For the differentiation of the subtypes of renal cell carcinoma, degree of enhancement is the most valuable parameter; enhancement pattern, the presence or absence of calcification, and tumor-spreading patterns can serve supplemental roles in the identification of the subtype of renal cell carcinoma.
Ovarian teratomas can be associated with various complications and demonstrate a wide spectrum of clinical and imaging features. The complications include torsion (16% of ovarian teratomas), rupture (1%-4%), malignant transformation (1%-2%), infection (1%), and autoimmune hemolytic anemia (<1%). These complications require different therapeutic strategies; therefore, timely and accurate diagnosis of these complications is important for optimal patient treatment. In cases of complicated ovarian teratomas, the clinical manifestations provide only limited information and often overlap with those of other diseases. Furthermore, ovarian teratomas may have unusual clinical and imaging manifestations, thereby leading to misdiagnosis. These unusual manifestations include immature teratomas, monodermal teratomas (struma ovarii), combination tumors and collision tumors containing teratomas, and mature cystic teratomas without demonstrable fat or with pure fatty components. To provide adequate treatment and prevent misdiagnosis, it is necessary to be familiar with the imaging findings of both the complications and the unusual manifestations of ovarian teratomas.
PurposeInactivation of TP53, which occurs predominantly by missense mutations in exons 4–9, is a major genetic alteration in a subset of human cancer. In spite of growing evidence that gain-of-function (GOF) mutations of p53 also have oncogenic activity, little is known about the clinical relevance of these mutations.MethodsThe clinicopathological features of high-grade serous ovarian carcinoma (HGS-OvCa) patients with GOF p53 mutations were evaluated according to a comprehensive somatic mutation profile comprised of whole exome sequencing, mRNA expression, and protein expression profiles obtained from the Cancer Genome Atlas (TCGA).ResultsPatients with a mutant p53 protein (mutp53) with a GOF mutation showed higher p53 mRNA and protein expression levels than patients with p53 mutation with no evidence of GOF (NE-GOF). GOF mutations were more likely to occur within mutational hotspots, and at CpG sites, and resulted in mutp53 with higher functional severity (FS) scores. Clinically, patients with GOF mutations showed a higher frequency of platinum resistance (22/58, 37.9%) than patients with NE-GOF mutations (12/56, 21.4%) (p=0.054). Furthermore, patients with GOF mutations were more likely to develop distant metastasis (36/55, 65.5%) than local recurrence (19/55, 34.5%), whereas patients with NE-GOF mutations showed a higher frequency of locoregional recurrence (26/47, 55.3%) than distant metastasis (21/47, 44.7%) (p=0.035). There were no differences in overall or progression-free survival between patients with GOF or NE-GOF mutp53.ConclusionThis study demonstrates that patient with GOF mutp53 is characterized by a greater likelihood of platinum treatment resistance and distant metastatic properties in HGS-OvCa.
Upregulation of granzyme B in CD8(+) and non-CD8(+) cells is an early phenomenon of small airway wall remodelling in centrilobular emphysema and suggests its possible role in the pathogenesis of COPD.
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