Refractory corticotroph adenomas

Abstract

The majority of corticotroph adenomas are benign but some are locally invasive, demonstrate high rates of recurrence, and exhibit a relatively poor response to often repeated surgical, medical, and radiation treatment. Herein, we summarize the currently known somatic and genetic mutations and other molecular factors that influence the pathogenesis of these tumors and discuss currently available therapies. Although recent molecular studies have advanced our understanding of the pathogenesis and behavior of these refractory corticotroph adenomas, these insights do not reliably guide treatment choices at present. Development of additional diagnostic tools and novel tumor-directed therapies that offer efficacious treatment choices for patients with refractory corticotroph adenomas are needed.

Investigating cellular similarities and differences between upper tract urothelial carcinoma and bladder urothelial carcinoma using single-cell sequencing

“…DEGs between UTUC and BLCA-derived M1 macrophages identified 281 upregulated DEGs and 298 downregulated DEGs. Upregulated DEGs included chemokines (CXCL16, CCL2, CCL3, CCL4L2, and CCL4) and cytoskeleton-associated genes (ACTB, TUBB, DYNLL1, RACK1, and PFN1) ( Supplementary Figure 2E ) ( 50 , 51 ), highlighting distinct immune modulatory and migratory capabilities between these two diseases.…”

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“…DEGs between UTUC and BLCA-derived M1 macrophages identified 281 upregulated DEGs and 298 downregulated DEGs. Upregulated DEGs included chemokines (CXCL16, CCL2, CCL3, CCL4L2, and CCL4) and cytoskeleton-associated genes (ACTB, TUBB, DYNLL1, RACK1, and PFN1) (Supplementary Figure 2E) (50,51), highlighting distinct immune modulatory and migratory capabilities between these two diseases.…”

Image_4.tif

“…DEGs between UTUC and BLCA-derived M1 macrophages identified 281 upregulated DEGs and 298 downregulated DEGs. Upregulated DEGs included chemokines (CXCL16, CCL2, CCL3, CCL4L2, and CCL4) and cytoskeleton-associated genes (ACTB, TUBB, DYNLL1, RACK1, and PFN1) (Supplementary Figure 2E) (50,51), highlighting distinct immune modulatory and migratory capabilities between these two diseases.…”