. Is there a test that utilises anti-PSA monoclonal antibodies to localise PSA-avid tumour in the body?

Early attempts to localize prostate cancer using anti PSMA monocolonal antibodies did exist, most notably caroomab pendetide labeled with indium-111 for SPECT imaging. İt was used ideally for patients with raising PSA post surgery when CT/Bone scan was negative. The use of it is limited due to high rates of false positive and false negative rates. And also because PSA is primarily intracellular, antibody binding accurs mainly in necrotic or membrane compromised cells rather than viable tumor tissue, leading to low sensitivity and suboptimal lesion detection.

 

This is a very important clinical question, especially when biochemical recurrence happens and conventional imaging doesn't show anything, which happens to all of us from time to time. There has been an effort to use monoclonal antibody-based imaging to find prostate cancer in this situation, strictly speaking. A well-known example is ¹¹¹In-capromab pendetide (Prostascint), which is a murine monoclonal antibody used in immunoscintigraphy. It targets antigens related to the prostate (more specifically, PSMA instead of PSA itself) and was made to find hidden disease, especially in people whose PSA levels are going up after prostatectomy. In practice, though, this method didn't work very well. One significant problem was low sensitivity, in part due to the antibody binding to an intracellular epitope, which may lead to a preference for detecting dead or damaged cells over viable tumor cells. Reported sensitivities were very low (as low as ~17% in some series), which made it much less useful in the clinic. Due to these constraints, capromab-based imaging is now predominantly regarded as a historical reference and is no longer extensively utilized in contemporary guidelines. More recently, researchers have been working on newer monoclonal antibodies (like J591) that target the extracellular domains of PSMA. However, even in this area, the field has been moving away from full antibodies because they take a long time to clear and don't show up well in images. PSMA-targeted PET imaging with small-molecule ligands, on the other hand, is what has really changed the way doctors work. These attach to the extracellular part of PSMA and give much better sensitivity and resolution. Current evidence indicates that PSMA PET can localize disease in instances of biochemical recurrence and has emerged as a crucial instrument for staging and restaging prostate cancer. So, to answer your question in a useful way: Yes, imaging based on monoclonal antibodies (including early "anti-prostate antigen" methods) has been created and used. But it isn't reliable enough to use every day right now, especially for people with low PSA and negative conventional imaging. PSMA PET has successfully supplanted these antiquated methods and is presently the most effective modality for identifying occult disease in this context. If PSA levels are rising after a prostatectomy and MRI/CT scans are negative, most centers would now use PSMA PET/CT scans instead of antibody-based scans. This is because the diagnostic yield is so much higher with PSMA PET/CT scans. 

Refer the refrences below for more details 

1.     https://www.sciencedirect.com/topics/neuroscience/capromab-pendetide-in-111?utm_source=chatgpt.com 

2.     https://en.wikipedia.org/wiki/Indium_%28111In%29_capromab_pendetide?utm_source=chatgpt.com 

3. https://snmmi.org/common/Uploaded%20files/Web/Clinical%20Practice/Appropriate%20Use%20Criteria/J%20Nucl%20Med-2020-Jadvar-552-62.pdf?utm_source=chatgpt.com 

4.     https://link.springer.com/article/10.1007/s00261-023-04002-z

 

Various preclinical and clinical studies have demonstrated that STAT3 plays a central  role in maintaining intestinal mucosal barrier function by promoting epithelial cell survival, proliferation, and wound healing.  STAT3 promotes the survival and proliferation of intestinal epithelial cells (IECs), preventing excessive cell death that would compromise the barrier. However, persistent and excessive activation of the STAT3 pathway is linked to inflammatory bowel disease (IBD) and colitis-associated cancer, indicating that it must be tightly regulated for its beneficial effects.