PeptideJournal
FAQ11 min read

Can Peptides Cause Cancer?

The straight answer: no peptide used in therapy has been proven to cause cancer in humans. But several peptides raise theoretical concerns because they activate biological pathways — growth factor signaling, angiogenesis, cell proliferation — that cancer also uses.

The straight answer: no peptide used in therapy has been proven to cause cancer in humans. But several peptides raise theoretical concerns because they activate biological pathways — growth factor signaling, angiogenesis, cell proliferation — that cancer also uses. The devil is in the details of which peptide, which pathway, and what the data actually shows versus what people fear.

This article separates the real science from the speculation.

Table of Contents

Why This Question Comes Up

The concern isn't random. It stems from basic biology: many therapeutic peptides work by stimulating growth. Growth hormone peptides stimulate GH and IGF-1, which promote cell proliferation. BPC-157 promotes angiogenesis (new blood vessel formation) to accelerate healing. GLP-1 agonists activate receptors found on thyroid C-cells.

Cancer, at its core, is uncontrolled cell growth. So the question is logical: if a peptide promotes growth, repair, and new blood vessel formation, could it also promote tumor growth?

The answer requires looking at each peptide individually, because the risks are different for each one.

GLP-1 Agonists and Thyroid Cancer: The Rodent Data

Every FDA-approved GLP-1 receptor agonist — semaglutide, tirzepatide, liraglutide, dulaglutide, exenatide — carries a boxed warning about thyroid C-cell tumors. This is the most prominent cancer concern in peptide therapy, and understanding where it comes from is important.

What the Rodent Studies Showed

In preclinical studies, GLP-1 receptor agonists caused thyroid C-cell tumors (medullary thyroid carcinoma) in rats and mice at clinically relevant doses. The mechanism: GLP-1 receptors are expressed on thyroid C-cells (the cells that produce calcitonin). In rodents, activating these receptors triggers C-cell proliferation, calcitonin release, and eventually tumor formation.

The rodent data was consistent and dose-dependent across multiple GLP-1 drugs, which is why the FDA requires the boxed warning.

The Species Problem

Here's the critical context: rodent thyroid C-cells and human thyroid C-cells are fundamentally different. Rodent C-cells express high levels of GLP-1 receptors. Human C-cells express much lower levels. The degree of C-cell proliferative response to GLP-1 activation in humans appears to be dramatically less than in rodents.

This isn't a theoretical distinction. It's been measured. Multiple studies have shown that GLP-1 receptor expression in human thyroid tissue is markedly lower than in rodent thyroid tissue. Additionally, the rodent studies used high doses administered over a significant portion of the animals' lifespans — conditions that don't directly translate to human clinical use.

What Human Studies Actually Show

The human data on GLP-1s and thyroid cancer is genuinely mixed — and that ambiguity is worth being honest about.

Studies Suggesting Increased Risk

A large international multicenter cohort study found that use of GLP-1 RA for 1-3 years was associated with an increased risk of all thyroid cancer (adjusted hazard ratio 1.58) and medullary thyroid cancer (adjusted HR 1.78). A 2024 meta-analysis calculated a 52% increase in thyroid cancer risk, translating to an absolute increase of 0.148 per 1,000 patient-years — meaning for every 1,349 patients treated for 5 years, approximately one additional thyroid cancer case would be expected.

Studies Finding No Increased Risk

A pooled analysis of multiple cohorts found no association between GLP-1RA use and increased thyroid cancer risk (pooled weighted HR 0.81, CI 0.59-1.12). A January 2025 international study found no evidence that GLP-1RA use increases thyroid cancer risk.

The Detection Bias Explanation

A Mayo Clinic study offered a compelling alternative explanation: the increased thyroid cancer diagnoses observed in the first year of GLP-1 therapy likely reflect detection bias, not causation. Patients starting GLP-1 drugs receive more medical attention, more bloodwork, and more physical exams — which naturally leads to earlier detection of pre-existing thyroid conditions that might otherwise have gone unnoticed.

This detection bias theory is supported by the timing pattern: the risk appears highest in the first year of use (when screening attention is highest) and doesn't increase with longer duration of therapy (which you'd expect if the drug were actually causing cancer).

The FDA's Position

The FDA has contraindicated GLP-1 agonists in patients with:

  • Personal history of medullary thyroid carcinoma (MTC)
  • Family history of MTC
  • Multiple endocrine neoplasia syndrome type 2 (MEN2)

This is a precautionary measure based on the rodent data, not proof that GLP-1 drugs cause thyroid cancer in humans. The European Medicines Agency (EMA) has not implemented the same contraindication, reflecting a different interpretation of the evidence.

BPC-157 and Angiogenesis: The Theoretical Concern

BPC-157 is a potent stimulator of angiogenesis — it promotes the formation of new blood vessels by upregulating VEGFR2 (vascular endothelial growth factor receptor 2) and activating the VEGFR2-Akt-eNOS signaling pathway.

Why This Concerns Oncologists

Angiogenesis is a double-edged sword. In healing, new blood vessels deliver oxygen and nutrients to damaged tissue, accelerating repair. In cancer, new blood vessels feed tumors and facilitate metastasis. The VEGF/VEGFR2 pathway is active in approximately half of human cancers, and anti-VEGF drugs (like bevacizumab/Avastin) are a major class of cancer treatment.

A 2023 pharmaceutical review noted that BPC-157's upregulation of VEGFR2 could "inadvertently support tumor growth and metastasis if cancer cells are present." This is a genuine concern grounded in well-established cancer biology.

What the Proponents Say

Researchers who study BPC-157 (primarily Dr. Predrag Sikiric's group in Croatia) have argued that BPC-157 has "prominent anti-tumor potential" and controls angiogenesis rather than simply promoting it. They cite studies showing BPC-157 alleviates cancer-related cachexia and inflammation in tumor-bearing animals.

What "Pro-Angiogenic" Actually Means in Practice

Every time a wound heals, angiogenesis happens. Every time you exercise, angiogenesis happens in your muscles. Physiological angiogenesis is normal and necessary. The concern with BPC-157 isn't that it promotes angiogenesis per se — it's whether it could promote pathological angiogenesis in a tumor context.

Healthy tissue has mechanisms to regulate and limit blood vessel growth once healing is complete. Cancer tissue hijacks these mechanisms, promoting uncontrolled angiogenesis to feed tumor growth. The question is whether BPC-157's angiogenic stimulation could tip the balance toward pathological blood vessel growth in someone with pre-existing cancer. This remains unanswered.

The Honest Assessment

No study has shown that BPC-157 causes cancer in any species. But:

  • The pro-angiogenic mechanism is real and well-documented
  • The VEGF/VEGFR2 pathway is a known cancer promoter
  • No cancer-specific safety studies have been conducted in humans
  • The anti-tumor claims are not supported by studies showing actual tumor inhibition

The prudent position: people with active cancer, a recent history of cancer, or strong cancer risk factors should avoid BPC-157 until cancer-specific safety data exists. For everyone else, the theoretical risk needs to be weighed against the theoretical and observed benefits.

This is the most robust dataset connecting a peptide-related pathway to cancer risk, and it's directly relevant to anyone using growth hormone secretagogues like CJC-1295, ipamorelin, GHRP-2, GHRP-6, or MK-677.

What the Evidence Shows

A landmark UK Biobank study of nearly 400,000 participants confirmed that higher circulating IGF-1 levels are positively associated with increased risk of:

  • Colorectal cancer — consistent association across multiple studies
  • Breast cancer — women with IGF-1 levels in the top 20% had 1.24x increased risk
  • Prostate cancer — a meta-analysis of 47 studies confirmed a positive association
  • Thyroid cancer — association identified in the UK Biobank data

The Mechanism

IGF-1 promotes cancer through several pathways:

  • Inhibiting apoptosis: IGF-1 activates the PI3K/Akt survival pathway, preventing programmed cell death — the mechanism the body uses to eliminate damaged or precancerous cells.
  • Stimulating proliferation: The Raf/MEK/ERK cascade promotes cell division.
  • Promoting immune evasion: IGF-1 upregulates PD-L1 (an immune checkpoint), helps tumors escape immune surveillance, and promotes immunosuppressive regulatory T-cell function.

The Critical Nuance

The IGF-1/cancer data is epidemiological — it shows association, not necessarily causation. People with naturally higher IGF-1 levels have higher cancer rates. This doesn't prove that artificially raising IGF-1 through peptides increases cancer risk, though it's biologically plausible.

Also important: the cancer risk correlates with chronically elevated IGF-1. Short-term, modest elevation from properly dosed GH peptides may carry different risk than lifelong high levels. The problem is that we don't have long-term studies on growth hormone peptide users to know with certainty.

Growth Hormone Peptides and Tumor Risk

Growth hormone replacement therapy (using actual recombinant GH, not peptide secretagogues) has been studied for cancer risk more extensively. The findings provide some guidance:

  • Large observational studies of adults on GH replacement therapy have not found an increased incidence of new cancers
  • GH replacement in childhood cancer survivors remains controversial — some studies show no increased recurrence risk, while others suggest caution
  • The Endocrine Society recommends against GH therapy in patients with active malignancy

Growth hormone peptides produce more modest and physiological IGF-1 elevations compared to direct GH injection. This theoretically means lower cancer risk. But again, long-term data specific to peptide secretagogues doesn't exist.

Peptides Being Studied to Fight Cancer

It's worth noting that the peptide-cancer relationship isn't one-directional. Multiple peptide-based therapies are being developed specifically against cancer:

  • Peptide-drug conjugates (PDCs): Peptides that target tumor-specific receptors, delivering chemotherapy directly to cancer cells while sparing healthy tissue.
  • Cancer vaccines: Peptide-based vaccines that train the immune system to recognize tumor-associated antigens.
  • Antimicrobial peptides: Some antimicrobial peptides (like LL-37) show direct anti-tumor activity in laboratory studies.
  • GLP-1 agonists themselves: Some research suggests GLP-1 activation may actually have anti-cancer properties in certain contexts, adding further complexity to the thyroid cancer question.

For more on this topic, see peptides for cancer research.

Skincare Peptides and Cancer: A Non-Concern

For completeness: topical skincare peptides like Matrixyl, Argireline, and GHK-Cu do not raise meaningful cancer concerns. They work locally in the skin, achieve minimal systemic absorption, and have decades of consumer safety data. While GHK-Cu does influence gene expression and has anti-inflammatory properties, studies suggest its gene-expression modulating effects may actually be protective — GHK-Cu has been shown to upregulate tumor suppressor genes and downregulate genes associated with cancer progression in cell culture studies.

Similarly, collagen peptide supplements taken orally are broken down into basic amino acids and small peptide fragments. They do not activate growth factor pathways or promote angiogenesis in any meaningful way. There is no cancer concern with oral collagen supplementation.

Context and Perspective

Risk needs context to be meaningful:

Absolute vs. relative risk. The highest thyroid cancer risk estimate from GLP-1 studies translates to approximately 1 extra case per 1,349 patients treated for 5 years. Meanwhile, the cardiovascular benefit from semaglutide (20% reduction in MACE events) saves many more lives than a tiny potential thyroid cancer risk threatens.

Background cancer rates. Medullary thyroid carcinoma has an annual incidence of about 0.2 per 100,000 people. Even a 50% relative increase would change this to 0.3 per 100,000 — still extremely rare.

Growth is not cancer. Promoting growth, angiogenesis, or cell proliferation doesn't cause cancer. Cancer requires specific genetic mutations that disable growth controls. Growth-promoting peptides could theoretically accelerate existing cancer or tip pre-cancerous cells over a threshold, but they don't create the genetic damage that initiates cancer.

Risk vs. benefit. Obesity itself is a major cancer risk factor, linked to 13 types of cancer. If a GLP-1 agonist produces significant weight loss, the cancer risk reduction from weight loss may outweigh any theoretical cancer risk from the drug itself.

Frequently Asked Questions

Should I get screened for cancer before starting peptides?

It's prudent to have a baseline health evaluation before starting any therapeutic peptide protocol, including standard cancer screening appropriate for your age and risk factors. For GLP-1 drugs, thyroid examination and a family history review are reasonable. For growth hormone peptides, ensuring IGF-1 levels stay within physiological range through monitoring is a smart precaution. For BPC-157, a discussion with your doctor about any cancer history or elevated risk is appropriate.

Can I use peptides if I've had cancer?

This depends on the cancer type, how long ago it was, and which peptide you're considering. FDA-approved GLP-1 drugs are specifically contraindicated only with medullary thyroid carcinoma family history. For other cancer histories, the decision should involve your oncologist. Growth hormone-stimulating peptides are generally not recommended for anyone with active malignancy, and caution is warranted for recent cancer survivors. Topical skincare peptides don't carry meaningful cancer risk.

Does BPC-157 cause cancer?

No study has demonstrated that BPC-157 causes cancer in any species. The concern is theoretical, based on its ability to promote angiogenesis through the VEGFR2 pathway — the same pathway that tumors use to grow new blood vessels. This doesn't mean BPC-157 causes cancer; it means the question hasn't been adequately studied. The absence of evidence isn't evidence of absence, nor is it evidence of presence.

Are GLP-1 drugs safe to take long-term regarding cancer risk?

The existing long-term data (up to 5+ years from clinical trials and post-market surveillance) has not identified a clear causal link between GLP-1 drugs and cancer in humans. The SELECT trial followed 17,604 patients for a mean of 39.8 months and did not report increased cancer incidence. Ongoing outcome trials (like SURMOUNT-MMO) will provide even longer-term data. The FDA continues to require monitoring and maintains the thyroid cancer warning as a precaution.

The Bottom Line

No peptide has been proven to cause cancer in humans. But the theoretical concerns aren't baseless — they're grounded in real biology.

GLP-1 agonists carry a rodent-derived thyroid cancer concern that human data has not confirmed. The weight of evidence suggests detection bias rather than causation, but definitive long-term data is still accumulating.

BPC-157's pro-angiogenic mechanism could theoretically support tumor growth, but this has never been observed. People with active cancer or strong risk factors should exercise particular caution.

Growth hormone peptides raise IGF-1 levels, and higher IGF-1 is epidemiologically linked to several cancer types. This is the most substantiated concern, though it reflects correlation rather than proven causation.

The responsible approach: discuss cancer risk factors with your doctor before starting any peptide therapy, maintain regular cancer screenings, monitor IGF-1 levels if using growth hormone peptides, and weigh the theoretical risks against the documented benefits for your specific situation.

References

  1. Silverii GA, et al. Glucagon-like peptide-1 receptor agonists and risk of thyroid cancer. Diabetes Obes Metab. 2024;26(3):e15382. Wiley
  2. Bezin J, et al. GLP-1 Receptor Agonists and the Risk of Thyroid Cancer. Diabetes Care. 2023;46(2):384-390. Diabetes Care
  3. Mayo Clinic. GLP-1RA and thyroid cancer: New study suggests detection bias. 2025. Mayo Clinic
  4. Hsieh MJ, et al. Therapeutic potential of pro-angiogenic BPC157 is associated with VEGFR2 activation. J Mol Med. 2017;95:323-333. PubMed
  5. UK Biobank / Oxford CEU. IGF-1 and cancer risk in 400,000 participants. Oxford CEU
  6. Watts EL, et al. Circulating IGF-1 and cancer risk: Mendelian randomization analysis. Int J Epidemiol. 2023;52(4):1154-1167. PubMed