Spectrum of imaging findings in hyperplastic cholecystosis and potential mimics.

Adenomyomatosis and cholesterolosis of the gallbladder, collectively termed hyperplastic cholecystosis, are commonly encountered incidental findings on imaging studies performed for a variety of indications including biliary colic or nonspecific abdominal pain. These pathologies are rarely the source of symptoms, generally considered benign and do not require further work-up. However, their imaging characteristics can overlap with more sinister conditions that should not be missed. In this review, the imaging findings of adenomyomatosis and cholesterolosis will be reviewed followed by other gallbladder pathologies that might mimic these conditions radiologically. Important differentiating factors will be discussed that can aid the radiologist in making a more confident imaging diagnosis.

Advanced MRI Protocols to Discriminate Glioma From Treatment Effects: State of the Art and Future Directions.

In the follow-up treatment of high-grade gliomas (HGGs), differentiating true tumor progression from treatment-related effects, such as pseudoprogression and radiation necrosis, presents an ongoing clinical challenge. Conventional MRI with and without intravenous contrast serves as the clinical benchmark for the posttreatment surveillance imaging of HGG. However, many advanced imaging techniques have shown promise in helping better delineate the findings in indeterminate scenarios, as posttreatment effects can often mimic true tumor progression on conventional imaging. These challenges are further confounded by the histologic admixture that can commonly occur between tumor growth and treatment-related effects within the posttreatment bed. This review discusses the current practices in the surveillance imaging of HGG and the role of advanced imaging techniques, including perfusion MRI and metabolic MRI.

CRY1-CBS binding regulates circadian clock function and metabolism.

Circadian disruption influences metabolic health. Metabolism modulates circadian function. However, the mechanisms coupling circadian rhythms and metabolism remain poorly understood. Here, we report that cystathionine ß-synthase (CBS), a central enzyme in one-carbon metabolism, functionally interacts with the core circadian protein cryptochrome 1 (CRY1). In cells, CBS augments CRY1-mediated repression of the CLOCK/BMAL1 complex and shortens circadian period. Notably, we find that mutant CBS-I278T protein, the most common cause of homocystinuria, does not bind CRY1 or regulate its repressor activity. Transgenic CbsZn/Zn  mice, while maintaining circadian locomotor activity period, exhibit reduced circadian power and increased expression of E-BOX outputs. CBS function is reciprocally influenced by CRY1 binding. CRY1 modulates enzymatic activity of the CBS. Liver extracts from Cry1-/- mice show reduced CBS activity that normalizes after the addition of exogenous wild-type (WT) CRY1. Metabolomic analysis of WT, CbsZn/Zn , Cry1-/- , and Cry2-/- samples highlights the metabolic importance of endogenous CRY1. We observed temporal variation in one-carbon and transsulfuration pathways attributable to CRY1-induced CBS activation. CBS-CRY1 binding provides a post-translational switch to modulate cellular circadian physiology and metabolic control.

Identification of Bladder Diverticular Stone on 99mTc-Methyl Diphosphonate Bone Scintigraphy and SPECT/CT.

We report a bladder diverticular stone with increased 99mTc-methyl diphosphonate uptake on bone scintigraphy and SPECT/CT. Diverticular stone is a known risk factor for bladder malignancy. The deposition of 99mTc-methyl diphosphonate on the crystal surface of the diverticular stone is a rare phenomenon but of clinical significance. Cystolitholapaxy is indicated to remove the diverticular stone and to reduce the risk of bladder cancer.

Adrenal Tumors Found During Staging and Surveillance for Colorectal Cancer: Benign Incidentalomas or Metastatic Disease?

OBJECTIVE: To evaluate the incidence of adrenal metastases in patient with colorectal cancer (CRC) and determine the clinical and radiographic features associated metastatic CRC to the adrenal glands. MATERIALS AND METHODS: The review of consecutive adults with newly diagnosed CRC found to have adrenal tumors > 1 cm in size on staging or surveillance CT scans with at least two scans to evaluate progression or stability of disease. RESULTS: Fifty-eight of 856 (6.8%) CRC patients had an adrenal tumor. Forty-three patients (74%) with 46 adrenal tumors had benign adrenal tumors, and 15 (26%) patients with 17 adrenal tumors had metastatic disease. On univariate analysis, patients with metastatic CRC had larger adrenal tumors (26.7 mm vs 12.4 mm, p < 0.01), a higher mean CEA (239 ng/mL vs 14.2 ng/mL, p = 0.03), and were more likely to have other sites of metastatic disease seen on imaging 8/43 (19%) vs 14/15 (93%), p < 0.01. On multivariable analysis, adrenal tumor size > 1.8 cm (OR 49.6 CI 8-306), CEA > 2.5 ng/mL (OR 15.8 CI 1.7-144) and other metastatic disease seen on imaging (OR 68.1 CI 7-661) were independently associated with adrenal metastases. CONCLUSION: CRC patients with small adrenal tumors, normal CEA levels and no evidence of other metastatic disease are unlikely to have spread to the adrenal glands. Adrenal tumors found during staging and surveillance of CRC patients should be evaluated with appropriate imaging and biochemical analysis.

Targeting glutamine metabolism slows soft tissue sarcoma growth.

Tumour cells frequently utilize glutamine to meet bioenergetic and biosynthetic demands of rapid cell growth. However, glutamine dependence can be highly variable between in vitro and in vivo settings, based on surrounding microenvironments and complex adaptive responses to glutamine deprivation. Soft tissue sarcomas (STSs) are mesenchymal tumours where cytotoxic chemotherapy remains the primary approach for metastatic or unresectable disease. Therefore, it is critical to identify alternate therapies to improve patient outcomes. Using autochthonous STS murine models and unbiased metabolomics, we demonstrate that glutamine metabolism supports sarcomagenesis. STS subtypes expressing elevated glutaminase (GLS) levels are highly sensitive to glutamine starvation. In contrast to previous studies, treatment of autochthonous tumour-bearing animals with Telaglenastat (CB-839), an orally bioavailable GLS inhibitor, successfully inhibits undifferentiated pleomorphic sarcoma (UPS) tumour growth. We reveal glutamine metabolism as critical for sarcomagenesis, with CB-839 exhibiting potent therapeutic potential.

Differences in Growth Rate on CT of Adrenal Adenomas and Malignant Adrenal Nodules.

OBJECTIVE. The purpose of this study is to determine the differences in growth rate of adrenal adenomas and malignant adrenal nodules. MATERIALS AND METHODS. This was a retrospective review of adults with an adrenal nodule seen at two different abdominal or chest CT examinations or PET/CT examinations. Patients in the adenoma group were included if they had a CT, MRI, or pathologic diagnosis of an adrenal adenoma. Patients in the malignant group were included if they had a pathologically proven malignant adrenal nodule. Nodule growth was defined as a change in the largest axial diameter greater than or equal to 3 mm. Growth rate was calculated by dividing the change in the longest axial diameter by the time between the first and last imaging examination. RESULTS. There were 105 adenomas and 26 malignant nodules. Of the 105 adenomas, 34 (32.4%; 95% CI, 23.6-42.2%) grew, three (2.9%; 95% CI, 0.6-8.1%) became smaller, and 68 (64.8%; 95% CI, 54.8-73.8%), were unchanged in size. All 26 (100%; 95% CI, 89.1-100%) malignant nodules grew. The mean (± SD) growth rate of adenomas was 1.0 ± 0.67 mm/year (range, 0.3-2.8 mm/year), compared with 58.4 ± 78.5 mm/year (range, 5.8-395.4 mm/year) for malignant nodules (p < 0.001). A growth rate of 3 mm/year distinguished adenomas from malignant nodules with a sensitivity of 100% (95% CI, 86.8-100%) and a specificity of 100% (95% CI, 96.6-100%). CONCLUSION. Approximately one-third of radiologically proven adrenal adenomas grew, all of which grew at a rate less than 3 mm/year. All malignant adrenal nodules grew, and all at a rate greater than 5 mm/year.