Tall Allen said...
Not really. Extracapsular extension means it is growing through the capsule ("extra" means outside of) that surrounds the prostate except at the apex where it becomes indistinct. As it breaks through the prostate capsule, it eats into the tissues in the prostate bed that surround it. Those tissues may include the neurovascular bundles, periprostatic fat, and various layers of tissue called fascia. Once it is out of the prostate, it can shed and spread cancer cells more easily. That's why it is a good idea to start with radiation for T3 because it treats a "safety" margin outside of the prostate where those invisible cancer cells may be nesting.
What may be confusing you is the clinical staging T4, which means that it has invaded such structures as the external sphincter, rectum, bladder, levator muscles, and/or pelvic wall.
So how much "margin" do most RO's use to treat the ECE that is possible?
Sounds like 3-4 mm is he distance the tumors can grow outside??
I found this:
https://www.ncbi.nlm.nih.gov/pubmed/10699615
Extent of extracapsular extension in localized prostate cancer.
Sohayda C1, Kupelian PA, Levin HS, Klein EA.
Author information
Abstract
OBJECTIVES:
To measure the radial extent of extracapsular penetration by tumor cells, thereby providing estimates of the margins needed around target volumes. New radiotherapeutic techniques, like brachytherapy and conformal radiotherapy, irradiate small volumes and reduce the dose to periprostatic tissues. Even in the early stages of localized prostate cancer, extracapsular extension (ECE) is commonly seen.
METHODS:
Two hundred sixty-five consecutive radical prostatectomy specimens were analyzed for the presence of ECE. ECE was found in 92 of all cases (35%); measurements were performed in 79 of the 92 cases. A total of 98 ECE sites were evaluated in the 79 cases. The distance of tumor outside the capsule was measured in millimeters. Extension less than 0.1 mm was considered as "focal".
RESULTS:
The site of ECE was posterolateral in 53% of cases, lateral in 24%, posterior in 13%, and at the base in 10%. The median amount of ECE at all sites was 1. 1 mm (mean 1.7). However, the range was wide; the minimum measurable extent was 0.1 mm and the maximum 10.0 mm. The extent was within 3.8 mm for 90% of all cases. By stratifying cases with favorable and unfavorable tumors, the 90th percentiles of ECE were as follows: 3.3 mm for favorable tumors (clinical Stage T1-2, initial prostate-specific antigen 10 ng/mL or less, and biopsy Gleason score 6 or less) and 3.9 mm for unfavorable tumors (clinical Stage T3, initial prostate-specific antigen greater than 10 ng/mL, or biopsy Gleason score 7 or greater).
CONCLUSIONS:
Most of the ECE was at posterolateral sites. The extent of disease outside the prostate was within 4 mm in 90% of cases. Since ECE was observed in 30% to 60% of all patients with clinical Stage T1-2 prostate cancer, only 3% to 7% of all such cases would have disease extent exceeding 4 mm. The present study provides useful estimates of the amount of ECE. These estimates could be potentially used in planning the target volumes for treatment of prostate cancer with either conformal radiotherapy or brachytherapy