Low-dose involved-field radiation in the treatment of non-hodgkin lymphoma: predictors of response and treatment failure.

Purpose: To investigate clinical and pathologic factors significant in predicting local response and time to further treatment after low-dose involved-field radiation therapy (LD-IFRT) for non-Hodgkin lymphoma (NHL).

Methods And Materials: Records of NHL patients treated at a single institution between April 2004 and September 2011 were retrospectively reviewed. Low-dose involved-field radiation therapy was given as 4 Gy in 2 fractions over 2 consecutive days.

Atypical metastases from prostate cancer: 10-year experience at a single institution.

Objective: The purpose of the study was to retrospectively review the frequency, sites, and patterns of atypical metastases from prostate cancer and to determine whether any correlation exists between the atypical sites and biochemical or histologic variables.

Materials And Methods: All available imaging studies of 620 consecutive patients with biopsy-proven prostate carcinoma seen at our institute between 1999 and 2009 were reviewed. Eighty-two patients (mean age, 72 years; age range, 58-87 years) with atypical sites of metastases were identified.

Interrogation of inhibitor of nuclear factor κB α/nuclear factor κB (IκBα/NF-κB) negative feedback loop dynamics: from single cells to live animals in vivo.

Full understanding of the biological significance of negative feedback processes requires interrogation at multiple scales as follows: in single cells, cell populations, and live animals in vivo. The transcriptionally coupled IκBα/NF-κB negative feedback loop, a pivotal regulatory node of innate immunity and inflammation, represents a model system for multiscalar reporters. Using a κB(5)→IκBα-FLuc bioluminescent reporter, we rigorously evaluated the dynamics of ΙκBα degradation and subsequent NF-κB transcriptional activity in response to diverse modes of TNFα stimulation.

PLAGL2 regulates Wnt signaling to impede differentiation in neural stem cells and gliomas.

A hallmark feature of glioblastoma is its strong self-renewal potential and immature differentiation state, which contributes to its plasticity and therapeutic resistance. Here, integrated genomic and biological analyses identified PLAGL2 as a potent protooncogene targeted for amplification/gain in malignant gliomas. Enhanced PLAGL2 expression strongly suppresses neural stem cell (NSC) and glioma-initiating cell differentiation while promoting their self-renewal capacity upon differentiation induction.

Identification of a ligand-induced transient refractory period in nuclear factor-kappaB signaling.

In response to a variety of extracellular ligands, nuclear factor-kappaB (NF-kappaB) signaling regulates inflammation, cell proliferation, and apoptosis. It is likely that cells are not continuously exposed to stimulating ligands in vivo but rather experience transient pulses. To study the temporal regulation of NF-kappaB and its major regulator, inhibitor of NF-kappaBalpha (IkappaBalpha), in real time, we utilized a novel transcriptionally coupled IkappaBalpha-firefly luciferase fusion reporter and characterized the dynamics and responsiveness of IkappaBalpha processing upon a short 30-s pulse of tumor necrosis factor alpha (TNFalpha) or a continuous challenge of TNFalpha following a 30-s preconditioning pulse.

A proteasomal stress response: pre-treatment with proteasome inhibitors increases proteasome activity and reduces neuronal vulnerability to oxidative injury.

We report here that exposure to low concentrations of proteasome inhibitors (e.g. 10-100 nm MG-132, 0.