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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: CustomerService@OncoPlexDx.com
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