Multi-Cancer Driver Interception
HELIXPAN
Available in the US from October 16
- Prescribed and reviewed by physicians
- Home kit or partner location
- Your report within 8 weeks, explained
After prostate, blood or skin cancer, or with a multi-organ history: the broadest reading of your drivers.
HELIXPAN is a physician-guided blood test that reads cancer drivers across tissues, rather than in one organ, in the cell-free DNA of your blood. It is for survivors of cancers the organ applications do not cover, such as prostate, blood or skin cancer, for family histories that span several organs, and for anyone who wants the widest view. Not sure where to start? Start here.
Is HELIXPAN for you?
HELIXPAN is for histories that do not fit inside one organ, and for people who want the widest view. Find the situation closest to yours.
I came through prostate cancer
Your PSA tests and urology visits continue. HELIXPAN reads drivers across tissues, including the androgen-receptor axis that matters in prostate cancer.
I came through a blood cancer
After lymphoma, leukemia or another blood cancer, your hematologist leads follow-up. HELIXPAN adds a reading with a confirmation step built to separate real signal from background.
I had melanoma, or bladder or kidney cancer
Skin and urinary tract cancers have no dedicated application. HELIXPAN is the one for you: it reads drivers across tissues, between your scheduled checks.
Cancer runs in my family, in several organs
When the history in your family spans several organs, a focused panel sees only part of it. HELIXPAN reads across tissues, test after test.
I want the broadest picture
You already track blood pressure, glucose and cholesterol. HELIXPAN adds a reading of cancer drivers across tissues, repeated over time, beside your age-based screenings.
I'm not sure where to start
If nothing points to one organ, start with HELIXPAN. Our physician reviews your questionnaire before anything is prescribed.
A third question
Two kinds of test are familiar. One tells you what you inherited. The other looks for cancer that is already there. HELIXAFE sits between them and asks something neither was built to answer.
- Hereditary testing
What did I inherit?
Reads the variants you were born with, such as BRCA1 or Lynch syndrome genes. The answer is fixed for life, so it is usually tested once.
- HELIXAFE
What is changing now?
Reads acquired driver changes in your blood, then reads them again, so you get a reference first and a direction after.
- Screening
Is there cancer to find?
Mammograms, colonoscopies, CT scans and other exams look for cancer, or precancer, that is already there.
How it works
- 1
Answer a short questionnaire
Choose your application, then share your health and family history in a short online questionnaire.
- 2
A physician prescribes
A Bioscience Institute physician reviews your answers and, if the test fits, prescribes it. Your kit ships overnight.
- 3
One blood draw
Use the kit at home, or visit a partner location. The sample then travels to a CLIA/CAP-certified laboratory.
- 4
Your report, explained
Within 8 weeks, with physicians and genomic counselors who explain each finding and what comes next.
What HELIXPAN follows
HELIXPAN is the widest panel in HELIXAFE: 52 genes, more than 900 point mutations, 99 gene fusions and 12 copy number alterations. In plain words, it reads three kinds of change (single-letter typos, genes broken and joined, extra gene copies) across tissues rather than in one organ.
- Drivers across tissues
- The core drivers shared by many solid tumors, read together rather than organ by organ.
- Tumor suppressor genes
- Genes such as TP53 that act as brakes on damaged cells. HELIXPAN follows the changes that weaken those brakes.
- More than 900 point mutations
- Single-letter changes in a gene's code, the most common kind of driver change.
- 99 fusions, 12 copy number changes
- Genes broken and rejoined to a partner, and genes present in extra copies. Both can lock a growth signal on.
- Prostate and rarer tumors
- The androgen-receptor axis for a prostate history, and drivers relevant to less common tumors.
- Real signal, not noise
- A confirmation step sets genuine signal apart from background, which matters most after a blood cancer or chemotherapy.
Your first HELIXPAN test is your reference across tissues. Repeat tests, through Continue Interception, are read against it, so you see a direction rather than a snapshot. Stable is a result in its own right. A change is a reason to talk with our physicians, who explain what it means for you.
Alongside every check you already do
Age-based screenings, PSA tests, skin checks, blood counts, scans and oncology visits look for cancer that is already there, and HELIXPAN replaces none of them. It works in the time between, reading what is changing across tissues in your blood, so an appointment is no longer the only moment you learn something. Keep every recommended screening and follow-up, exactly as scheduled.
What you receive
Your blood draw kit
Shipped overnight anywhere in the US, with what you need for a draw at home. Prefer a partner location? That works too.
Laboratory analysis
Your cell-free DNA is read with next-generation sequencing in a CLIA/CAP-certified laboratory, on the panel you chose.
A structured report
Within 8 weeks: which acquired changes are present in the genes your application reads, and how strong each signal is.
Physician and genomic counselor review
Bioscience Institute physicians and genomic counselors review your result and explain it against your personal and family history.
What HELIXAFE is not
- Not a replacement for any exam. Keep every recommended screening and follow-up, exactly as scheduled.
- Not a cancer verdict. A result does not tell you whether you have cancer; it is information your physicians help you use.
- Not a look at what you inherited. It reads changes acquired during life, not the variants you were born with.
- Not for under-18s or without a prescription. For adults 18 and over, prescribed and reviewed by Bioscience Institute physicians.
Questions people ask
I came through prostate cancer. Which HELIXAFE application fits?
HELIXPAN. None of the organ applications focuses on the prostate, and HELIXPAN reads across tissues, including the androgen-receptor axis. Your PSA tests, scans and urology visits continue exactly as planned. Our physician reviews your history before prescribing.
How is HELIXPAN different from a multi-cancer blood test?
Multi-cancer blood tests look for signs of a cancer that is already there. HELIXPAN asks something else: which acquired driver changes are in your blood now, and how they move from one test to the next. It is not built to look for cancer, and it replaces none of your screenings.
Does HELIXPAN read tumor suppressor genes?
Yes. Tumor suppressor genes, such as TP53, act as brakes that stop damaged cells from dividing. HELIXPAN reads them alongside growth genes, gene fusions and extra gene copies, 52 genes in all. Our physicians explain in plain words which changes, if any, appear in your report.
Which cancers does HELIXPAN relate to?
HELIXPAN follows the genes on its panel and the cancer types those genes are known to drive, no further. Because it reads across tissues, it suits histories that reach beyond one organ. No blood test reads everything, and our physicians explain what the panel means for your history.
After a blood cancer, won't my blood carry changes anyway?
It can. After lymphoma, leukemia or their treatment, blood cells sometimes carry acquired changes of their own. HELIXPAN includes a confirmation step designed to tell genuine signal from that background, and our physicians read every result with your history in front of them.
What does a positive HELIXPAN result mean?
It means acquired changes were found in one or more genes on the panel, and the report shows how strong each signal is. That is not the same as having cancer. Our physicians and genomic counselors explain it against your personal and family history. If it calls for a closer look, they tell you what to raise with your doctors or refer you to a specialist.
I'm healthy and proactive. Is HELIXPAN worth it?
If you are 18 or over and want the broadest reading, HELIXPAN gives you a reference now and, with repeat tests, a direction over the years. It is not a general health score, and it does not replace the screenings recommended for your age. Our physician reviews your questionnaire first.
Should I choose HELIXPAN or an organ application?
If your history points clearly to the digestive tract, the lungs, or the breast and gynecologic organs, the matching application focuses there. If it spans more than one area, or none of them, HELIXPAN is the one. Still unsure? Start with HELIXPAN.
The science behind it
HELIXAFE grows out of Bioscience Institute's work on cell-free DNA, the small fragments of DNA that cells release into the blood. Its peer-reviewed research on cell-free DNA in healthy people, published in 2019, underpins how HELIXAFE reads acquired changes. The platform is patent-protected, and every sample is analyzed in a CLIA/CAP-certified laboratory.
For healthcare professionals
Request the clinician briefPanel specifications and clinical indications for each application, for physicians and genetic counselors.
Patient? Switch viewMonitoring genomic instability - namely the progressive accumulation of genetic mutations - is key to primary cancer interception and to reducing the risk of future tumour development
HELIXPAN is a test designed to identify genomic instability through a peripheral blood sample.
This parameter is assessed by monitoring the frequency of mutations and represents a key indicator of the prodromal phase of solid tumours. The DNA extracted from the sample is sequenced using advanced Next Generation Sequencing (NGS) technologies. The subsequent bioinformatic analysis enables the identification of potential mutations in the genes under investigation.
HELIXPAN investigates and quantifies the presence of mutations in both tumour suppressor genes and driver genes, with the aim of assessing their effectiveness in preserving genomic stability. When repeated over time, the test can reveal a progressive accumulation of somatic mutations, which would support the persistent inactivation of these genes and the resulting genomic instability.
Origin of Somatic Mutations
From embryonic development onwards, an individual’s DNA undergoes thousands of daily damages due to a wide range of environmental, chemical, or biological factors such as:
- Genotoxicity
- Mutagenic chemical substances
- Tobacco smoke
- DNA replication errors
- Oxidative stress
- Ultraviolet radiation
- Ionising radiation
- Environmental pollution
- Viruses
These damages are normally repaired by Tumour Suppressor Genes, thereby intercepting the development of serious diseases such as cancer. These genes play a fundamental role in the cellular response, promoting the repair of damaged DNA, intercepting uncontrolled cell proliferation, and inhibiting cancerous transformation.
Impact on DNA and Ageing Processes
When Tumor Suppressor Genes lose their function, damage goes unrepaired and transforms into Somatic Mutations that can compromise genomic stability. Temporary loss of gene function is not critical, whereas permanent inactivation results in a progressive accumulation of somatic mutations, which characterizes the prodromal phase of carcinogenesis, known as Genomic Instability.
Genomic Instability is thus an indicator of Tumor Suppressor Gene inactivity. These genes play key roles in regulating the cell cycle, DNA repair, and programmed cell death of damaged cells. When inactive, the cell loses vital control mechanisms that normally protect against cancer development. This loss can lead to multiple consequences that facilitate neoplastic transformation and tumour progression.
In addition to Tumour Suppressor Genes, HELIXPAN also investigates whether somatic mutations are present in Driver Genes. When mutated or abnormally expressed, these genes push cells towards cancerous transformation and contribute directly to tumour growth and survival.
Genomic Instability is considered a primary cause of ageing and age-related diseases, such as cancer. The progressive accumulation of somatic mutations (Genomic Instability) identified by HELIXPAN suggests that critical genome control mechanisms, typically governed by Tumour Suppressor and Driver Genes, are not functioning correctly, leading to an acceleration of associated pathologies.
Health Consequences
The time required for cancer development, starting from the first signs of genomic instability, varies greatly and depends on numerous factors.
There is no fixed or predictable timeframe within which a cell with an inactive Tumour Suppressor Gene and Genomic Instability becomes cancerous.
Generally, the process can take from a few years to several decades. For instance, some forms of leukaemia may develop relatively quickly, while other cancers, such as prostate or breast cancer, may take many years to emerge from a single altered cell. Each case can differ significantly depending on specific circumstances.
Conventional Approaches to Restoring Tumour Suppressor Gene Function
Various approaches have been developed to attempt the restoration of Tumour Suppressor Gene function or to mitigate the effects of their inactivation. The main strategies for gene reactivation include the use of DNA-demethylating agents and gene therapy, which involves introducing a functional copy of the Tumour Suppressor Gene.
Strategies for the Reactivation of Tumour Suppressor Genes
Identify Gene Inactivation
Recognise inactive Tumour Suppressor Genes through molecular analysis and genetic profiling
Apply Gene Therapy
Introduce a functional copy of the gene using viral vectors or other delivery mechanisms
Administer Drugs
Use pharmacological agents to restore protein function and reactivate suppressed pathways
Modify DNA
Chemically modify DNA to restore function through epigenetic modifications and demethylation
Restore Gene Function
Achieve reactivation of tumour suppressor gene function and restore normal cellular control
HELIXPAN: Innovative Genomic Monitoring Backed by Scientific Evidence
The accumulation of genetic alterations and epigenetic changes over a person’s lifetime can lead to genomic instability in normal cells. The immune system recognises and eliminates most mutated cells, but some may evade this control and initiate tumour development.
Liquid biopsy, being minimally invasive, allows longitudinal monitoring over time in healthy individuals of tissue progression events from normal to precancerous and eventually neoplastic conditions.
The genes analysed with the HELIXPAN test were selected based on current scientific literature, data from clinical studies, and guidelines provided by the NCCN (National Comprehensive Cancer Network).
HELIXPAN: Our Comprehensive Analysis
The HELIXPAN test is performed by analysing circulating nucleic acids (DNA and RNA) extracted from the patient’s plasma (cell-free total nucleic acid, cfTNA).
Specifically, the panel includes 52 genes and evaluates over 900 SNVs (single nucleotide variations), 12 CNV-gains (copy number increases), and 99 gene fusions. Additionally, for the MET gene, the test assesses the exon 14 splicing (skipping) mutation.
- Hotspot Genes (SNVs) and small insertions/deletions (indels): APC, AKT1, ALK, AR, ARAF, BRAF, CHEK2, CTNNB1, DDR2, EGFR, ERBB2, ERBB3, FBXW7, ESR1, FGFR1, FGFR2, FGFR3, FGFR4, FLT3, GNA11, GNAQ, GNAS, HRAS, IDH1, IDH2, KIT, KRAS, MAP2K1, MAP2K2, MET, MTOR, NRAS, NTRK1, NTRK3, PDGFRA, PIK3CA, PTEN, RAF1, RET, ROS1, SF3B1, SMAD4, SMO, TP53
- Gene fusions: ALK, BRAF, ERG, ETV1, FGFR1, FGFR2, FGFR3, MET, NTRK1, NTRK3, RET, ROS1
- De novo (non-hotspot) variants in TP53: The panel covers approximately 80% of the TP53 gene. Identified non-HS variants are reported if their allelic frequency is ≥ 1%.
- MET exon 14 skipping
- Copy number amplifications (CNAs): CCND1, CCND2, CCND3, CDK4, CDK6, EGFR, ERBB2, FGFR1, FGFR2, FGFR3, MET, MYC
Under optimal conditions, the test can identify sequence variants with an allelic frequency greater than 0.1%. The Limit Of Detection (LOD) achieved in the analysis for each patient is provided in the technical report.
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Scientific content reviewed by the Bioscience Institute Scientific Board. · Last updated
The information on this page is for general education and does not replace a consultation with a physician.