Internal use only (affix UID label here) Clinical Requisition Form Quantitative protein expression analysis by SRM-mass spectrometry and mutation analysis by NGS Please fax completed form with pathology reports (if available) and insurance information to 888.977.1386. * Indicates required information. Ordering physician information Patient information Institution name:* Ordering NPI#:* physician:* Address:* Last name:* Address:* City:*State: Date of birth:* Medical record number: Zip:* Phone:*Fax:* First name:* City:*State: Gender:* Zip:* Female Male Pathology information Insurance information Location name:* Address:* Name Relationship of insured:* to patient: Bill to:* Insurance Medicare Patient Hospital/Institution City:*State:* Patient status:* Hospital inpatient Hospital outpatient Non-hospital patient Hospital discharge date (if Medicare):* Zip:* Phone:*Fax: Specimen information Specimen ID:* ICD9 Date and location code(s):* of collection: Additional instructions: Specimen source: Date retrieved from archive (if applicable): Protein expression analysis Comprehensive cancer protein panel Available for all solid tumors. Targeted therapy markers: ALK, AXL, EGFR, FGFR2, HER2, HER3, IGF1R, KRAS, MET, MSLN, PD-L1, RON, ROS1 ChemoPlex panel: Androgen Receptor, ERCC1, FR-α, hENT1, RRM1, SPARC, TOPO1, TOPO2A ChemoPlexTM protein panel Androgen Receptor, ERCC1, FR-α, hENT1, RRM1, SPARC, TOPO1, TOPO2A Lung cancer protein panel Breast cancer protein panel Gastrointestinal cancer protein panel HPV-infection associated protein p16 Targeted therapy markers: AXL, EGFR, HER2, HER3, IGF1R, MET, PD-L1, ROS1 ChemoPlex panel: Androgen Receptor, ERCC1, FR-α, hENT1, RRM1, SPARC, TOPO1, TOPO2A Targeted therapy markers: EGFR, FGFR2, HER2, HER3, IGF1R, KRAS, MET, MSLN, PD-L1, RON ChemoPlex panel: Androgen Receptor, ERCC1, FR-α, hENT1, RRM1, SPARC, TOPO1, TOPO2A Genomic analysis Available for head and neck cancers. Available when ordered with protein expression analysis. Genetic mutation analysis panel (NGS, 50 genes) Targeted therapy markers: ALK, AXL, EGFR, HER2, HER3, IGF1R, KRAS, MET, MSLN, PD-L1, ROS1 ChemoPlex panel: Androgen Receptor, ERCC1, FR-α, hENT1, RRM1, SPARC, TOPO1, TOPO2A NSCLC Differentiation: CK5, CK7, TP63, TTF-1 Available for colon, lung and melanoma. For gene list see page 2. ALK rearrangement analysis (FISH) Available for NSCLC. Statement of medical necessity This requisition constitutes an order for services. I certify the services are medically indicated and necessary, and they will assist me in treating my patient. Authorized signature Printed nameDate OncoPlex Diagnostics - Attention: Clinical Specimen Receiving 9620 Medical Center Drive, Suite 100 • Rockville, MD 20850 Phone: 301.977.3654 • Fax: 888.977.1386 • Email: [email protected] Dr. Robert Heaton, Medical Director • Maryland Business License # 1872 CLIA # 21d2043150 SPC-001.02, v17 Protein clinical marker background information ALK Approximately 3-5% of NSCLCs express a mutant ALK protein, most commonly due to a genetic rearrangement where the ALK gene recombines with another gene. When mutant ALK is expressed in tumor cells, the tumor will likely show a positive response to ALK targeted treatments. Androgen Receptor Prostate, breast and bladder cancers can use androgen receptor (AR) signaling for growth. Triple negative breast cancers expressing AR represent a unique breast cancer subtype: AR-positive TNBC. Drugs that disrupt AR binding of androgens are approved for prostate cancer, and many are currently in clinical trials for breast cancer. AXL Overexpression of the AXL protein has been observed in breast, pancreatic and lung cancers. Specific inhibition of the AXL kinase shows tumor growth inhibiting activity in pre-clinical studies and AXL specific inhibitors are currently in clinical trials. EGFR Tumors overexpressing the EGFR protein are reported to have an improved response to anti-EGFR therapies. Certain EGFR mutations are associated with response to erlotinib and afatinib, which are approved for NSCLC and pancreatic cancers. ERCC1 A protein involved in DNA repair, ERCC1 is overexpressed in NSCLC, ovarian and other cancers. Expression of ERCC1 can cause resistance to platinum-based therapies. FR-α Overexpression of FR-α has been observed in breast, mesothelioma, lung, ovarian and colorectal cancers. Due to its critical role in folate uptake FR-α is a potential biomarker of tumor response to anti-folate chemotherapy. FGFR2 Overexpression of the FGFR2 protein in gastric cancers or disregulated signaling activity initiated by FGFR2 in squamous cell carcinomas has been observed to influence tumor growth and metastasis. Many FGFR2 targeted agents are in clinical development. hENT1 Nucleoside analogs such as gemcitabine depend on hENT1 for effective delivery into the cell. Multiple studies have shown that expression of hENT1 result in better overall survival in gemcitabine treated patients. HER2 The HER2 protein is frequently overexpressed in breast, gastric, gastroesophageal and other cancers. There are many approved targeted therapies for HER2. HER3 Expression of HER3 is associated with worse survival in patients with solid tumors. HER3 is reported to be a resistance mechanism for trastuzumab and to predict response to pertuzumab in breast cancer. Many HER3 targeted agents are in clinical development. IGF1R Dysregulation of IGF1R signaling is observed in gastric, liver, prostate, colorectal, NSCLCs and Ewings sarcoma, resulting in tumor growth and proliferation. KRAS KRAS protein overexpression and gene amplification represent a mechanism by which cancer cell growth is dysregulated. Patients that have KRAS amplification or mutations may be more responsive to MEK/ERK pathway inhibition. MET MET amplification and protein over expression has been found in gastroesphageal and lung cancers. Many therapies targeting MET are under evaluation in clinical trials. MSLN Mesothelin is expressed at high levels in mesothelioma, and can also be found in pancreatic adenocarcinomas, breast and ovarian cancers and lung adenocarcinomas. Mesothelin targeted agents are in clinical development. p16 p16 expression is indicative of HPV infection in head and neck cancers. Squamous cell carcinomas of the head and neck with high expression of p16 have favorable prognosis compared to p16 negative tumors. PD-L1 Tumor cells that express the PD-L1 protein can activate the T-cell localized PD-1 receptor to evade immune system mediated cell death. PD-L1 expression has been associated with response to both PD-L1 and PD-1 targeted therapies. RON Overexpression of the RON protein is associated with poor overall survival in GI and breast cancers. Tumors co-expressing both RON and MET receptors demonstrate worse overall survival. ROS1 ROS1 translocations are found in approximately 2% of lung adenocarcinomas. The ROS1 protein may be effectively targeted with ALK inhibitors. RRM1 The RRM1 protein is a critical component of the DNA repair mechanism. Tumor cells that express high levels of RRM1 may be more resistant to gemcitabine. SPARC The SPARC protein may play a role in accumulating albumin-conjugated drugs in tumor cells due to its high affinity for albumin. Several studies suggest that SPARC overexpression is associated with improved response to nab-paclitaxel. TOPO1 An enzyme that alters supercoiling of double stranded DNA during DNA replication. Higher expression of TOPO1 has been associated with improved response to TOPO1 inhibitors. TOPO2A An enzyme that alters the supercoiling of double stranded DNA during cell division. High TOPO2A protein expression or TOPO2A gene amplification has been associated with benefit from anthracycline-based chemotherapy. Tumor genetic mutation analysis ABL1 BRAF EGFR FGFR1 GNAS IDH2 KRAS NPM1 PTPN11 SMO AKT1 CDH1 ERBB2 FGFR2 GNAQ JAK2 MET NRAS RB1 SRC ALK CDKN2A ERBB4 FGFR3 HNF1A JAK3 MLH1 PDGFRA RET STK11 APC CSF1R EZH2 FLT3 HRAS KDR MPL PIK3CA SMAD4 TP53 ATM CTNNB1 FBXW7 GNA11 IDH1 KIT NOTCH1 PTEN SMARCB1 VHL
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