Inflammation is a known driver of carcinogenesis which is the initiation of cancer formation.
A Mount Sinai research team observed that prostate cancer patients with pelvic inflammation had poor outcomes.
This is the first study to look at the link between pelvic inflammation and prostate cancer biology and outcomes.
This study reports a significant association of pelvic inflammation with advanced prostate cancer in a large cohort of men undergoing robot-assisted laparoscopic prostatectomy (RALP) for localised prostate cancer.
Prostate cancer patients with pelvic inflammation had elevated expression of inflammation-associated genes and cancer-driving pathways in their tumours.
Increased systemic inflammation with activation of the IL6-STAT pathway was seen in prostate cancer patients with pelvic inflammation.
The presence of pelvic inflammation in prostate cancer patients suggests aggressive disease with a potential to develop biochemical recurrence and metastasis.
This study is highly relevant as it allows us to closely follow prostate cancer patients with pelvic inflammation for metastasis.
It also suggests that inhibiting the STAT-IL6 pathway would benefit these patients.
Pelvic inflammation was associated with adverse pathology and higher biochemical recurrence rates in prostate cancer patients.
Prostate cancer patients with pelvic inflammation had elevated expression of inflammation-associated genes and cancer-driving pathways in their tumours that drive reoccurrence or metastasis.
Tumour inflammation promotes prostate cancer carcinogenesis.
However, the implications of pelvic inflammation and its effect on prostate cancer have never been studied.
In this study, researchers retrospectively investigated the association of pelvic inflammation with PCa aggressiveness and its impact on oncological outcomes in a large cohort of men undergoing RALP for localised PCa.
Overall, pelvic inflammation was a significant predictor of AP in both univariate and multivariate analyses.
“We have observed that prostate cancer patients with adhesions or scar tissues had a higher likelihood of aggressive disease. With further in-depth analysis, we discovered that pelvic inflammation is a driver of aggressive prostate phenotype. Until now, chronic inflammation within the prostate was considered a significant contributor to prostate cancer progression. However, our studies, for the first time, demonstrate that inflammation away from the prostate could be equally important. Therefore, managing inflammation in high-risk prostate cancer patients is critical and could be achieved by diet and other intervention strategies,” says Dr Ash Tewari.
“This study fundamentally contributes to the growing literature demonstrating inflammation’s negative impact on cancer progression. The role of pelvic inflammation in prostate cancer progression has never been studied, and our study in a large cohort of patients provides mechanistic insights that could explain how pelvic inflammation contributes to prostate cancer progression and biochemical recurrence. We are pursuing multi-institutional collaborations to validate our findings in other cohorts. Our long-term objective is to develop blood or urine-based biomarker to monitor inflammation status in our prostate cancer patients,” adds Dr Dimple Chakravarty, the lead author.
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