> For the complete documentation index, see [llms.txt](https://myhealingcommunity.gitbook.io/myhealingcommunity-docs/llms.txt). Markdown versions of documentation pages are available by appending `.md` to page URLs; this page is available as [Markdown](https://myhealingcommunity.gitbook.io/myhealingcommunity-docs/breast-cancer/triple-negative/lar-subtype-triple-negative-ar-positive.md). # LAR-Subtype Triple-Negative (AR-Positive) Some **triple-negative breast cancers** are strongly positive for the **androgen receptor**, or **AR**. This pattern is often called the **luminal androgen receptor**, or **LAR**, subtype. LAR TNBC deserves its own treatment discussion because it does not behave like the more familiar basal-like form of TNBC. It often shows lower proliferation, lower **neoadjuvant response** to standard chemotherapy, and a stronger pull toward pathway-led trial matching. The key question is not whether it is still triple-negative. It is which biology is actually driving the disease. If you are starting from the broader TNBC picture, see [Triple-Negative](/myhealingcommunity-docs/breast-cancer/triple-negative.md). This page goes deeper on the subgroup where **AR signalling**, **PI3K/AKT/mTOR** alterations, and occasional **ERBB2** mutations can shape the next step. ### In this section Jump to: * [What LAR TNBC means](#what-lar-tnbc-means) * [Why LAR TNBC behaves differently](#why-lar-tnbc-behaves-differently) * [Markers worth checking on reports](#markers-worth-checking-on-reports) * [TKIs for ERBB2-mutant LAR](#tkis-for-erbb2-mutant-lar) * [How sequencing fits in](#how-sequencing-fits-in) * [Treatment and trial directions](#treatment-and-trial-directions) * [Selected trials and how to use them](#selected-trials-and-how-to-use-them) * [Standard options that still matter](#standard-options-that-still-matter) * [Supportive and experimental research areas](#supportive-and-experimental-research-areas) * [Questions to ask your team](#questions-to-ask-your-team) * [Related pages](#related-pages) * [Selected references](#selected-references) ### What LAR TNBC means LAR TNBC is still **triple-negative** on standard **ER**, **PR**, and **HER2** testing. The difference is that the tumour shows strong **AR** expression and often carries a more luminal, hormone-linked transcriptional program rather than a classic basal-like one. It is best understood as a biologically distinct subset within TNBC, not as a contradiction of the triple-negative label. That distinction matters clinically. A tumour can be triple-negative on routine receptors and still be shaped by **AR signalling**, lower cell-cycle activity, and a different pattern of therapeutic vulnerability. This is one reason LAR disease can look less explosive at diagnosis yet still be frustrating in the neoadjuvant setting, where pathologic complete response rates are often lower than in more proliferative basal-like TNBC. ### Why LAR TNBC behaves differently LAR tumours often show **lower proliferation** than basal-like TNBC, which helps explain why they may grow more slowly and why **Ki-67** can be lower. That same biology can also make them less chemosensitive. In practical terms, a subtype that is less dependent on rapid cell cycling may produce a weaker **pathologic complete response** to standard neoadjuvant chemotherapy, even when the cancer is still very real and still needs standard treatment planning. Lower response does not mean lower relevance. It means the biology may be pointing toward a different vulnerability. Relapse timing can differ as well. Basal-like TNBC often carries a more front-loaded recurrence pattern. Some LAR cancers appear to relapse later, which fits with a less proliferative but more persistent biology. That does not make LAR safer. It changes the time course and the trial logic. The genomic background also tends to differ. **PIK3CA** alterations are enriched in this subtype, which is one reason **AR plus PI3K/AKT/mTOR** combinations keep resurfacing in early-phase studies. A subset of LAR tumours also carries **ERBB2** mutations despite remaining **HER2-negative** by routine testing. Those cases can fall into a separate therapeutic conversation from classic HER2-amplified breast cancer. ### Markers worth checking on reports #### Androgen receptor **AR IHC** is the starting point, not the whole story. Strong staining raises interest in **AR-focused trials** and combination strategies, but **AR-positive** does not always mean truly **LAR-like**. Some tumours stain for AR and still behave more like basal TNBC, which is why wider molecular profiling can add useful context. The most actionable details are the **percentage of AR-positive cells**, staining intensity, and whether the rest of the pathology fits a luminal-pattern tumour rather than a high-grade basal one. Those details help separate a biologically meaningful AR signal from a more incidental finding. #### Ki-67 **Ki-67** gives a rough sense of proliferation. LAR tumours often show lower **Ki-67** than basal-like TNBC, which fits the slower-cycling biology, but it is only one clue. A lower number supports the pattern. It does not prove the subtype by itself. What matters most is the combination of findings. **AR positivity**, a lower **Ki-67**, and luminal-featured molecular profiling together are more informative than any one marker alone. #### PIK3CA and the PI3K-AKT-mTOR pathway **PIK3CA** mutations are enriched in LAR TNBC, and broader **PI3K/AKT/mTOR** pathway changes can matter even when the report does not show a classic hotspot mutation. This is one of the clearest examples of biology shaping trial direction. If this pathway is altered, it strengthens the rationale for **AR blockade** plus **PI3K**, **AKT**, or **mTOR** targeting, usually in a trial-based setting rather than as standard care. This is also one reason genomic testing matters more in LAR disease than it might in a more straightforward basal-like case. The pathway enrichment is not incidental background noise. It can be part of the subtype logic. #### ERBB2 mutations Some LAR tumours carry activating **ERBB2** mutations without **HER2** amplification. These alterations usually do not appear on standard **HER2 IHC** or **FISH** testing, so they can be missed on routine pathology while still mattering biologically and potentially therapeutically. This changes the treatment conversation in a very specific way. In the right setting, an **ERBB2-mutant** result can raise interest in **HER2-targeted TKIs**, even though the cancer does not fit the usual **HER2-positive** category. The therapeutic logic here comes from the mutation, not from overexpression or amplification. The next two sections explain what that means in practice. First, they define **TKIs for ERBB2-mutant LAR**. Then they show how sequencing is what usually finds these alterations in the first place. #### TKIs for ERBB2-mutant LAR When this page mentions **TKIs** in LAR-type TNBC, it means **HER2-targeted oral tyrosine kinase inhibitors**, especially **neratinib**, used because sequencing shows an activating **ERBB2** (**HER2**) mutation. This is different from the usual breast-cancer setting, where HER2 drugs are used because the tumour is **HER2-positive** on **IHC** or **FISH**. Here, the reason to consider a HER2 TKI is the mutation itself rather than conventional **HER2** overexpression or amplification. What is known most clearly right now is that **neratinib** has the strongest direct evidence in **HER2** or **ERBB2-mutant** breast cancer, including metastatic TNBC, and has shown meaningful activity in mutation-positive but non-amplified disease. In TNBC specifically, studies such as **SUMMIT** support neratinib, sometimes with **trastuzumab**, in heavily pretreated **ERBB2-mutant** disease. **Lapatinib** is also a HER2 TKI used in breast cancer, but the mutation-focused signal is stronger for neratinib, and some HER2 mutations may respond less well to older HER2-directed drugs. **Tucatinib** is an important HER2 drug in breast cancer, but the evidence base in **HER2-mutant**, **HER2-non-amplified** TNBC is not as established as it is for neratinib in this specific setting. This remains a **precision-oncology** or **trial-based** discussion, not a standard shortcut for all LAR TNBC. It matters in the subset with a genuine activating **ERBB2** mutation. A practical way to raise this with your oncologist is: > "I understand this cancer is still HER2-negative on standard IHC or FISH testing. If a multi-gene next-generation sequencing panel on the tumour, or a liquid biopsy, were to show an activating ERBB2 mutation, is that the sort of mutation that could make a HER2 tyrosine kinase inhibitor such as neratinib, possibly with trastuzumab, relevant for me in a clinical-trial or precision-oncology setting?" #### How sequencing fits in Routine **ER**, **PR**, and **HER2** tests do not look for **ERBB2** (**HER2**) mutations. Those are usually found on a multi-gene **next-generation sequencing**, or **NGS**, panel, which many centres now use in metastatic or high-risk cancers to look for targetable changes. That is why sequencing can change the picture even when routine pathology does not. In LAR TNBC, it can clarify not only **ERBB2** but also other subtype-relevant findings such as **PIK3CA**, **PTEN**, **BRCA1/2**, and broader pathway changes. In countries such as the **USA** and **Australia**, this kind of profiling is becoming more common in advanced breast cancer, especially when trial matching is part of the discussion, but access is still uneven and it is not universal. If a report does not mention mutations at all, it is reasonable to ask whether tumour **NGS**, including **ERBB2**, **PIK3CA**, and related drivers, or **liquid-biopsy profiling** would add useful information in your setting. For more on circulating-tumour-DNA strengths and blind spots, see [Liquid Biopsy for HER2-Positive Resistance](/myhealingcommunity-docs/breast-cancer/her2-positive/her2climb/liquid-biopsy-for-her2-positive-resistance.md). The disease context is different, but the practical limits of mutation detection still apply. #### BRCA1, BRCA2, and HRD LAR TNBC can still carry **BRCA1/2** variants or wider **HRD** features. That matters because subtype biology does not cancel out DNA-repair biology. If **BRCA1/2** or **HRD** is present, **platinum drugs** and **PARP inhibitors** can still be highly relevant in selected cases. This is an important guardrail. A tumour can look LAR-enriched and still fit established TNBC treatment logic when homologous recombination repair is weak. #### PD-L1 and immune context LAR tumours often have lower immune activity than more inflamed TNBC subtypes. **PD-L1** expression may be lower, and **TILs** may be less prominent, which can reduce enthusiasm for assuming the same level of benefit from chemo-immunotherapy seen in more immune-active disease. That said, immune context still matters. If **PD-L1** is positive or **TILs** are meaningfully present, those findings should stay in the discussion. The point is not that immunotherapy never matters in LAR TNBC. It is that the subgroup often looks less immune-hot, so the biology needs closer reading. This is part of why trial matching can differ from the usual TNBC reflex toward immune-led approaches. ### Treatment and trial directions The main LAR treatment themes stay fairly consistent, but they need careful framing. Standard TNBC treatment still matters first. What changes is the level of interest in biologically matched combinations when the tumour shows clear **LAR** features, limited **neoadjuvant response**, or pathway findings that make a trial more compelling. Most LAR-focused strategies fall into five buckets: * **AR blockade alone** * **AR blockade plus CDK4/6 inhibition** * **AR blockade plus PI3K-AKT-mTOR inhibition** * **HER2-targeted TKIs** when **ERBB2** mutations are present * **Immune or senescence-focused combinations** in more experimental settings Each bucket reflects a different part of the subtype biology. **AR blockade** asks whether the tumour is truly androgen-driven, although single-agent benefit has generally looked modest and subset-dependent rather than universal. **AR plus CDK4/6** targets the more luminal, cell-cycle-linked side of LAR disease. **AR plus PI3K/AKT/mTOR** fits the enrichment of pathway alterations such as **PIK3CA**. **HER2-targeted TKIs** matter in the subset with **ERBB2** mutations rather than amplification. The more speculative end of the field includes **immune** and **senescence** directions, especially where treatment pressure may leave behind persistent survivor populations. The table below gives concrete examples. That is usually more useful than discussing the biology in the abstract. ### Selected trials and how to use them This table is a discussion tool. It is not a treatment checklist. A trial can look highly relevant on paper and still not fit because of stage, prior treatment, organ function, country, timing, or access. In LAR TNBC, that mismatch happens often enough that report wording matters. The difference between **AR-positive**, **LAR-enriched**, **PIK3CA-mutant**, **ERBB2-mutant**, or poor **neoadjuvant response** disease can completely change which trial is actually worth pursuing. #### Selected AR-focused and LAR-relevant trials This version focuses on studies with direct registry links or clear public listings. | Trial | Trial link | Main drugs or strategy | Eligibility hooks that may matter | Why it matters in LAR-type TNBC | | ------------------------------------------------------------------------ | -------------------------------------------------------------------------------- | ------------------------------------------------------------------------------------------------ | ------------------------------------------------------------------------------------------------------------------------------------ | ----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------- | | **Enzalutamide in advanced AR-positive TNBC** (`MDV3100-11`, phase II) | [ClinicalTrials.gov `NCT01889238`](https://clinicaltrials.gov/study/NCT01889238) | **Enzalutamide**, a second-generation androgen-receptor inhibitor | Advanced or metastatic **AR-positive TNBC**, generally with **AR staining of 10% or higher** | One of the foundational AR-targeting studies in TNBC. It helped show that a subset of AR-positive tumours can derive clinical benefit from AR blockade | | **Bicalutamide in AR-positive TNBC** (phase II) | [ClinicalTrials.gov `NCT02353988`](https://clinicaltrials.gov/study/NCT02353988) | **Bicalutamide**, a first-generation AR blocker | **ER-negative**, **PR-negative**, **AR-positive** metastatic breast cancer | Helped validate AR as a meaningful target in selected TNBC cases and still helps frame off-label or combination AR discussions | | **Enzalutamide plus paclitaxel before surgery** (phase IIB) | [ClinicalTrials.gov `NCT02689427`](https://clinicaltrials.gov/study/NCT02689427) | **Enzalutamide plus paclitaxel** in the neoadjuvant setting | Stage I to III **AR-positive TNBC** before surgery, especially when anthracycline response is poor or the biology looks LAR-enriched | Relevant because it asks whether adding AR blockade can improve outcomes in a subtype that often responds poorly to standard neoadjuvant chemotherapy | | **Palbociclib plus bicalutamide** (phase I/II) | [ClinicalTrials.gov `NCT02605486`](https://clinicaltrials.gov/study/NCT02605486) | **CDK4/6 inhibition plus AR blockade** | **AR-positive** metastatic breast cancer, including **ER-negative** disease that overlaps with LAR-type TNBC | One of the clearest examples of a biologically matched combination strategy for luminal-like, CDK4/6-linked LAR biology | | **Ribociclib plus bicalutamide in AR-positive TNBC** (`BTCRC BRE15-024`) | [ClinicalTrials.gov `NCT03090165`](https://clinicaltrials.gov/study/NCT03090165) | **Ribociclib plus bicalutamide**, combining CDK4/6 and AR inhibition | Advanced **AR-positive TNBC** | This trial directly targets two recurring LAR vulnerabilities — **AR signalling** and **cell-cycle dependence** | | **Taselisib plus enzalutamide in AR-positive TNBC** | [ClinicalTrials.gov `NCT02457910`](https://clinicaltrials.gov/study/NCT02457910) | **PI3K inhibition plus AR blockade** | **AR-positive TNBC**, especially if genomic profiling shows **PIK3CA** or broader **PI3K/AKT/mTOR** pathway changes | One of the most important mechanistic trial directions for LAR disease because PI3K-pathway alterations are enriched in this subtype | | **Darolutamide in AR-positive advanced TNBC** | [ClinicalTrials.gov `NCT03383679`](https://clinicaltrials.gov/study/NCT03383679) | **Darolutamide**, a newer AR inhibitor, compared against **capecitabine** in a randomised study | Advanced **AR-positive TNBC** after prior treatment, with **AR positivity of 10% or higher** in the reported study | A newer trial direction in this setting. Useful because it gives one of the most up-to-date datasets on whether modern AR inhibition works best in molecularly androgen-dependent tumours rather than all AR-positive tumours | | **Enzalutamide with or without mifepristone versus physician's choice** | [ClinicalTrials.gov `NCT06099769`](https://clinicaltrials.gov/study/NCT06099769) | **Enzalutamide** alone or **enzalutamide plus mifepristone** versus physician's choice treatment | Metastatic **AR-positive TNBC** or **ER-low** breast cancer | Useful current study to watch because it explores whether refining AR blockade can improve outcomes in AR-positive metastatic breast cancer | #### Notes for using the links * [ClinicalTrials.gov](https://clinicaltrials.gov/) is the best starting point for inclusion criteria, recruitment status, locations, and contact details. * Some older studies are completed or closed. They still matter because they built the evidence base for newer AR-focused trials. * Trial status can change quickly. Confirm the current listing with your oncology team or a trial navigator. #### How to use this table with your team Start by matching each trial to the exact wording in the pathology or genomic report. LAR trial matching works best when the biology is described precisely, not loosely. The most useful hooks are: * **AR percentage** and staining strength * A **LAR** or **androgen-response** signature, if profiling was done * **PIK3CA**, **PTEN**, **ERBB2**, **PD-L1**, **BRCA1/2**, and **HRD** results * Whether the setting is **early-stage poor-response disease** or **metastatic disease** Not every **AR-positive** TNBC is truly **LAR-like**. Some tumours stain for AR but still behave more like basal TNBC. That is why wider profiling can matter. It helps explain why one AR-focused strategy may fit better than another, and why some patients may be better served by standard TNBC pathways than by forcing a subtype match that is not biologically convincing. ### Standard options that still matter LAR TNBC still follows the wider TNBC treatment framework. That includes standard chemotherapy, surgery, radiation, and biomarker-led decisions. The subtype label should refine planning. It should not erase standard-of-care treatment that is still supported by stage and biomarker evidence. Key points still include: * **Anthracycline-taxane chemotherapy** still matters, especially in early-stage disease * **Platinum** still matters when **BRCA1/2** or **HRD** is relevant * **Pembrolizumab** still matters in selected **PD-L1-positive** metastatic or high-risk early-stage settings * **PARP inhibitors** still matter in selected **gBRCA1/2** disease The main difference is that LAR often pushes more attention toward **additional molecular testing** and **clinical-trial matching**, especially when chemotherapy response is weaker than hoped or when residual disease remains after neoadjuvant treatment. That is the balance to keep in view: standard treatment remains central, while subtype biology helps identify where trial-based escalation or a more targeted plan may make sense. ### Supportive and experimental research areas These approaches are not standard treatment for LAR TNBC. They fit best as supportive or experimental ideas to discuss carefully with your team, especially when the aim is to complement rather than replace standard care. The useful question is whether a compound maps onto the actual subtype biology, not whether it sounds broadly anti-cancer. #### Metabolic support themes Several off-label or low-cost strategies connect to recurring LAR themes such as metabolic dependence, steroid and cholesterol biology, inflammatory signalling, and **PI3K/AKT/mTOR** overlap. The most useful companion page here is [TNBC Off-Label Drugs in Treatment Resistance Research](/myhealingcommunity-docs/breast-cancer/triple-negative/treatment-resistance-research/tnbc-off-label-drugs-in-treatment-resistance-research.md), which covers the mechanism detail in more depth. Research interest includes: * **Metformin** for mitochondrial and **AMPK** effects. See [TNBC Off-Label Drugs in Treatment Resistance Research](/myhealingcommunity-docs/breast-cancer/triple-negative/treatment-resistance-research/tnbc-off-label-drugs-in-treatment-resistance-research.md) and [Berberine & Metformin](/myhealingcommunity-docs/natural-medicines/berberine-in-oncology/berberine-and-metformin.md) * **Statins** for mevalonate-pathway and cholesterol-steroid signaling effects. See [TNBC Off-Label Drugs in Treatment Resistance Research](/myhealingcommunity-docs/breast-cancer/triple-negative/treatment-resistance-research/tnbc-off-label-drugs-in-treatment-resistance-research.md) * **Melatonin** for circadian, mitochondrial, and antioxidant support * **Aspirin** and related anti-inflammatory approaches in selected settings. See [TNBC Off-Label Drugs in Treatment Resistance Research](/myhealingcommunity-docs/breast-cancer/triple-negative/treatment-resistance-research/tnbc-off-label-drugs-in-treatment-resistance-research.md) These ideas are strongest as mechanism-based, preclinical, or early-clinical leads. They are not substitutes for standard treatment. In LAR disease, they are most interesting when they intersect with **AMPK/mTOR** control, mitochondrial stress handling, mevalonate-pathway biology, or inflammatory programs that may help tumours tolerate treatment. That framing is especially relevant for **metformin**, **statins**, and **melatonin**, which keep appearing because they overlap with real pathway questions rather than generic wellness claims. #### Natural compounds and pathway overlap Several natural compounds studied across TNBC also overlap with LAR biology, especially where **PI3K/AKT**, inflammatory signalling, oxidative stress handling, or senescence programs are relevant. The broader overview is [TNBC Natural Compounds in Treatment Resistance Research](/myhealingcommunity-docs/breast-cancer/triple-negative/treatment-resistance-research/tnbc-natural-compounds-in-treatment-resistance-research.md), but the key point here is that these compounds are being tracked because they touch plausible mechanisms, not because they are established LAR treatments. Examples include: * [Curcumin in breast cancer](/myhealingcommunity-docs/natural-medicines/curcumin-in-oncology/curcumin-evidence-by-cancer-type/breast-cancer.md) and related polyphenols with **PI3K-AKT**, **NF-kB**, and inflammatory pathway effects * [TNBC Natural Compounds in Treatment Resistance Research](/myhealingcommunity-docs/breast-cancer/triple-negative/treatment-resistance-research/tnbc-natural-compounds-in-treatment-resistance-research.md) for **pterostilbene**, blueberry compounds, **piperlongumine**, and other TNBC-relevant natural compounds * [Berberine & Metformin](/myhealingcommunity-docs/natural-medicines/berberine-in-oncology/berberine-and-metformin.md) for a metabolic-support angle that may overlap with LAR biology * **Sulforaphane** as a lower-toxicity adjunct with oxidative-stress, detoxification, and signalling relevance across breast-cancer research. For current supplier notes and product links, see [Trusted Suppliers and Discounts](/myhealingcommunity-docs/cancer-patient-community-supports/trusted-suppliers-and-discounts.md) * **Senolytic or senomorphic compounds** that may overlap with the emerging senescence theme. See [Senescence — The Second Escape Route](/myhealingcommunity-docs/treatment-resistance/treatment-resistance/senescence-the-second-escape-route.md) and [Senolytic Pulse Protocol](/myhealingcommunity-docs/senolytic-pulse-protocol.md) The emerging **senescence** angle deserves special caution and interest in equal measure. If treatment pressure pushes a subset of cells into a persistent, therapy-tolerant state, then [Senescence — The Second Escape Route](/myhealingcommunity-docs/treatment-resistance/treatment-resistance/senescence-the-second-escape-route.md) becomes directly relevant to how recurrence biology is framed. This is especially worth watching when combination treatment induces growth arrest without fully clearing disease. That remains an experimental, mechanism-first area. It is not standard of care. For practical sourcing, this site already points readers toward group-trusted options for compounds such as **curcumin**, **EGCG**, **boswellia**, and **sulforaphane**. See [Trusted Suppliers and Discounts](/myhealingcommunity-docs/cancer-patient-community-supports/trusted-suppliers-and-discounts.md) for the current product list and supplier notes. Most of this evidence is **preclinical** or early-phase. Subtype-specific human data are limited, and these approaches are best framed as adjunctive, trial-adjacent, or exploratory rather than established treatment. ### Questions to ask your team * Does this tumour look biologically **LAR**, or only **AR-positive** on IHC? * Have I had **NGS testing** that includes **PIK3CA**, **PTEN**, and **ERBB2**? * If an activating **ERBB2** mutation is present, would that make a **neratinib-based** trial or precision-oncology option realistic even if standard HER2 testing is negative? * Is the current goal **neoadjuvant response**, **metastatic control**, or **trial matching** after standard treatment? * Are there any local or international **AR-focused** or **PI3K/CDK4/6-focused** trials that fit now? ### Related pages * [Triple-Negative](/myhealingcommunity-docs/breast-cancer/triple-negative.md) * [Liquid Biopsy for HER2-Positive Resistance](/myhealingcommunity-docs/breast-cancer/her2-positive/her2climb/liquid-biopsy-for-her2-positive-resistance.md) * [TNBC Off-Label Drugs in Treatment Resistance Research](/myhealingcommunity-docs/breast-cancer/triple-negative/treatment-resistance-research/tnbc-off-label-drugs-in-treatment-resistance-research.md) * [TNBC Natural Compounds in Treatment Resistance Research](/myhealingcommunity-docs/breast-cancer/triple-negative/treatment-resistance-research/tnbc-natural-compounds-in-treatment-resistance-research.md) * [Trusted Suppliers and Discounts](/myhealingcommunity-docs/cancer-patient-community-supports/trusted-suppliers-and-discounts.md) * [Senescence — The Second Escape Route](/myhealingcommunity-docs/treatment-resistance/treatment-resistance/senescence-the-second-escape-route.md) * [Senolytic Pulse Protocol](/myhealingcommunity-docs/senolytic-pulse-protocol.md) ### Selected references * [LAR TNBC review](https://pmc.ncbi.nlm.nih.gov/articles/PMC9381326/) * [AR-positive TNBC biology and treatment overview](https://academic.oup.com/narcancer/article/4/2/zcac018/6609689) * [Potential therapeutic targets in LAR breast cancer](https://www.dovepress.com/potential-therapeutic-targets-for-luminal-androgen-receptor-breast-can-peer-reviewed-fulltext-article-OTT) * [Enzalutamide in AR-positive TNBC](https://ascopost.com/issues/june-10-2017/targeting-the-androgen-receptor-in-breast-cancer/) * [PI3K-pathway context in LAR TNBC](https://www.frontiersin.org/journals/genetics/articles/10.3389/fgene.2024.1440430/full) * [ClinicalTrials.gov](https://clinicaltrials.gov/) {% hint style="warning" %} This page is for education only. It is not medical advice. Supportive and experimental options should always be reviewed with a qualified clinician. {% endhint %} {% hint style="info" %} LAR TNBC research is moving quickly. Trial matching often depends on detailed pathology and molecular testing. {% endhint %} --- # Agent Instructions This documentation is published with GitBook. GitBook is the documentation platform designed so that both humans and AI agents can read, navigate, and reason over technical content effectively. Learn more at gitbook.com. ## Querying This Documentation If you need additional information that is not directly available in this page, you can query the documentation dynamically by asking a question. Perform an HTTP GET request on the current page URL with the `ask` query parameter, and the optional `goal` query parameter: ``` GET https://myhealingcommunity.gitbook.io/myhealingcommunity-docs/breast-cancer/triple-negative/lar-subtype-triple-negative-ar-positive.md?ask=&goal= ``` `ask` is the immediate question: it should be specific, self-contained, and written in natural language. `goal` is optional and describes the broader end goal you are ultimately trying to accomplish on behalf of the user. GitBook uses it to tailor the answer towards what is most useful for that goal. The response will contain a direct answer to the question and relevant excerpts and sources from the documentation. Use this mechanism when the answer is not explicitly present in the current page, you need clarification or additional context, or you want to retrieve related documentation sections.