Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

Small cell carcinoma of the bladder (SCCB) is a rare and aggressive variant of bladder cancer requiring multimodal treatment. We present a case of an 82-year-old male with SCCB with bulky pelvic adenopathy treated with a novel neoadjuvant combination of carboplatin, etoposide, and durvalumab with complete response of the small cell component. We also describe a rare complication of retinopathy resulting from this treatment. This study presents the potential efficacy and promise of adding immunotherapy to neoadjuvant chemotherapy for SCCB to achieve a long-term cure.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12395055PMC
http://dx.doi.org/10.1016/j.eucr.2025.103165DOI Listing

Publication Analysis

Top Keywords

small cell
12
carboplatin etoposide
8
etoposide durvalumab
8
bladder cancer
8
novel carboplatin
4
durvalumab neoadjuvant
4
neoadjuvant therapy
4
therapy treatment
4
treatment small
4
cell bladder
4

Similar Publications

Role of hydrogen sulfide in catalyzing the formation of NO-ferroheme.

Nitric Oxide

September 2025

Department of Physics, Wake Forest University, Winston-Salem, NC 27109, USA; Translational Science Center, Wake Forest University, Winston-Salem, NC 27109, USA. Electronic address:

We recently demonstrated a rapid reaction between labile ferric heme and nitric oxide (NO) in the presence of reduced glutathione (GSH) or other small thiols in a process called thiol-catalyzed reductive nitrosylation, yielding a novel signaling molecule, labile nitrosyl ferrous heme (NO-ferroheme), which we and others have shown can regulate vasodilation and platelet homeostasis. Red blood cells (RBCs) contain high concentrations of GSH, and NO can be generated in the RBC via nitrite reduction and/or RBC endothelial nitric oxide synthase (eNOS) so that NO-ferroheme could, in principle, be formed in the RBC. NO-ferroheme may also form in other cells and compartments, including in plasma, where another small and reactive thiol species, hydrogen sulfide (HS/HS), is also present and may catalyze NO-ferroheme formation akin to GSH.

View Article and Find Full Text PDF

Unveiling anaphylatoxins: Pioneering cancer therapies through complement system insights.

Biochim Biophys Acta Rev Cancer

September 2025

Department of Neurosurgery, The First Hospital of China Medical University, Nanjing Street 155, Heping District, Shenyang 110001, PR China. Electronic address:

The complement system, a cornerstone of innate immunity, plays pivotal roles in both defense and pathology, particularly through its anaphylatoxins, C3a and C5a. These small peptides, generated during complement activation, not only mediate pro-inflammatory responses but also contribute to the progression of various cancers by modulating the tumor microenvironment (TME). Anaphylatoxins influence tumor cell proliferation, epithelial-mesenchymal transition, angiogenesis, immune suppression, and therapy resistance via key signaling pathways such as PI3K/AKT, MEK/ERK, and p38 MAPK.

View Article and Find Full Text PDF

Unraveling the nexus in the neuro-neoplastic progression of colorectal cancer: Potential role of β2-adrenergic receptor (β2-AR).

J Adv Res

September 2025

Department of Physiology and Biophysics, Weill Cornell Medicine-Qatar, Education City, Qatar Foundation, Doha P.O. Box 24144, Qatar. Electronic address:

Background: Studies on the interaction of cancer cells with other cells (fibroblasts, endothelial cells, and immune cells) of the tumor microenvironment (TME) have led to the development of many novel targeted therapies. More recently, the notion that neuronal cells of the TME could impact various processes supporting cancer progression has gained momentum. Tumor-associated neurons release neurotransmitters into the TME that, in turn, bind to specific receptors on different target cells, supporting cancer progression.

View Article and Find Full Text PDF

Regulated release of small extracellular vesicles directs neutrophil recruitment in cutaneous wound healing.

J Invest Dermatol

September 2025

Department of Surgery, University of California San Diego, La Jolla, CA, United States; Department of Dermatology, University of California San Diego, La Jolla, CA, United States. Electronic address:

Normal cutaneous wound healing is a multicellular process that involves the release of small extracellular vesicles (sEVs) that coordinate intercellular communication by delivery of sEV payloads to recipient cells. We have recently shown how the pro-reparative activity of inflammatory cell sEVs, especially macrophage and neutrophil-derived sEVs, in the wound bed is dysregulated in impaired wound healing. Here we show that loss of Rab27A, a small GTPase that has a regulatory function in sEV secretion, reduces the release of neutrophil and macrophage-derived sEVs.

View Article and Find Full Text PDF