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Non-alcoholic fatty liver disease (NAFLD) is the most prevalent liver disorder worldwide. It comprises a spectrum of conditions that range from steatosis to non-alcoholic steatohepatitis, with progression to cirrhosis and hepatocellular carcinoma. Currently, there is no FDA-approved pharmacological treatment for NAFLD. The pathogenesis of NAFLD involves genetic and environmental/host factors, including those that cause changes in intestinal microbiota and their metabolites. In this review, we discuss recent findings on the relationship(s) of microbiota signature with severity of NAFLD and the role(s) microbial metabolites in NAFLD progression. We discuss how metabolites may affect NAFLD progression and their potential to serve as biomarkers for NAFLD diagnosis or therapeutic targets for disease management.

Lutetium Lu-177 dotatate is the first peptide receptor radionuclide therapy approved by the US Food and Drug Administration. Well-designed studies in Europe have shown dramatic effectiveness in improving progression-free survival in patients with gastroenteropancreatic neuroendocrine tumors, which are progressive and generally metastatic. This therapy is a molecular targeted therapy linking a beta-emitting radioisotope to dotatate, which binds tightly to somatostatin receptors on neuroendocrine tumors cells. Various adverse effects of this therapy have been reported in the literature, including potential toxicity to renal, hepatic, and hematologic tissues and risk of second malignancy. read more Our study sought to explore acute adverse effects in this patient population.

We tracked adverse effects and patient experience in our first year of therapy experience with this new agent.

In our first 12 patients who received Lutetium Lu-177 dotatate, tumor flare reactions occurred in 5 patients due to worsening symptoms of bone or soft tissue metastasis. This flare reaction can be mitigated with short course of corticosteroid therapy or other strategies.

Flare reaction is common in patients with progressive metastatic gastroenteropancreatic neuroendocrine tumors and can be managed successfully with several strategies.

Flare reaction is common in patients with progressive metastatic gastroenteropancreatic neuroendocrine tumors and can be managed successfully with several strategies.

To provide an overview of the major randomized trials that support the use of hypofractionated post-mastectomy radiation therapy for locally advanced breast cancer patients.

PubMed was systematically reviewed for publications reporting use of of hypofractionated radiation therapy in patients requiring post-mastectomy radiation.

Standard fractionation, which is typically delivered over 5 to 7 weeks, is considered the standard of care in setting of post-mastectomy radiation therapy (PMRT). Modern data has helped to establish hypofractionated whole breast irradiation, which consists of a 3- to 4-week regimen, as a new standard of care for early-stage breast cancer. Hypofractionated whole breast irradiation has also laid the groundwork for the exploration of a hypofractionated approach in the setting of hypofractionated post-mastectomy radiation therapy.

While standard fractionation remains the most commonly utilized regimen for PMRT, recently published trials support the safety and efficacy of a hypofractionated approach. Ongoing trials are further investigating the use of hypofractionated PMRT.

While standard fractionation remains the most commonly utilized regimen for PMRT, recently published trials support the safety and efficacy of a hypofractionated approach. Ongoing trials are further investigating the use of hypofractionated PMRT.

This study aimed to investigate intra- and interfraction motion during liver stereotactic body radiation therapy for the purpose of planning target volume (PTV) margin estimation, comparing deep inspiration breath hold (DIBH) and deep expiration breath hold (DEBH).

Pre- and posttreatment kV cone beam computed tomography (CT) images were acquired for patients with liver cancer who were treated using stereotactic body radiation therapy with DIBH or DEBH. A total of 188 images were analyzed from 18 patients. Positioning errors were determined based on a comparison with planning CT images and matching to the liver. Treatment did not proceed until errors were ≤3 mm. Standard deviations of random and systematic errors resulting from this image matching process were used to calculate PTV margin estimates.

DIBH errors are generally larger than DEBH errors, especially in the anterior-posterior and superior-inferior directions. Posttreatment errors tend to be larger than pretreatment errors, especially for DIBH. Standard deviations of random errors are larger than those of systematic errors. Considering both pre- and posttreatment cone beam CT images, PTV margins for DIBH and DEBH are estimated as anterior-posterior, superior-inferior, right-left = (5.7, 6.3, 3.0) mm and (3.1, 3.4, 2.8) mm, respectively.

This study suggests that DEBH results in more reproducible target positioning, which could in turn justify the use of smaller PTV margins.

This study suggests that DEBH results in more reproducible target positioning, which could in turn justify the use of smaller PTV margins.The main treatment modalities for localized prostate cancer are surgery and radiation. Surgery removes the whole prostate gland, whereas with radiation therapy the irradiated prostate remains within the patient's body. Biomarkers specific to the prostate gland should become undetectable after surgery, but this is not the case when radiation therapy is used, as residual prostate cells may still be metabolically active. Here, we review the role of tumor markers of toxicity and response to radiation therapy in patients with prostate cancer, including prostate specific antigen, human kallikrein 2, osteopontin, prostate cancer associated 3, citrulline, and others.

Preclinical and clinical data indicate that radiation therapy acts as an immune modifier, having both immune-stimulatory and immunosuppressive effects on the tumor-immune microenvironment (TIME). 3.3'-diindolylmethane (DIM) sensitizes tumor cells to radiation and protects mice from lethal doses of total body irradiation. We hypothesize that protecting nontumoral cells from the adverse effects of radiation treatment (RT) may help to correct immunosuppression resulting from radiation.

We generated tumor graft models using immune-competent and immune-deficient mouse strains. Narrow-beamed radiation was targeted to tumor sites using shielding. Tumor regression was monitored after DIM and RT versus RT alone. The effects of DIM on the efficacy of RT were assessed using immunohistochemistry staining and gene expression profiling. Complete blood counts, clonogenic cell survival assays, and global gene expression profiling of cultured cells were performed to study DIM's radioprotective effects on normal cells.

DIM enhanced tumor regression after RT in immune-competent but not immune-deficient mice.

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