Prostate Health Sensor Demo

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Prostate Health Sensor

John Doe
N8C9841
COVER LETTER

Dear Mr. Doe,

Your sample for the analysis arrived on 05/02/2018 in the laboratory and was evaluated
according to the highest laboratory quality standards (ISO 15189). The results were
evaluated and released by two independent geneticists and molecular biologists. After
obtaining the results, your personal report was compiled. We hereby transmit the
results to you in the format of your choice.
We would like to thank you for your trust and hope that you are satisfied with our
service. We are always open for questions and suggestions, please do not hesitate to
contact us. This is the only way we can continuously improve our services.
We hope the analysis meets your expectations.

Kind regards,

Dr. Daniel Wallerstorfer BSc. Florian Schneebauer, MSc.


Laboratory Director Laboratory Manager
Prostate Health Sensor

Personal analysis results for:


John Doe | Date of birth: 01/02/1985

Order number:
N8C9841

This report contains personal medical information that is highly


confidential. Data protection must be ensured.

N8C9841 Page 1 of 26
GENETICS

How genes influence our health


The human body consists of about 50 trillion individual cells. Most of
these cells have a nucleus which contains 46 chromosomes. A chromosome
consists of a very closely wound thread, the DNA "double helix."
DNA, the genetic code, is
Chromosome the blueprint of the human
Cells body. This genetic code
Body (50 trillion cells) consists of approximately
3.1 billion molecules, which
are each represented by a
letter. About 1% of this code
makes up the genes. Each
gene is an instruction for
the body, usually with a
single function. For
example, some genes tell
the body how to color the
iris and differences in these
genes produce different eye
DNA double helix A = healthy colors. Every function of the
G = risk body is controlled by one or
more genes, including the
way we break down food or
medication.

Lactase gene (LCT) Thrombosis gene


(FV)

Our genes are not completely error-free. The genes of each person are changed slightly by
environmental effects. Most of these changes have no effect. A small number have a harmful
effect. An even tinier number can produce a beneficial effect. Parents pass these changes,
including defects, to their children. Thus most of our genetic defects are inherited from our
parents.

In addition, our genes developed to help us live in a completely different world, and some of the
traits in our genes can interact with our modern environment to create negative effects on our
body. For example, the genetic predisposition to store dietary fat quickly and lose it slowly is
beneficial for people who go through times when food is scarce: they have a better chance of
surviving because their bodies use fat efficiently and store it for leater. However, in the modern
world, this trait is harmful because it programs the body to gain weight quickly and lose weight

N8C9841 Page 2 of 26
slowly. Genes increase our risk of heart attacks, trigger asthma and allergies, cause lactose
intolerance, and many other disorders.

Genetic traits can affect our health. While some genetic defects cause disease in all cases, most
genetic traits just increase our risk of developing a disease. For example, a person may have
genes that increase their risk for diabetes. However, not everyone at risk for diabetes actually
develops the disease. Furthermore, even people with a high risk of diabetes can lower their risk
with the right diet and exercise plan. Other genetic traits only cause illness when they are
triggered by a specific environmental feature. For example, lactose intolerance is a genetic
condition that causes a person who drinks milk to have digestive issues. A lactose-intolerant
person who never drinks milk will not have any symptoms.

Thanks to the latest technologies, it is now possible to test specific genes to determine if you
have genetic traits that are linked to various diseases. Based on the results of the analysis, we
can develop a prevention program that significantly reduces your personal disease risk and
helps you stay healthy.

A healthy lifestyle will decrease your risk of many diseases whether or not you have specific
information about your genetic traits. However, we provides you with additional information
that may point out other changes to your lifestyle that are not part of standard medical advice.
There are many examples, but one of the traits we test for is a gene that increases your body’s
ability to absorb iron. If you have this trait, you must not take iron supplements as the iron
would accumulate and cause a life threatening disease called hemochromatosis.

Experts estimate that every person carries about 2,000 genetic defects, which may affect their
health, and, in some cases, cause illnesses. A variety of factors can cause changes in our genes
(also called mutations). In a few cases, these mutations can benefit us. However, the vast
majority either have no effect or have a negative impact on our health. The best-known cause
of mutations, as depicted in the media and Hollywood, is radioactivity. Radioactive rays and
particles actually impact the DNA in our cells and physically alter our genes. In the movies,
these changes or mutations often lead to the creation of monsters like Godzilla, or characters
with supernatural powers, as in X-Men. In reality, they mostly go unnoticed or cause deadly
diseases, such as cancer, or congenital abnormality for newborns. Mutations are also caused by
substances in burned food. The substances enter the cells and damage our genes, which can
lead to colon cancer, among other form of cancer. UV radiation from the sun can also damage
our genes and cause diseases such as skin cancer.

External influences can affect individual genes and disrupt their function, but the majority of
our defective genes are inherited from our parents. Each embryo receives half of its genes from
the father and half of its genes from the mother, resulting in a new human being with some of
the characteristics of each parent. Whether a genetic defect is passed on, is determined
randomly, and it may be that some of the children carry the defective gene and others do not.

Each person is the unique product of generations of accumulation and combination of


different genetic traits. Some of those traits have negative effects on our health. With the
latest technology, it is now finally possible to examine one's genes and determine his personal
health risks and strengths. In many cases, taking advantage of this knowledge, and following
some precautionary measures, the diseases may be prevented. This is the next step in
preventive medicine and a new generation of health care.

N8C9841 Page 3 of 26
Action index
Discuss risks marked in orange or red with your doctor. All other results do not require any
further attention assuming there are no current medical conditions.

Prostate Health Sensor

N8C9841 Page 4 of 26
PHARMACO GENETICS
Not ordered

ONCOLOGY

CARDIOVASCULAR SYSTEM
Not ordered

NEUROLOGY
Not ordered

METABOLISM
Not ordered

MOVEMENT
Not ordered

DIGESTION
Not ordered

OPHTHALMOLOGY
Not ordered

ODONTOLOGY
Not ordered

OTHERS
Not ordered

SCIENCE

ADDITIONAL INFORMATION
Prostate Health Sensor
Effective prevention and treatment of prostate cancer
ANDROLOGY

Prostate
The prostate is a sex gland. It lies below the bladder, near the beginning of the urethra,
and is about the size and shape of a chestnut. It consists of several glands that produce
a secretion that is discharged during ejaculation into the urethra, where it is mixed
with the sperm. Thus, it plays an important role in reproduction. Unfortunately, the
prostate is also associated with a number of diseases, some of which can be serious or
even fatal. As a result, every man should undergo an annual examination of the
prostate after the age of 45.
Benign prostatic hyperplasia (BPH) is a non- at a later stage through symptoms such as
cancerous enlargement of the prostate gland urinary symptoms, bone pain, weight loss,
caused by the abnormal proliferation of and anemia. The main complaints arising are
certain cells. The disease is very common and referring to urination disorders: delayed
usually develops with age. The risk of an onset, a weak jet, drip or the interruption of
enlarged prostate depends on genetic and the urinary stream during urination. Residual
lifestyle factors. About 10-20% of men urine often remains in the bladder. Other
between age 50 and 59 have this condition, frequently observed symptoms include:
and 25-35% of men in between 60 and 69. In increased or predominantly nocturnal
contrast to prostate cancer, the symptoms of urination, frequent urination in small
prostate enlargement develop very rapidly. quantities, difficulty, or pain when urinating.
Typical symptoms are: pain during urination; Due to pressure damage to nerves of the
frequent urination; difficult, long-lasting sacrum area, erection problems may also
urination supported by abdominal pressure. occur. Visible blood in the urine or sperm is
If the bladder is significantly obstructed, rare but significant. A prostate tumor does
urine may accumulate in the kidney, which not cause discomfort, and so
can cause a life-threatening condition. An symptoms usually appear only after the
enlarged prostate can be treated either with tumor has spread to nearby lymph nodes or
medication, depending on the extent, or into the bones. At that point, the most
reduced surgically using a laser beam. common symptoms are pain in the spine and
However, the best option remains pelvis. In most cases, bone metastases are the
prevention. Since benign enlargement of the predominant disease, and they are also the
prostate is closely related to an unfortunate most common cause of death from prostate
combination of genes and lifestyle, cancer. The advanced stage is often
modifications in lifestyle can greatly reduce accompanied by anemia and weight loss.
the risk of disease for genetically predisposed Prostate cancer can only be treated
people. successfully before it has spread, so early
detection is crucial for effective treatment.
Prostate cancer is one of the most common That is why men over the age of 45 should be
cancers for men. About 15% of men will be tested annually for prostate cancer.
diagnosed with prostate cancer at some point Treatment options include surgery with
in life. In most cases, prostate cancer does complete removal of the prostate, radiation
not produce symptoms until it has therapy, hormone therapy, and in some cases,
progressed, and so it is usually detected only chemotherapy.

N8C9841 Page 8 of 26
If the cancer is treated early, before spreading
to other tissues, the 5-year survival rate is
approximately 90%. After the cancer spreads,
the 5-years survival rate is only around 35%,
which is why early detection is so important.
The lifetime risk for the diagnosis of
"prostate cancer" is about 11%. It is estimated
that approximately 20% of patients with
prostate cancer die. About half of the cases of
prostate cancer are caused by genetic
variations. Now it is possible to test these
genes and to determine the personal risk
prior to the occurrence of prostate cancer. If
the risk is significantly increased, a
preventive program can significantly reduce
the risk of developing of the disease.
Additionally, you can detect potential
diseases at an early stage through a more
intensive monitoring program and allow for
its timely treatment. More serious and
unpleasant consequences can be prevented in
most cases.

N8C9841 Page 9 of 26
ANDROLOGY

Relevant genes for prostate


Several genetic variations have been identified, which taken individually slightly increase or
decrease the risk of prostate cancer. Taken together, they have a significant impact on the risk
probability. The analysis of relevant genetic variations came to the following conclusion:

Genetic traits
SYMBOL rs NCBI POLYMORPH GENOTYPE
TCF2 rs4430796 G>A A/A
LOC124685 rs1859962 T>G T/G
8q24 region2 rs16901979 C>A C/C
8q24 region3 rs6983267 T>G T/G
8q24 region1 rs1447295 C>A C/C
VDR rs2107301 C>T C/T
8q24 rs4242382 G>A G/G
8q24 rs7837688 T>G G/G
8q24 rs2011077 A>G G/G
RNASEL rs627928 G>T G/T

LEGEND: rsNCBI = description of examined genetic variation, POLYMORPHISM = form of the genetic
variation, GENOTYPE = personal analysis result

N8C9841 Page 10 of 26
Summary of effects
Here you can see a summary of the impact your genetic variations have on your health and your
body:

➤ Your risk of developing prostate cancer is lower than that of the general population.

What is your risk of prostate cancer?


LOW AVERAGE RISK HIGHER

When are checkups recommended?


FROM 45 YEARS EARLIER

N8C9841 Page 11 of 26
ANDROLOGY

Prevention
You do not have an elevated genetic risk for this disease. In fact, your genetic profile
actually gives you a below-average chance of contracting against this disease. You
should follow only the general rules of a healthy life and submit to annual prostate
examination after the age of 45 years. In this way, the age-related (non-genetic) forms
of prostate diseases can be recognized and treated in time.

N8C9841 Page 12 of 26
ANDROLOGY

Effect on relevant drugs


Your genetic profile has an impact on the effect of drugs prescribed for prostate cancer and
associated diseases. This information can help your doctor choose the correct dosage of the right
medications to minimize side effects.

Painkillers (analgesics)
Painkillers effect Breakdown Adverse recommended alternative?
Reaction dose*
alfentanil ~% %
buprenorphine ~% %
codeine (FDA!) ~% %
enflurane ~% %
fentanyl ~% %
halothane ~% %
hydrocodone ~% %
isoflurane ~% %
levacetylmethadol ~% %
lidocaine ~% %
methadone ~% %
methoxyflurane ~% %
oxycodone ~% %
paracetamol ~% %
phenacetin ~% %
ropivacaine ~% %
sevoflurane ~% %
tramadol (FDA!) ~% %
zolmitriptan ~% %

Drugs for traveling sickness (antiemetic)


Drugs for easing the feeling effect Breakdown Adverse recommended alternative?
of sickness Reaction dose*

aprepitant ~% %
dolasetron ~% %
domperidone ~% %
metoclopramide ~% %

N8C9841 Page 13 of 26
Anti-cancer drugs (chemotherapy)
Drugs for the treatment effect Breakdown Adverse recommended alternative?
and prevention of cancer Reaction dose*

anastrozole ~% %
cyclophosphamide ~% %
docetaxel ~% %
doxorubicin ~% %
erlotinib ~% %
etoposide ~% %
gefitinib ~% %
ifosfamide ~% %
imatinib ~% %
nilutamide ~% %
paclitaxel ~% %
sorafenib ~% %
sunitinib ~% %
tamoxifen (FDA!) ~% %
temsirolimus ~% %
teniposide ~% %
vemurafenib ~% %
vinblastine ~% %
vincristine ~% %
vindesine ~% %

Recommended dosage for the doctor: ~ 100% (simply use the normal dosage), ~ 20% (start with a low dosage
and if necessary increase it under supervision), 0% (if possible use an alternative drug), 200% (start normally at
100% dosage and if necessary increase up to 200%)

REMEMBER: Only your doctor can prescribe the correct drugs and dosage.
NEVER stop taking a drug or change the dose: consult your doctor instead!

N8C9841 Page 14 of 26
PHARMACO GENETICS
Not ordered

ONCOLOGY

CARDIOVASCULAR SYSTEM
Not ordered

NEUROLOGY
Not ordered

METABOLISM
Not ordered

MOVEMENT
Not ordered

DIGESTION
Not ordered

OPHTHALMOLOGY
Not ordered

ODONTOLOGY
Not ordered

OTHERS
Not ordered

SCIENCE

ADDITIONAL INFORMATION
SCIENCE
This chapter shows the science behind the test.
SCIENCE

Prostate Health Sensor


TCF2 - Transcription factor 2 (rs4430796)
The transcription factor 2 (TCF-2 or HNF1B) forms a heterodimer with TCF1, and activates, or inhibits, the expression of different
target genes. The polymorphism rs4430796 is associated with an increased risk of prostate cancer.
RES Genotype POP Possible results
X A/A 34% Increased risk of prostate cancer (OR: 1.4)
A/G 44% No increased risk of prostate cancer
G/G 23% No increased risk of prostate cancer
References
Zheng et al. Cumulative association of five genetic variants with prostate cancer. N Engl J Med. 2008 Feb 28,358(9):910-9.

Levin et al. Chromosome 17q12 variants contribute to risk of early-onset prostate cancer. Cancer Res. 2008 Aug 15,68(16):6492-5.

Gudmundsson et al. Two variants on chromosome 17 confer prostate cancer risk, and the one in TCF2 protects against type 2 diabetes. Nat Genet.
2007 Aug,39(8):977-83.

LOC124685 - Myosin, light chain 6, alkali, smooth muscle and non-muscle pseudogene
(rs1859962)
A genome-wide association study has shown that the polymorphism rs1859962 on chromosome 17q24.3 is associated with an
increased risk of prostate cancer.
RES Genotype POP Possible results
T/T 34% No increased risk of prostate cancer
X T/G 47% No increased risk of prostate cancer
G/G 19% Increased risk of prostate cancer (OR: 1.28)
References
Sun et al. Cumulative effect of five genetic variants on prostate cancer risk in multiple study populations. Prostate. 2008 Sep 1,68(12):1257-62.

Levin et al. Chromosome 17q12 variants contribute to risk of early-onset prostate cancer. Cancer Res. 2008 Aug 15,68(16):6492-5.

Zheng et al. Cumulative association of five genetic variants with prostate cancer. N Engl J Med. 2008 Feb 28,358(9):910-9

8q24 region 2 (rs16901979)


Several studies have shown that different polymorphisms on 8q24 increase the risk of prostate cancer.
RES Genotype POP Possible results
A/A 8% Increased risk of prostate cancer (OR: 1.53)
A/C 26% Increased risk of prostate cancer (OR: 1.53)
X C/C 66% No increased risk of prostate cancer
References
Zheng et al. Cumulative association of five genetic variants with prostate cancer. N Engl J Med. 2008 Feb 28,358(9):910-9

Cheng et al. 8q24 and prostate cancer: association with advanced disease and meta-analysis. Eur J Hum Genet. 2008 Apr,16(4):496-505.

Levin et al. Chromosome 17q12 variants contribute to risk of early-onset prostate cancer. Cancer Res. 2008 Aug 15,68(16):6492-5.

N8C9841 Page 18 of 26
8q24 region 3 (rs6983267)
Several studies have shown that different polymorphisms on 8q24 increase the risk of prostate cancer.
RES Genotype POP Possible results
T/T 20% No increased risk of prostate cancer
X T/G 39% Increased risk of prostate cancer (OR: 1.25)
G/G 42% Increased risk of prostate cancer (OR: 1.25)
References
Haiman et al. A common genetic risk factor for colorectal and prostate cancer. Nat Genet. 2007 Aug,39(8):954-6.

Yeager et al. Genome-wide association study of prostate cancer identifies a second risk locus at 8q24. Nat Genet. 2007 May,39(5):645-9. Epub 2007
Apr 1.

Zheng et al. Cumulative association of five genetic variants with prostate cancer. N Engl J Med. 2008 Feb 28,358(9):910-9.

Cheng et al. 8q24 and prostate cancer: association with advanced disease and meta-analysis. Eur J Hum Genet. 2008 Apr,16(4):496-505.

8q24 region 1 (rs1447295)


Several studies have shown that different polymorphisms on 8q24 increase the risk of prostate cancer.
RES Genotype POP Possible results
A/A 5% Increased risk of prostate cancer (OR: 1.22)
A/C 27% Increased risk of prostate cancer (OR: 1.22)
X C/C 69% No increased risk of prostate cancer
References
Zheng et al. Association between two unlinked loci at 8q24 and prostate cancer risk among European Americans. J Natl Cancer Inst. 2007 Oct
17,99(20):1525-33. Epub 2007 Oct 9.

Amundadottir et al. A common variant associated with prostate cancer in European and African populations. Nat Genet. 2006 Jun,38(6):652-8. Epub
2006 May 7.

Freedman et al. Admixture mapping identifies 8q24 as a prostate cancer risk locus in African-American men. Proc Natl Acad Sci U S A. 2006 Sep
19,103(38):14068-73. Epub 2006 Aug 31.

VDR - vitamin D (1,25- dihydroxyvitamin D3) receptor (rs2107301)


The VDR gene encodes the vitamin D receptor, part of the steroid receptors family. It is a transcription factor that regulates the
activity of specific target genes, and thus affects the metabolism. The rs2107301 polymorphism is associated with an increased
risk of prostate cancer.
RES Genotype POP Possible results
T/T 49% Increased risk of prostate cancer (OR: 2.47)
X T/C 35% Increased risk of prostate cancer (OR: 1.11)
C/C 16% No increased risk of prostate cancer
References
Schäfer et al. No association of vitamin D metabolism-related polymorphisms and melanoma risk as well as melanoma prognosis: a case-control
study. Arch Dermatol Res. 2012 Jul,304(5):353-61.

Holt et al. Vitamin D pathway gene variants and prostate cancer risk. Cancer Epidemiol Biomarkers Prev. 2009 Jun,18(6):1929-33.

Holick et al. Comprehensive association analysis of the vitamin D pathway genes, VDR, CYP27B1, and CYP24A1, in prostate cancer. Cancer Epidemiol
Biomarkers Prev. 2007 Oct,16(10):1990-9.

N8C9841 Page 19 of 26
8q24 (rs4242382)
Several studies have shown that different polymorphisms on 8q24 increase the risk of prostate cancer.
RES Genotype POP Possible results
A/A 6% Increased risk of prostate cancer (OR: 2.1)
A/G 26% Increased risk of prostate cancer (OR: 1.91)
X G/G 68% No increased risk of prostate cancer
References
Zheng et al. Association between two unlinked loci at 8q24 and prostate cancer risk among European Americans. J Natl Cancer Inst. 2007 Oct
17,99(20):1525-33. Epub 2007 Oct 9.

Zheng et al. Cumulative association of five genetic variants with prostate cancer. N Engl J Med. 2008 Feb 28,358(9):910-9.

Fitzgerald et al. Analysis of recently identified prostate cancer susceptibility loci in a population-based study: associations with family history and
clinical features. Clin Cancer Res. 2009 May 1,15(9):3231-7.

8q24 (rs7837688)
Several studies have shown that different polymorphisms on 8q24 increase the risk of prostate cancer.
RES Genotype POP Possible results
T/T 2% No increased risk of prostate cancer
T/G 18% Increased risk of prostate cancer (OR: 1.91)
X G/G 81% Increased risk of prostate cancer (OR: 1.67)
References
Zheng et al. Association between two unlinked loci at 8q24 and prostate cancer risk among European Americans. J Natl Cancer Inst. 2007 Oct
17,99(20):1525-33. Epub 2007 Oct 9.

Zheng et al. Cumulative association of five genetic variants with prostate cancer. N Engl J Med. 2008 Feb 28,358(9):910-9.

Lindstrom et al. Characterizing associations and SNP-environment interactions for GWAS-identified prostate cancer risk markers--results from BPC3.
PLoS One. 2011 Feb 24,6(2):e17142.

8q24 (rs2011077)
Several studies have shown that different polymorphisms on 8q24 increase the risk of prostate cancer.
RES Genotype POP Possible results
A/A 62% No increased risk of prostate cancer
A/G 30% Increased risk of prostate cancer (OR: 2.4)
X G/G 8% Increased risk of prostate cancer (OR: 6.2)
References
Ma et al. Polymorphisms of fibroblast growth factor receptor 4 have association with the development of prostate cancer and benign prostatic
hyperplasia and the progression of prostate cancer in a Japanese population. Int J Cancer. 2008 Dec 1,123(11):2574-9.

N8C9841 Page 20 of 26
RNASEL - Ribonuclease L (2',5'-oligoisoadenylate synthetase-dependent) (rs627928)
RNase L, encoded by the RNASEL gene, is a ribonuclease that metabolizes viral and cellular RNA. The rs627928 polymorphism is
associated with an increased risk of prostate cancer.
RES Genotype POP Possible results
T/T 30% Increased risk of prostate cancer (OR: 1.4)
X T/G 44% Increased risk of prostate cancer (OR: 1.24)
G/G 26% No increased risk of prostate cancer
References
Mi et al. An update analysis of two polymorphisms in encoding ribonuclease L gene and prostate cancer risk: involving 13,372 cases and 11,953
controls. Genes Nutr. 2011 Nov,6(4):397-402.

Breyer et al. Genetic variants and prostate cancer risk: candidate replication and exploration of viral restriction genes. Cancer Epidemiol Biomarkers
Prev. 2009 Jul,18(7):2137-44.

Li et al. RNASEL gene polymorphisms and the risk of prostate cancer: a meta-analysis. Clin Cancer Res. 2006 Oct 1,12(19):5713-9.

LEGEND: RES = your personal analysis result (marked with an X), GENOTYPE = different variations of the
gene (called alleles), POP = percent of the general population that have this genetic result, POSSIBLE
RESULTS = influence of the genetic variation.

N8C9841 Page 21 of 26
PHARMACO GENETICS
Not ordered

ONCOLOGY

CARDIOVASCULAR SYSTEM
Not ordered

NEUROLOGY
Not ordered

METABOLISM
Not ordered

MOVEMENT
Not ordered

DIGESTION
Not ordered

OPHTHALMOLOGY
Not ordered

ODONTOLOGY
Not ordered

OTHERS
Not ordered

SCIENCE

ADDITIONAL INFORMATION
ADDITIONAL INFORMATION
In this chapter you will receive useful and helpful information
CERTIFICATIONS

Certifications
Our laboratory is one of the most modern and automated laboratories in Europe, and has
numerous certifications and quality assurance systems that meet international standards or
even exceed them. The various fields of business are certified separately to the highest
standards.

Analysis for Lifestlye-purposes Medical interpretation of genetic


Certified through analysis in our ISO 15189 analyses
certified laboratory Certified through analysis in our ISO 15189
certified laboratory

Scientific release of analysis results Company and office


Licensed for medical genetic analyses by the Certified through ISO 9001
Austrian government

N8C9841 Page 24 of 26
CUSTOMER SERVICE

Customer Service
Questions or comments about our service?

Our customer service team is happy to help with any enquiries, questions or problems. You can contact
us in the following ways:

➤ office@novogenia.com
➤ +43 662 42 50 99 11

Our team is looking forward to your call. Customer satisfaction is our first priority. If you are not fully
satisfied with our service, please let us know. We will do our best to help find a satisfactory solution to
your problem.

Contact | Impressum
DNAhealthControl
(part of Novogenia Group)
Saalachstrasse 92
5020 Salzburg
Österreich

N8C9841 Page 25 of 26
TECHNICAL DETAILS

Technical details
Address Established analysis methods
Musterstrasse 1 qRT-PCR, DNA sequencing, fragment length
1234 Musterstadt analysis, CNV assay, GC-MS, Immunocap ISAC,
AUSTRIA Cytolisa

Order number Detection rate


N8C9841 ~>99%

Date of birth Report generated


01/02/1985 07/02/2018

Performed analyzes Current version


M7PRO V512

Ordering company Analyzing company


DNAhealthControl DNA Plus - Zentrum für Humangenetik
(part of Novogenia Group) Georg Wrede Strasse 13
Saalachstrasse 92 83395 Freilassing
5020 Salzburg Deutschland
Österreich

Laboratory Director Laboratory Manager

Dr. Daniel Wallerstorfer Bsc. Florian Schneebauer, MSc.

N8C9841 Page 26 of 26
NOTES:
0000000000000
Prostate Health Sensor
John Doe
0000000000000 N8C9841
DEMO

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