Triple Negative Breast Cancer overview, complementary and alternative treatments

Triple Negative Breast Cancer overview, complementary and alternative treatments

Is TNBC so hard to beat, or is it just that it does not succumb to conventional drugs and no oncologist treats the things that really matter? Here we review possible ways you could help yourself improve your personal odds of survival, according to research.

Triple-negative breast cancer (TNBC) is an aggressive form of breast cancer that accounts for 15-20 per cent of all breast cancer cases.

 

It is defined by the absence of three key receptors: Oestrogen receptors (ER), Progesterone receptors (PR), and Human epidermal growth factor receptor 2 (HER2).


Because of this, TNBC does not respond to classic hormonal therapies nor treatments targeting HER2, which limits treatment options and contributes to its more challenging prognosis compared to other breast cancer types.


TNBC tends to grow and spread more quickly, is more likely to recur, and is more commonly diagnosed in younger women, Black women, and individuals with a BRCA1 mutation. Most triple-negative breast cancers have a basal-like genetic pattern. This term means that the breast cancer cells look somewhat like the cells that line the breast ducts, the tubes in the breast where milk travels.

 

TNBC Treatment options

 

The uniqueness of TNBC doesn't stop oncologists using standard chemotherapy - this may reduce the size of tumours, but it will rarely get rid of the cancer. Paclitaxel and Carboplatin may be given at the outset. Other chemotherapy options include anthracycline-based regimens like AC (doxorubicin and cyclophosphamide) or EC (epirubicin and cyclophosphamide).

 

Immunotherapy - this is increasingly used in conjunction with chemotherapy.  Pembrolizumab (Keytruda), an anti-PD-1 immune checkpoint inhibitor, is approved for use with chemotherapy before surgery. It may also be used on its own after surgery. The use of chemotherapy with immunotherapy is controversial. It is well known that antibiotics and PPIs given immediately before or during immunotherapy can ruin the performance of the immunotherapy. So, experts ask why would chemotherapy not do the same?


In patients whose tumour expresses PD-L1, Atezolizumab (Tecentriq), a PD-L1 inhibitor, has been studied in combination with chemotherapy in neoadjuvant settings.

 

For patients with inherited BRCA1 or BRCA2 mutations, PARP inhibitors such as olaparib (Lynparza) and talazoparib (Talzenna) are approved for both early-stage and metastatic TNBC.

 

In metastatic TNBC, several newer therapies have been introduced since 2018. For example, Trodelvy, an antibody-drug conjugate targeting Trop-2, is approved for patients whose cancer has progressed on at least two prior lines of therapy. We have rarely seen this 'work'.

 

At this point, you may be wondering if any standard drug offers any long term benefit with TNBC. And you'd be quite justified. The reason is a failure to understand what the differences of TNBC are from the norm, and then to target them, largely because those differences are not usually treated by the current cancer industry.

 

What can you do if you have TNBC?

 

1) Why does TNBC not succumb to breast cancer drugs? 

 

This is a metabolic cancer with epigenetic causes - it’s not caused by a new mutation in your DNA. As Christine Meyr of Sloan Kettering told the world, cancer drivers are not found in your DNA - you have a mutation in your copying process and this is reversible. TNBC cancer shows a complex network of epigenetic, metabolic, and microenvironmental drivers that underlie its aggression and drug resistance. So said a major research study on this cancer.

 

Yes, you can have an inherited mutation in your DNA, such as BRCA1 and sometimes BRCA2. And these can be treated with PARP drugs. But research (1) from Stanford Medicine was very clear - having an inherited mutation may increase your risk of developing a cancer, but plays no role in your survival time.

 

In fact, in TNBC, about 20-30% of people even have a postive oestrogen receptor β (ERβ) but regulation its 'tethering partners' (Fos, Jun, Fra1), render the ERβ ineffective in regulating proliferation and inflammation.

 

TNBC is usually caused by Metabolic Dysfunction. Your metabolism has gone wrong. You ate badly, smoked, drank too much, were attacked by environmental toxins, had low vitamin D, high blood sugar, high cholesterol, were overweight, stressed, had gut problems etc. etc.. Hence existing drugs can't treat it because they don’t promote good metabolism, build your microbiome or correct metabolic dysfunction. Arguably, they make matters worse.

 

You correct epigenetic issues naturally.

 

There are foods shown to reduce the aggression of TNBC, notably Luteolin (lemons), Turmeric, DIM (broccoli) and Rose Hips. We have an article on seven natural compounds shown to fight TNBC.

 

We have research showing that a good diet, particularly consuming a Rainbow Diet slashes TNBC risk.

 

There are also strong bioactive compounds known to correct breast cancer and TNBC epigenetically.

 

In case you are wondering ‘What is Epigenetics?’ we have an article on Epigenetics and reversing cancer.

 

And here are just some of the compounds that can correct Epigenetic changes - 25 Epigenetic compounds that have been shown to reverse cancer.

 

2) Natural compounds and TNBC 

 

Of course, there’s no Phase 3 Clinical trial research on natural compounds helping fight a cancer as difficult as TNBC. Who would pay for it? But there is research, and here are just a few of the research papers on PubMed:

 

Berberine benefits with TNBC - How berberine helps fight TNBC.

 

And Turmeric induces apoptosis of TNBC cells (5)

 

And Melatonin inhibits TNBC progression (6)

 

And a bioavailable Honokiol was shown to kill TNBC cells (7)

 

And Honokiol inhibits lung metastases by regulating macrophage activity in TNBC (8)

 

And a combination of Quercetin and Turmeric inhibits TNBC (9).

 

And Quercetin may reduce spread of TNBC (10).

 

And Lycopene - induces cell cycle arrest and also acts by inhibiting the Wnt/β-catenin signaling pathway, a key driver of TNBC progression (11). We might not use lycopene during chemotherapy because it is an alpha carotene and a strong antioxidant. from deep sea plants and certain strains of spirulina

 

And Phycocyanin, a pigment protein complex from deep sea plants and certain strains of spirulina, has anti-cancer activity, and restricted spread and colonisation in TNBC (12).

 

And a blend of organic Medicinal Mushrooms - Reishi, Maitake, Cordyceps, Shiitake, Agaricus - caused apoptosis of lung mets in mice given TNBC (13). 

 

3) The TNBC tumour microbiome and biofilms

 

The tumour microbiome in TNBC is not of much interest to your oncologist but it exhibits distinct features, including the lowest bacterial diversity among all breast cancer types! What does that mean? You make antibodies every minute of everyday to the bacteria in your gut. Lower diversity = lowered antibodies and a lowered adaptive immune system.

 

TNBC has a higher abundances of bacteria such as Aggregatibacter and Caulobacter, which are known to form biofilms (protective, blocking films) and are associated with conditions like periodontitis and endocarditis (2).

 

Conventional drugs rarely break down biofilms, but there are many natural compounds that are strong in breaking down biofilms - 

 

* Garlic extract and its active components allicin, ajoene, and L-homoserine lactone, have demonstrated the ability to reduce biofilm formation from pathogens such as Pseudomonas aeruginosa and Staphylococcus aureus.

  

* Oil of oregano, rich in carvacrol and thymol, also exhibits potent anti-biofilm activity against various bacterial species.

 

* Cranberry polyphenols, pomegranate extract, apple cider vinegar and manuka honey have all been noted for breaking down biofilm structures.

 

Additionally, studies have found that the tumour microbiota in TNBC has higher levels of pathogenic bacteria such as Prevotella, Brevundimonas, Arcanobacterium, Escherichia, Sphingobacterium, Actinomyces, and Rothia, and shows higher signals for viral presence of Herpesvirus members and yeasts/fungi such as Piedra.

 

Mouth pathogens such as Fusobacterium are present in the tumours, and this bacterium seems capable of binding to Gal-3 (see later) and increasing drug resistance, while reducing tumour suppression.

 

4) The Gut microbiome in TNBC -

 

Dysbiosis and lower levels of Bacteroides species such as Alistipes, play a significant role in cancer progression and treatment response (chemo, radio and immunotherapy). Yes, the TNBC gut microbiome blocks the drugs!!

 

So get rid of the blockers. Researchers are currently studying the effects of improving the gut microbiome to improve treatment outcomes (e.g by using probiotics, prebiotics, dietary interventions, and even fecal microbiota transplantation). I've been doing this for years with TNBC patients!!! We kill the bad and replenish the good - these things correct metabolic dysfunction. (All illness starts in the gut - Hippocrates)

 

A full gut rebuild would be advisable for someone with TNBC. See the end of this article for how to 'Heal your Gut'.

 

5) Viruses in TNBC - 

 

High-risk human papillomaviruses (HPVs) and Epstein-Barr virus (EBV) are frequently detected in triple-negative breast cancer (TNBC). In a study of 70 TNBC cases from Croatia (3), high-risk HPVs were present in 53% (37/70) of samples, while EBV was detected in 36% (25/70). How many oncologists think to get rid of the viruses driving your cancer?

 

6) High Galectin 3

 

Gal-3 is a protein produced in varying amounts by different cancer cells. Sarcoma, Neuroendocrine, and TNBC have the highest levels of Gal-3 in their cells. It promotes tumour growth, metastases, immune system depletion and chemo-resistance. As we said above, the bacterium Fusobacterium can enhance Galectin-3. Oncologists do nothing to eradicate Fusobacterium (try artemisinin) and have nothing to block Galectin-3 but Gal-3 can be blocked by Modified Citrus Pectin.

 

7) Cancer Stem Cells (CSCs) are a major factor

 

Oncologists have no drugs capable of dealing with CSCs. These CSCs, often identified by markers such as CD44+CD24-/ALDH1+, are more prevalent in TNBC compared to the other breast cancer subtypes and are responsible for the disease's high rates of relapse, recurrence and resistance to chemotherapy and radiotherapy (4). There are off-label drugs such as Niclosamide, Doxycycline or Ivermectin that can deal with CSCs, and a good number of natural compounds such as Holy Basil, with Turmeric and Resveratrol, which kill CSC's in vivo. We have an article on the top natural compounds that can treat Cancer Stem Cells.

 

8) p53 and TNBC

 

Oncologists should test you for TP53 or p53 - it's the tumour suppressor protein, and is missing in 80% of TNBC - they call it a mutation, but actually it's a deficiency. I’m a biochemist and we understand these things. p53 or TP53 is the controller of the mitochondrial genome - there are 37 genes in the mitochondria (your cell's power stations) and these keep the energy system running perfectly in your body. A p53 deficiency occurs with low energy production and leads to a more aggressive cancer. This could be due to a poor diet, too much salt, stress, low iodine, magnesium etc.. It is a metabolic issue and we look at known ways to correct p53 deficiency here.

 

9) BRCA1/2 inherited genes - 

 

Inherited mutations are a key driver of TNBC, with prevalence rates of up to 20% among TNBC patients, as opposed to a 3-5% occurrence in the general population. More cases are due to BRCA1 than BRCA2. You should be tested and if positive you could take a PARP and/or the long list of natural compounds that behave like a PARP inhibitor. TNBC incidence is also greater in younger women patients and this has shown a marked increase since Covid, as noted by Yale Medicine.

 

10) The crucial importance of Lymphocytes in TNBC

 

TNBC is characterised by a high density of tumour-infiltrating lymphocytes (TILs), being more prevalent in TNBC than in other breast cancer subtypes. These TILs are closely associated with improved outcomes, including a higher likelihood of pathological complete response to neoadjuvant chemotherapy and better overall survival. The immune infiltrate in TNBC tumours includes not only T- lymphocytes but also B-lymphocytes.

 

The problem is that all chemo drugs and antibiotics like Doxycycline lower your lymphocytes and this lowers your survival times. Radiotherapy is the worst - it lowers lymphocytes and damages the immune memory of B-lymphocytes. According to UCLA expert Professor Soon-Shiong, just a 10 per cent lowering of your lymphocytes reduces survival times by 43 per cent and Doctors have no way of restoring their levels.

 

Patients should ensure they always have good levels of lymphocytes (above 2.2). They can achieve this through high doses of organic Turkey Tail Powder, Echinacea, Astragalus and Cats Claw. According to Patrick Soon -Shiong, oncologists rarely even try to rebuild lymphocytes after conventional treatments and this leaves patients with TNBC with a strong risk of lowered survival times. We believe you should immediately aim to restore levels to around 2.2 - 2.6 after all treatments. Your lymphocytes are your primary attack cells.

 

Lymphocytes also have receptors for vitamin D on their surface - vitamin D acts as a hormone and it activates the lymphocytes. Your vitamin D level is thus crucial too. Below 80 nmol/L (or 32 ng/ml) is deficiency (Harvard), and healthy levels are over 125 nmol/L or 50 ng/ml.

 

You can learn more about the crucial role of Lymphocytes and how to boost them here.

 

Go to: How to heal your Gut

 

********

References

 

1. Women with genetic mutations fare no worse with breast or ovarian cancer, study finds;  Stanford Medicine News

2. Unravelling novel microbial players in the breast tissue of TNBC patients: a meta-analytic perspective;  Hannah H. Rashwan et al; npj Biofilms and Microbiomes volume 11, Article number: 182 (2025) 

3. Presence of high-risk HPVs, EBV, and MMTV in human triple-negative breast cancer; Ishita Gupta et al; Human vaccine immunotherapy 2021 Nov 2;17(11):4457-4466

4. Regulation of cancer stem cells in triple negative breast cancer; Norman Fultang et al; Cancer Drug Resist. 2021 Jun 19;4(2):321–342.

5. Curcumin induces apoptosis of triple-negative breast cancer cells by inhibition of EGFR expression; Xiao-Dong Sun et al; Mol Med Rep. 2012 Dec;6(6):1267-70

6. Melatonin inhibits triple-negative breast cancer progression through the Lnc049808-FUNDC1 pathway; Anli Yang et al; Cell Death Dis, 2021 Jul 16;12(8):712.

7. Honokiol nanomicellar formulation produced increased oral bioavailability and anticancer effects in triple negative breast cancer (TNBC); Chandraiah Godugu et al; Colloids Surf B Biointerfaces. 2017 May 1:153:208-219.

8. Honokiol prevents lung metastasis of triple-negative breast cancer; Mei Mei et al; Eur J Pharmacol. 2023 Nov 15:959:176076.   

9. Synergistic anticancer action of quercetin and curcumin against triple-negative breast cancer cell lines; Sai Kundur et al; J Cell Physiol. 2019 Jul;234(7):11103-11118.

10. Quercetin regulates β-catenin signaling and reduces the migration of triple negative breast cancer; Asha Srinivasan et al; Mol Carcinog. 2016 May;55(5):743-56.

11. A Comprehensive Review on the Molecular Mechanism of Lycopene in Cancer Therapy; Muhammad Maaz et al, Food Sci Nutr. 2025 Jul 13;13(7):e70608.

12. Molecular mechanism of anti-cancer activity of phycocyanin in triple-negative breast cancer cells; Ravi M et al;  BMC Cancer 15, 768 (2015).

13. From a Medicinal Mushroom Blend a Direct Anticancer Effect on Triple-Negative Breast Cancer: A Preclinical Study on Lung Metastases; Elisa Roda et al; Molecules. 2020 Nov 18;25(22):5400.

 

 

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