RT when the second allele of INI1 is also mutated (5), and families who are carriers of a mutation in this gene are predisposed to rhabdoid syndrome (7). Furthermore, mice heterozygous for Ini1͞hSNF5 mutations develop rhabdoid tumors with a high frequency because of loss of heterozygosity at the Ini1 locus (8-10).INI1͞hSNF5 is a component of the chromatin-remodeling mammalian SWI͞SNF complex (11). Reintroduction of this gene into rhabdoid cell lines causes G 0 -G 1 arrest and affects the transcription of several cell c...

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alphaE2 is an effective agent for inhibition of DHT-induced PSA, cyclin A, cyclin D1 gene expression, and cell proliferation in LAPC-4 cells, and tumor growth in LAPC-4 xenograft mice.