http://basicmed.med.ncku.edu.tw/admin/up_img/981106-1.pdf

CD4+ T Cells Regulate Pulmonary Metastasis of Mammary Carcinomas by Enhancing Protumor Properties of Macrophages

Immuno-oncology is an emerging field that has revolutionized cancer treatment Most immunomodulatory strategies focus on enhancing T cell responses, but there has been a recent surge of interest in harnessing the relatively underexplored natural killer (NK) cell compartment for therapeutic interventions NK cells show cytotoxic activity against diverse tumour cell types, and some of the clinical approaches originally developed to increase T cell cytotoxicity may also activate NK cells Moreover, increasing numbers of studies have identified novel methods for increasing NK cell antitumour immunity and expanding NK cell populations ex vivo, thereby paving the way for a new generation of anticancer immunotherapies The role of other innate lymphoid cells (group 1 innate lymphoid cell (ILC1), ILC2 and ILC3 subsets) in tumours is also being actively explored This Review provides an overview of the field and summarizes current immunotherapeutic approaches for solid tumours and haematological malignancies

Natural killer cells and other innate lymphoid cells in cancer.

Innate immune cells can constitute a substantial proportion of the cells within the tumor microenvironment and have been associated with tumor malignancy in patients and animal models of cancer; however, the mechanisms by which they modulate cancer progression are incompletely understood. Here, we show that high levels of cathepsin protease activity are induced in the majority of macrophages in the microenvironment of pancreatic islet cancers, mammary tumors, and lung metastases during malignant progression. We further show that tumor-associated macrophage (TAM)-supplied cathepsins B and S are critical for promoting pancreatic tumor growth, angiogenesis, and invasion in vivo, and markedly enhance the invasiveness of cancer cells in culture. Finally, we demonstrate that interleukin-4 (IL-4) is responsible for inducing cathepsin activity in macrophages in vitro and in vivo. Together, these data establish IL-4 as an important regulator, and cathepsin proteases as critical mediators, of the cancer-promoting functions of TAMs.

/pdf/il-4-induces-cathepsin-protease-activity-in-tumor-associated-4bt28h75b0.pdf

IL-4 induces cathepsin protease activity in tumor-associated macrophages to promote cancer growth and invasion

The discovery that the tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) can induce apoptosis of cancer cells without causing toxicity in mice has led to the in-depth study of pro-apoptotic TRAIL receptor (TRAIL-R) signalling and the development of biotherapeutic drug candidates that activate TRAIL-Rs The outcome of clinical trials with these TRAIL-R agonists has, however, been disappointing so far Recent evidence indicates that many cancers, in addition to being TRAIL resistant, use the endogenous TRAIL-TRAIL-R system to their own advantage However, novel insight on two fronts - how resistance of cancer cells to TRAIL-based pro-apoptotic therapies might be overcome, and how the pro-tumorigenic effects of endogenous TRAIL might be countered - gives reasonable hope that the TRAIL system can be harnessed to treat cancer In this Review we assess the status quo of our understanding of the biology of the TRAIL-TRAIL-R system - as well as the gaps therein - and discuss the opportunities and challenges in effectively targeting this pathway

/pdf/exploring-the-trails-less-travelled-trail-in-cancer-biology-10gpea7hru.pdf

Exploring the TRAILs less travelled: TRAIL in cancer biology and therapy

Unlike other members of the TNF superfamily, the TNF-related apoptosis-inducing ligand (TRAIL, also known as Apo2L) possesses the unique capacity to induce apoptosis selectively in cancer cells in vitro and in vivo. This exciting discovery provided the basis for the development of TRAIL-receptor agonists (TRAs), which have demonstrated robust anticancer activity in a number of preclinical studies. Subsequently initiated clinical trials testing TRAs demonstrated, on the one hand, broad tolerability but revealed, on the other, that therapeutic benefit was rather limited. Several factors that are likely to account for TRAs' sobering clinical performance have since been identified. First, because of initial concerns over potential hepatotoxicity, TRAs with relatively weak agonistic activity were selected to enter clinical trials. Second, although TRAIL can induce apoptosis in several cancer cell lines, it has now emerged that many others, and importantly, most primary cancer cells are resistant to TRAIL monotherapy. Third, so far patients enrolled in TRA-employing clinical trials were not selected for likelihood of benefitting from a TRA-comprising therapy on the basis of a valid(ated) biomarker. This review summarizes and discusses the results achieved so far in TRA-employing clinical trials in the light of these three shortcomings. By integrating recent insight on apoptotic and non-apoptotic TRAIL signaling in cancer cells, we propose approaches to introduce novel, revised TRAIL-based therapeutic concepts into the cancer clinic. These include (i) the use of recently developed highly active TRAs, (ii) the addition of efficient, but cancer-cell-selective TRAIL-sensitizing agents to overcome TRAIL resistance and (iii) employing proteomic profiling to uncover resistance mechanisms. We envisage that this shall enable the design of effective TRA-comprising therapeutic concepts for individual cancer patients in the future.

/pdf/getting-trail-back-on-track-for-cancer-therapy-2xgo2qs2df.pdf

Getting TRAIL back on track for cancer therapy

It has been observed that different IEEE 802.11 commercial cards produced by different vendors experience different performance, either when accessing alone the channel, as well as when competing against each other. These differences persist also when thorough measurement methodologies (such as RF shielding, laptop rotation, etc) are applied, and alignment of the environmental factors (same laptop models, traffic generators, etc) is carried out. This paper provides an extensive experimental characterization of the backoff operation of six commercial NIC cards. It suggests a relevant methodological approach, namely a repeatable, well defined, set of experiments, for such a characterization. Low level backoff distribution measurements are taken through a custom equipment developed in our laboratory. Our work allows to detect both a non-standard backoff behavior of some commercial cards (in terms of minimum contention window size and neglection of EIFS times), as well as potential implementation limits (in either the card hardware/firmware and/or the software driver) which appear to severely alter the card performance in challenging conditions.

Experimental Assessment of the Backoff Behavior of Commercial IEEE 802.11b Network Cards

Colorectal cancer has provided an important model to test the stem cell hypothesis of cancer origin, which implies that cancer arises as a result of genetic aberrations in stem cells leading to deregulation of the proliferation/differentiation balance. We and others have demonstrated that, similarly to other solid tumors, colon carcinogenesis and progression are dictated by highly apoptosis-resistant stem-like cells. Our data have suggested that protection from apoptosis is achieved by autocrine production of interleukin-4 (IL-4) through up-regulation of anti-apoptotic mediators. In this study, we extend our analysis to another apoptosis inhibitor widely expressed in tumors, namely survivin (also known as BIRC-5, baculoviral IAP repeat-containing protein 5). We show that this protein, with important roles in cell death counteraction and mitotic progression control, is regulated by the IL-4 pathway in colon rectal cancer stem cells (CR-CSC). Hence, the presence of IL-4 increases survivin levels in our model while cytokine neutralization has opposing effects. Treatment with cytokine neutralizing agent or with leflunomide, Stat6 inhibitor, have similar consequences on survivin localization, increasing its nuclear pool, an observation known to be correlated with a good prognosis in colon cancer patients. These results demonstrate that IL-4, through activation of the STAT-6 signaling pathway, is involved in survivin expression levels as well as its localization. These findings shed more light on the molecular mechanisms involved in IL-4-mediated chemoresistance.

Survivin is regulated by interleukin-4 in colon cancer stem cells

A hardware implementation of an adaptive noise canceller (ANC) is presented. It has been synthesized within an FPGA, using a modified version of the least mean square (LMS) error algorithm. The results obtained so far show a significant decrease of the required gate count when compared with a standard LMS implementation, while increasing the ANC bandwidth and signal to noise (S/N) ratio. This novel adaptive noise canceller is then useful for enhancing the S/N ratio of data collected from sensors (or sensor arrays) working in noisy environment, or dealing with potentially weak signals.

Efficient FPGA implementation of an adaptive noise canceller

The IEEE 802.11 DCF protocol is known to be fair in terms of long-term resource repartition among the contending stations. However, when considering real scenarios, where commercial 802.11 cards interact, very unpredictable as well as sometimes surprising behaviors emerge. Motivation of this paper is to investigate the reasons of the very evident disagreement between the theoretical IEEE 802.11 DCF protocol models and its practical implementations. In particular, we try to characterize the card behavior not only in terms of perceived throughput, but also in terms of low-level channel access operations. In fact, the simple throughput analysis does not allow to identify what affecting parameters, both in terms of transceivers architectures and MAC layer deployments, determine the performance differentiation among the cards. To this purpose, we implemented a tunable DCF network card, in which all MAC parameters are programmable and all the baseband signals are available, and we used this card as a probe instrument. We registered the low-level access operations of commercial cards in terms of access times revealed by the carrier sense function of our probe card. By comparing these times, we surprisingly proved that the most evident performance differences are not due to PHY layer issues, but to the MAC implementations, which often seem to do not respect the standard specifications.

On the fidelity of IEEE 802.11 commercial cards

A prototype of a Software Defined Radio (SDR) platform has been successfully designed and tested implementing a reconfigurable IEEE 802.11 and ZigBee receiver. The system exploits the reconfiguration capability of an FPGA for implementing a number of receiver configurations that share the same RF front-end. Configurations can be switched at run time, or can share the available logic and radio resource.

/pdf/an-fpga-based-software-defined-radio-platform-for-the-2-4ghz-30mk74b20q.pdf

An FPGA-Based Software Defined Radio Platform for the 2.4GHz ISM Band

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