PTEN/TMPRSS2:ERG

For patients with atypical/HGPIN diagnoses, and those with biopsy Gleason Scores 3+3 and 3+4, PTEN/TMPRSS2:ERG molecular testing can help predict prostate cancer aggressiveness, providing additional information to make informed treatment decisions.

 
  • Anticipate prostate cancer aggressiveness, confirming genetic changes before the cancer develops and metastasizes
  • Differentiate patients requiring aggressive treatment from those appropriate for active surveillance
  • Determine monitoring intervals and treatment plans for diagnoses of HGPIN, atypical, and low Gleason Scores of 6 and 7

Appropriate treatment decisions require individual patient assessment.

Reflex to PTEN and ERG for your atypical and HGPIN patients.

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PTEN

PTEN is a tumor suppressor gene. When cancer (or the potential for cancer) is present, the PTEN gene acts as a suppressor of that cancer. If PTEN is positive (a “hemizygous deletion” or “homozygous deletion”) this means the PTEN gene is no longer present, representing the potential for aggressive cancer in your patient.

Utilize the association between PTEN deletion and early onset of disease recurrence and survival rate.2

Partial or complete deletion of the PTEN (Phosphatase and Tensin) biomarker more accurately indicates the aggressiveness of prostate cancer in patients with diagnoses of High-Grade Prostatic Intraepithelial Neoplasia (HGPIN) and cancer with low Gleason scores of 6 and 7.


ERG: Better information for you and your patients leads to confident treatment decisions.

ERG is a gene located on one chromosome (chromosome 21). A positive ERG test represents a “fusion” on the ERG gene with another gene on that same chromosome. Specifically, ERG and TMPRSS2 come into contact with each other and produce a positive ERG test.  


The ERG FISH test provides an analytical sensitivity of 94.5% and specificity of 100% for detection of TMPRSS2:ERG fusion.3

Possible ERG FISH outcomes:

Metamark ERG testing can distinguish between three different types of ERG fusion, each with a greater level of severity/potential outcome for your patient.

No Fusion

The ERG and TMPRSS2 genes are separated by HMGN1 and DSCAM genes.

Fusion by Deletion

The HMGN1 and DSCAM genes are deleted, allowing TMPRSS2 and ERG to come into close contact and fuse.

Fusion by Insertion

The HMGN1 and DSCAM genes move locations, allowing TMPRSS2 and ERG to come into close contact and fuse.

Fusion Plus

Additional copy numbers of the TMPRSS2/ERG gene fusion are present in the sample.

PTEN PLUS ERG: Greater insight into the progress of your prostate cancer patient

 

Use enhanced information to build a customized treatment plan.

PTEN and ERG determine the rate of disease progression, and can help guide the selection of appropriate therapy for your patient.




References:
  1. Wilt T, Brawer M, Jones K, et al. Radical Prostatectomy versus Observation for Localized Prostate Cancer. N Eng J Med. 2012;367(3):203-213.
  2. Yoshimoto M, Cunha IW, Coudry RA, et al. FISH anal ysis of 107 prostate cancers shows that PTEN genomic deletion is associated with poor clinical outcome. British J of Cancer. 2007;97:678-685.
  3. Schelling LA, Cheng L, et al. (2013) Frequent TMPRSS2-ERG rearrangement in prostatic small cell carcinoma detected by FISH: the superiority of fluorescence in situ hybridization over ERG immunohistochemistry. Human Pathology 44:2227-2233.
  4. Yoshimoto M, Joshua AM, Cunha IW, Coudry RA, Fonseca FP, et al. (2008) Absence of TMPRSS2: ERG fusions and PTEN losses in prostate cancer is associated with a favorable outcome. Mod Path 21:1451-1460

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