Understanding Breast Cancer Management Guidelines

Chapter 1

What Is Breast Cancer? A Biological Primer

Your body is made of about 37 trillion cells, each following a precise programme: divide a set number of times, do your job, and then die to make room for replacements. Cancer happens when a cell's internal programme breaks — it starts dividing without the usual off-switch, accumulating mutations until it is no longer recognisable as a breast cell and no longer obeys the body's rules.

Breast cancer almost always starts in one of two places:

• The milk ducts — tubes that carry milk to the nipple. Cancer starting here is called ductal carcinoma, the most common type.
• The milk-producing lobules — small glands at the end of the ducts. Cancer here is called lobular carcinoma.

The Lymphatic System: The Cancer Highway

Alongside your blood vessels runs a second network of tiny tubes called the lymphatic system. It drains fluid from tissues and filters it through small bean-shaped structures called lymph nodes. For breast cancer, the most clinically important lymph nodes are the axillary nodes — the cluster sitting in your armpit (axilla). If cancer cells enter the lymphatic vessels in the breast, the axillary nodes are the first place they typically travel to, which is why so much of breast cancer management focuses on whether these nodes are involved.

Chapter 2

Detecting the Problem: The Triple Test

When a woman presents with a breast lump, the first priority is to determine what it is before any treatment begins. The NCG guideline mandates what is called the Triple Test — three independent assessments that together give a highly reliable answer.

Component	What it involves	What it tells us
1. Clinical Examination	A breast surgeon physically examines the lump — its size, texture, whether it is mobile or fixed, whether the skin over it or the nipple is affected.	Preliminary suspicion level; identifies features like skin dimpling (peau d'orange) or nipple retraction that suggest invasive disease.
2. Bilateral Imaging	Mammogram: low-dose X-ray of both breasts. Ultrasound: sound-wave image, especially useful in younger women (denser breast tissue). MRI in selected cases (very dense breasts, suspected multiple tumours).	Reveals the shape, size, and margins of the lump; detects suspicious calcifications; assesses the other breast for concurrent lesions.
3. Histopathology	A needle is inserted into the lump to extract a tissue sample (core biopsy, preferred) or cells (FNAC — Fine Needle Aspiration Cytology). A pathologist examines this under a microscope.	The definitive answer: is this cancer or not? If cancer: what type? What is its grade? What are its receptor markers?

Possible Outcomes of the Triple Test

The imaging sorts lumps into three categories, each with its own follow-up:

• Benign-looking cyst (confirmed on ultrasound): A fluid-filled sac. Simple cysts can be left alone. Cysts with blood-stained fluid or a solid component need biopsy.
• Benign-looking solid mass: Still needs a biopsy to be certain.
• Suspicious solid mass: Biopsy is mandatory. If biopsy says malignant, the cancer pathway begins.

Chapter 3

Grading and Staging: How Serious Is It?

Once malignancy is confirmed, the next question is: how far has it gone, and how aggressive is it? Two independent systems answer this.

Grading: Measuring Aggressiveness

A pathologist looks at the cancer cells under a microscope and scores three features, each on a scale of 1–3:

• Tubule formation: Do the cancer cells still form tube-like structures (as normal breast cells do)? Grade 1 means they do; Grade 3 means they look nothing like normal breast tissue.
• Nuclear pleomorphism: Are the cell nuclei (the command centres) of uniform size and shape? Irregular, enlarged nuclei score 3.
• Mitotic count: How rapidly are the cells dividing? More divisions per microscopic field = higher score.

The three scores are added together to give a total of 3–9, which maps to a Grade I (score 3–5, well-differentiated, slow-growing), Grade II (score 6–7, intermediate), or Grade III (score 8–9, poorly-differentiated, fast-growing) tumour.

Staging: Measuring Spread — The TNM System

The international TNM staging system classifies a cancer on three axes:

Letter	Stands For	What it measures
T	Tumour	Size and local extent of the primary tumour in the breast Tis = in situ only (no invasion) T1 = ≤ 2 cm  |  T2 = 2–5 cm T3 = > 5 cm  |  T4 = invades chest wall or skin
N	Nodes	Whether and how many regional lymph nodes are involved N0 = no nodes involved  |  N1 = 1–3 axillary nodes N2 = 4–9 nodes or fixed nodes  |  N3 = 10+ nodes or supra/infraclavicular
M	Metastasis	Whether cancer has spread to distant organs (lungs, liver, bones, brain) M0 = no distant spread  |  M1 = distant metastases confirmed

The combination of T, N, and M gives the overall stage (I–IV). The NCG guidelines practically organise patients into three management groups:

Chapter 4

Receptor Biology: The Molecular Fingerprint

Perhaps the most important discovery in breast cancer medicine in the last 30 years is that not all breast cancers are the same — even if they look identical under a microscope, they can behave completely differently and respond to completely different treatments. The key is the cancer's receptor profile.

Think of receptors as docking ports on the surface of the cancer cell. Different molecules can dock at these ports and tell the cell to grow faster. By identifying which ports are present (and which are missing), doctors can choose treatments that specifically target the fuel sources the cancer depends on.

Estrogen Receptor (ER) and Progesterone Receptor (PR)

Estrogen and progesterone are female hormones. Cancer cells that carry ER and PR are using these hormones as growth signals. If you cut off the hormone supply — either by blocking the receptor (Tamoxifen) or by stopping the body from making estrogen (Aromatase Inhibitors) — the cancer is deprived of its fuel and may shrink or stop growing.

ER status is reported as positive (the receptor is present) or negative (absent). Intensity (weak/moderate/strong) and the Allred Score (0–8, combining proportion of cells staining + staining intensity) further quantify how hormone-sensitive the cancer is.

HER2 (Human Epidermal Growth Factor Receptor 2)

HER2 is a growth-factor receptor that, in normal cells, helps regulate cell growth. In about 15–20% of breast cancers, the gene encoding HER2 is amplified — duplicated many extra times — and the cancer cell bristles with far more HER2 receptors than normal, effectively keeping its growth accelerator permanently floored. These tumours tend to grow fast and spread early.

The critical insight is that this dependency is also a vulnerability: drugs like Trastuzumab (Herceptin) are engineered antibodies that bind specifically to HER2 and block its signalling, with remarkable effectiveness.

The Three Clinical Subtypes

Subtype	ER/PR	HER2	Characteristic
Luminal (HR+/HER2−)	Positive	Negative	Hormone-driven. Usually slower-growing. Responds well to hormone therapy. Most common subtype.
HER2-positive	Any	Positive	Growth-factor driven. Aggressive but now highly treatable with targeted anti-HER2 drugs.
Triple-Negative (TNBC)	Negative	Negative	No hormone or HER2 receptors. Cannot use targeted therapies. Chemotherapy is the mainstay. Often more aggressive.

Chapter 5

The Three Clinical Scenarios

With the Triple Test complete and receptor status known, the treatment path diverges based on how far the cancer has progressed. Here is how each scenario unfolds.

Scenario A: Operable Breast Cancer (OBC)

This is the earliest-stage group. The tumour is small, nodes are either clear or only minimally involved, and there is no distant spread. Surgery is feasible upfront — the question is: which type of surgery?

The patient's preference and tumour characteristics create three branches:

1. Wants BCS and is eligible → Breast-Conserving Surgery (lumpectomy + radiation)
2. Wants BCS but tumour is too large relative to breast size → NACT first (to shrink the tumour), then BCS if it responded well
3. Does not want BCS or has contraindications → Mastectomy

Scenario B: Locally Advanced Breast Cancer (LABC)

The tumour is too large or too locally invasive (e.g., involves skin or chest wall) for upfront surgery to be safe or effective. The standard approach is neoadjuvant chemotherapy (NACT) — chemotherapy given before surgery, with the goal of shrinking the tumour enough to make surgery possible.

After NACT the surgeon reassesses: if the tumour has responded and surgery is now feasible, it proceeds (MRM or BCS as appropriate). If there is no response, alternative chemotherapy or direct mastectomy is considered.

Scenario C: Metastatic Breast Cancer (MBC)

Distant spread has been confirmed (typically to lungs, liver, bones, or brain). Surgery on the primary tumour does not cure the patient in this setting. Treatment is systemic — treating the whole body — to control growth, relieve symptoms, and extend life. Palliative care is initiated early.

Chapter 6

Surgery: Removing the Tumour

Breast-Conserving Surgery (BCS)

Also called lumpectomy or wide local excision. Only the tumour and a surrounding rim of healthy tissue (the "margin") are removed. The rest of the breast is preserved. This requires radiation afterwards to eliminate any microscopic cells that might remain in the breast.

Contraindications to BCS (situations where mastectomy is mandatory regardless of patient preference):

• Diffuse micro-calcifications spread across the breast
• Persistent positive margins after re-excision attempts
• Poor patient compliance (radiation follow-up is non-negotiable with BCS)
• Previous radiation to the chest or breast
• Relative: multicentricity (tumour in multiple separate areas of the breast)

Modified Radical Mastectomy (MRM)

Removal of the entire breast along with the overlying skin, the nipple-areola complex, and the axillary lymph nodes. The pectoralis major muscle (the large chest muscle) is preserved — this distinguishes a "modified" from the older "radical" mastectomy. Many patients are eligible for breast reconstruction at the same sitting.

Chapter 7

The Lymph Node Problem: Managing the Axilla

Removing the primary tumour is not enough if cancer has already spread to the axillary lymph nodes. The question is how to handle those nodes — and the approach has evolved significantly in the last two decades.

Why does it matter?

If lymph nodes contain cancer cells and those nodes are left in place, the cells can continue spreading. Removing them (axillary dissection) provides both prognostic information (how many nodes are involved?) and therapeutic benefit (removing a reservoir of cancer). However, removing too many nodes causes lymphoedema — chronic, sometimes severe swelling of the arm because the lymphatic drainage is disrupted. This is why modern practice tries to be as conservative as possible.

The Sentinel Lymph Node Biopsy (SLNB)

The sentinel node is the first lymph node downstream from the tumour — the first place cancer cells would travel. The surgeon injects a dye or a small amount of radioactive tracer near the tumour and watches where it drains; the first node that lights up is the sentinel.

If the sentinel node is negative (no cancer cells found), it is overwhelmingly likely that all other nodes are also clear — so no further dissection is needed. The patient is spared the morbidity of a full axillary clearance. If the sentinel node is positive, the surgeon completes a full axillary lymph node dissection (ALND) — removing all Level I–III nodes.

Post-NACT Axilla Management

Patients who were clinically node-positive before NACT but become clinically node-negative after chemotherapy (the chemo shrank the nodal disease) can sometimes be managed with SLNB rather than full axillary dissection — but only if strict criteria are met. If still node-positive, complete axillary dissection is mandatory.

Chapter 8

Chemotherapy: Killing the Remaining Cells

Surgery removes the visible tumour. Radiation cleans up the local area. But microscopic cancer cells may have already slipped into the bloodstream, circulating invisibly. Systemic chemotherapy is designed to hunt and kill these cells wherever they are hiding.

How Chemotherapy Works

Most standard chemotherapy drugs target rapidly-dividing cells — they interfere with cell division in various ways:

• Anthracyclines (Adriamycin/Doxorubicin, Epirubicin): Intercalate into DNA and block the enzymes needed to uncoil it for replication. Cancer cells die. Unfortunately, so do some normal rapidly-dividing cells (hence hair loss, mucositis). Dose-limited by cardiotoxicity over time.
• Taxanes (Paclitaxel, Docetaxel): Stabilise the mitotic spindle — the molecular scaffold cells use to pull chromosomes apart during division. The cell freezes mid-division and dies.
• Cyclophosphamide: An alkylating agent that cross-links DNA strands so they cannot be read. Works across the cell cycle.

The Regimens: Why Different Combinations?

Drugs are combined because cancer cells can develop resistance to any single agent. Using three drugs simultaneously makes it much harder for any one mutation to confer complete resistance. The combinations are abbreviated:

• AC: Adriamycin (doxorubicin) + Cyclophosphamide
• EC: Epirubicin + Cyclophosphamide
• TC: Taxane (docetaxel) + Cyclophosphamide
• CMF: Cyclophosphamide + Methotrexate + 5-Fluorouracil
• TCH: Taxane + Carboplatin + trastuzumab (H = Herceptin)

"q 3 wk" = every 3 weeks; "q wk" = weekly. "DD" = dose-dense, meaning every 2 weeks with growth-factor support.

Chemotherapy by Receptor Subtype: Why Different Patients Get Different Drugs

HR+/HER2− patients with T1/T2 N0 (low-risk early cancer)

If the tumour is under 2 cm, Grade I or II, strongly hormone-receptor positive, and the patient is postmenopausal — hormone therapy alone may be sufficient. The biological reasoning: the cancer's main driver is estrogen, and blocking estrogen is effective. Adding chemotherapy would increase toxicity without meaningfully improving outcomes. But if any of these favourable features are absent, chemotherapy is added.

TNBC (Triple-Negative)

With no hormone receptor and no HER2, there is nothing to "target" specifically — so chemotherapy is the only systemic weapon. Regimens tend to be more intensive, often including taxanes. For TNBC patients who receive NACT and do not achieve a pathological complete response (meaning residual tumour is found at surgery), maintenance capecitabine (an oral chemotherapy) significantly improves outcomes — this is a category (b) recommendation.

HER2-positive

These patients receive chemotherapy plus Trastuzumab (anti-HER2 targeted antibody), typically starting with the taxane component. Adding Trastuzumab to chemotherapy roughly halves the risk of recurrence in HER2+ disease. Trastuzumab is then continued as maintenance therapy for a total of 6–12 months. Patients with residual disease after NACT may benefit from TDM-1 (Trastuzumab emtansine) — a drug that attaches a toxin directly to the Trastuzumab antibody, delivering a payload specifically to HER2-expressing cells.

Chapter 9

Hormone Therapy: Cutting Off the Fuel Supply

For ER and/or PR positive cancers, hormones are the petrol the cancer runs on. Hormone therapy (also called endocrine therapy) works by either blocking the hormone receptors or reducing the amount of estrogen circulating in the body. It is taken for a minimum of 5 years after primary treatment.

Premenopausal Women

Before menopause, most estrogen is produced by the ovaries. The primary drug is:

• Tamoxifen (20 mg daily): A selective estrogen receptor modulator (SERM) — it binds to the estrogen receptor in breast cells but blocks it rather than activating it. For high-risk or node-positive patients, 10 years of Tamoxifen is recommended (rather than 5) as it further reduces late recurrence.
• Tamoxifen + Ovarian Function Suppression (OFS): For high-risk premenopausal patients, suppressing the ovaries (via medication, radiation, or surgery) removes the estrogen source entirely, and then adding an Aromatase Inhibitor (see below) further drives estrogen levels to near zero. This combination is more effective than Tamoxifen alone but more toxic.

Postmenopausal Women

After menopause, ovarian estrogen production ceases. But estrogen is still made in small amounts by converting precursors in fat tissue and the adrenal glands — a process catalysed by an enzyme called aromatase. Postmenopausal women can use:

• Aromatase Inhibitors (AIs) — Letrozole, Anastrozole, Exemestane: Block aromatase, reducing circulating estrogen by >95%. More effective than Tamoxifen in postmenopausal women. However, they can cause joint pain and accelerate bone loss.
• Tamoxifen: Still an option, especially when AIs are not tolerated.
• Extended therapy (for high-risk patients): 5 years Tamoxifen followed by 5 years of AI; or 7–10 years of AI. Breast cancer can recur 10–20 years after diagnosis — extended endocrine therapy reduces this late-recurrence risk.

Chapter 10

Targeted Therapy: Precision Attack on HER2

Conventional chemotherapy is relatively non-specific — it kills any rapidly dividing cell. Targeted therapy is different: it is designed to interfere with a specific molecular abnormality present in cancer cells but not (or minimally) in normal cells.

Trastuzumab (Herceptin)

A monoclonal antibody — a protein engineered to bind specifically to the HER2 receptor on the surface of cancer cells. It works through several mechanisms:

• Blocks the HER2 receptor from receiving growth signals
• Marks the cancer cell for destruction by the immune system
• May directly trigger cell death

In HER2+ invasive breast cancer, Trastuzumab is the standard of care — for 6 months (category b) or at least 12 weeks (minimum category a). Adding it to chemotherapy roughly halves recurrence risk.

Importantly: Trastuzumab only works if the tumour is truly HER2-positive. This is why pathology must confirm HER2 status by IHC (immunohistochemistry) scoring the protein level (0/1+ = negative, 2+ = equivocal requiring additional FISH test, 3+ = positive) before prescribing it.

TDM-1 (Trastuzumab Emtansine)

An "antibody-drug conjugate" — Trastuzumab with a potent cytotoxic drug (emtansine) chemically attached. The Trastuzumab component finds HER2-positive cells and docks on them; the emtansine payload is then released inside the cell, killing it. For patients with residual HER2-positive disease after NACT + Trastuzumab, adjuvant TDM-1 improves outcomes (category c in NCG 2019 — evidence has strengthened since).

Chapter 11

Radiation Therapy: The Local Clean-Up

Radiation uses high-energy X-rays (or electrons) to damage the DNA of cells in a defined volume of tissue. Cancer cells, having lost the ability to repair DNA damage, die disproportionately. Normal cells sustain damage too but are better at repairing it.

When Is Radiation Used?

Clinical situation	Radiation target	Standard dose
Post-BCS, any stage (T1/T2 N0)	Whole breast + tumour bed boost	40 Gy / 15 fractions / 3 weeks (hypofractionation)
Post-BCS, DCIS	Whole breast ± boost for high-grade or close margins or age ≤50	Same as above; elderly low-grade DCIS may omit RT
Post-mastectomy, T1/T2 N0	No indication for RT	—
Post-mastectomy, T1/T2 N1 (except select low-risk)	Chest wall + supraclavicular fossa	40 Gy / 15 fractions
Post-mastectomy, T3N0	Chest wall + individualised nodal RT	40 Gy / 15 fractions
Advanced (T3N1–3, T4, N2–3)	Chest wall / whole breast + supraclavicular fossa + axilla if residual	40 Gy / 15 fractions; or 50 Gy / 25 fractions if high cardiac dose

Special Radiotherapy Considerations

Boost to the tumour bed

After whole-breast radiation, an extra dose ("boost") of 10–14 Gy is delivered to the area where the tumour was. Boost is recommended for high-grade tumours, young patients (≤50 years), or close margins — situations where residual microscopic disease risk is highest.

APBI — Accelerated Partial Breast Irradiation

In carefully selected low-risk patients (age >40, small tumour ≤3 cm, clear margins, no lymphovascular invasion, no extensive DCIS component), radiation can be limited to just the tumour bed rather than the whole breast. Treatment is completed faster. This is a category (b) recommendation — only at centres with experience in the technique.

Left-sided cancers and cardiac protection

The heart sits behind the left side of the chest wall. For left-sided cancers, radiation fields must carefully spare the heart. If standard tangential fields result in excessive cardiac dose (heart-to-field distance >1 cm or central lung distance >3 cm), special techniques are used:

• DIBH (Deep Inspiration Breath Hold): Patient takes a deep breath and holds it during each radiation pulse. The inflated lungs push the heart away from the chest wall, increasing the separation between the treatment field and the heart.
• Prone positioning: Patient lies face-down; gravity pulls the breast away from the chest wall.
• IMRT/IGRT: Computer-optimised beam modulation to sculpt the dose distribution around critical structures.

Oligo-metastatic disease and SBRT

A small but important subset of metastatic patients have oligo-metastatic disease — a limited number (≤5) of small metastatic lesions in a single organ. In these patients, aggressively treating all metastatic sites with radiation (typically SBRT) can potentially achieve long-term remission. SBRT delivers a very high dose to a precisely targeted small volume — 24–30 Gy in a single fraction, or 30 Gy in 5 fractions. The extreme precision limits damage to surrounding tissue.

Chapter 12

Metastatic Disease: When Cancer Has Spread

When cancer reaches distant organs, the biology of management changes fundamentally. The goal is no longer cure but disease control with maximum quality of life. The guidelines emphasise early palliative care involvement alongside systemic treatment.

First Steps in MBC

On diagnosis of metastatic disease:

• Re-biopsy the metastatic site if feasible — receptor status can change between primary and metastatic disease
• CECT of chest/abdomen/pelvis and bone scan to map all sites of disease
• Early palliative care referral, pain clinic referral, and occupational therapy for symptom management

Systemic Therapy by Receptor Subtype

HR+ / HER2− MBC (most common)

Unless there is visceral crisis (rapidly failing organs), hormone therapy is tried first — it is less toxic than chemotherapy and can control disease for years. The sequence:

1. First line: Tamoxifen or Aromatase Inhibitor ± CDK4/6 inhibitor (drugs like Palbociclib that further brake cell division)
2. Second line: Fulvestrant (a pure estrogen receptor antagonist) ± CDK4/6 inhibitor; or Exemestane + Everolimus (blocks a cell growth pathway called mTOR)
3. Endocrine resistance: Transition to single-agent chemotherapy
4. Visceral crisis at any time point: Chemotherapy immediately

HER2+ MBC

• First line: Taxane + Trastuzumab (± Pertuzumab, a second anti-HER2 antibody that blocks a complementary signalling pathway)
• Second line: TDM-1, or Capecitabine + Lapatinib (a small-molecule HER2 inhibitor that penetrates cell membranes differently from antibodies)

TNBC MBC

Without targetable receptors, chemotherapy is the mainstay. Taxanes and platinum-based agents are most effective. There is no single recommended first-line regimen — choice depends on prior treatments and patient fitness.

Palliative Radiation for Metastases

Even in the metastatic setting, targeted radiation can provide major symptom relief:

• Bone metastases: A single dose of 8 Gy to a painful bone provides good pain relief for most patients. For impending fracture or spinal cord compression, 20 Gy in 5 fractions is used.
• Brain metastases: Multiple brain metastases are treated with whole-brain radiation (20 Gy / 5 fractions, or 30 Gy / 10 fractions). A single brain metastasis in an otherwise well-controlled patient can be treated with neurosurgery or stereotactic radiosurgery (SRS) — a highly precise single-session radiation treatment.

Chapter 13

Patient Journey Walkthroughs

The guidelines are most easily understood through concrete examples. Here are three representative patient journeys.

Patient A — Early Luminal Cancer

58-year-old postmenopausal woman. 1.5 cm lump in left breast, discovered on routine mammogram. Biopsy: Grade II infiltrating ductal carcinoma, ER strongly positive (Allred 7/8), PR positive, HER2 negative. Ultrasound axilla: no enlarged nodes. Clinical stage: T1 N0 M0.

Patient B — Locally Advanced TNBC

38-year-old premenopausal woman. Presents with 7 cm left breast mass, palpable axillary nodes, skin oedema. Core biopsy: Grade III infiltrating ductal carcinoma, ER negative, PR negative, HER2 negative (Triple-Negative). CT and bone scan: no distant metastases. Clinical stage: T3 N2 M0. LABC.

Patient C — HER2+ Metastatic Disease

52-year-old postmenopausal woman. Previously treated 4 years ago (early HER2+ BC, received adjuvant Trastuzumab). Now presents with chest pain and breathlessness. CT: multiple liver metastases and pleural effusion. Bone scan: multiple bone metastases. Biopsy of liver metastasis confirms: ER positive, HER2 positive (3+ on IHC). Stage IV, de novo relapse. HER2 receptor confirmed positive on rebiopsy.

Appendix

Glossary

ALND (Axillary Lymph Node Dissection)

Surgical removal of the lymph nodes in the armpit (Level I–III). Provides staging information and removes a potential reservoir of cancer cells.

Allred Score

A combined score (0–8) quantifying estrogen receptor positivity from a pathology slide — adds proportion of cells staining to staining intensity. Score ≥6 is considered strongly positive.

Anthracycline

A class of chemotherapy drugs (e.g., Adriamycin/doxorubicin, epirubicin) that interfere with DNA replication. Highly effective in breast cancer but limited by cumulative cardiotoxicity.

APBI (Accelerated Partial Breast Irradiation)

A radiation technique treating only the tumour bed (rather than the whole breast) over a shorter course. For select low-risk patients only.

BCS (Breast-Conserving Surgery)

Removal of the tumour and a clear margin of surrounding tissue, preserving the remainder of the breast. Always combined with radiation.

CDK4/6 Inhibitors (Palbociclib, Ribociclib, Abemaciclib)

Drugs that block proteins (cyclin-dependent kinases 4 and 6) needed for cells to progress through the cell cycle. Used alongside hormone therapy in HR+ MBC.

DCIS (Ductal Carcinoma In Situ)

Cancer cells confined within the milk duct, not yet invasive. If left untreated, some (not all) DCIS will progress to invasive cancer over years.

DIBH (Deep Inspiration Breath Hold)

A radiation technique in which the patient holds a deep breath during radiation delivery, physically separating the heart from the treatment field.

ER (Estrogen Receptor)

A protein on breast cancer cells that binds estrogen and responds by promoting cell growth. ER-positive cancers are susceptible to hormone therapies.

FNAC (Fine Needle Aspiration Cytology)

A biopsy technique using a thin needle to aspirate cells from a lump. Less information than core biopsy (no tissue architecture, no receptor testing), but acceptable when core biopsy is unavailable.

HER2 (Human Epidermal Growth Factor Receptor 2)

A growth-factor receptor protein. When overexpressed (HER2-positive), it drives aggressive cancer growth. Targeted by drugs like Trastuzumab.

IHC (Immunohistochemistry)

A laboratory technique using antibody-based staining to detect specific proteins (ER, PR, HER2) in tissue sections. The primary method for receptor testing.

LABC (Locally Advanced Breast Cancer)

Breast cancer that is large or locally extensive (skin/chest wall involvement, or extensive nodal disease) but without confirmed distant metastases.

Lymphoedema

Chronic swelling of the arm caused by disruption of lymphatic drainage after axillary dissection or radiation. Can be permanent and debilitating.

MBC (Metastatic Breast Cancer)

Breast cancer that has spread to distant organs (lungs, liver, bones, brain). Also called Stage IV or advanced breast cancer.

MRM (Modified Radical Mastectomy)

Removal of the entire breast, overlying skin, nipple-areola, and axillary lymph nodes, preserving the chest-wall muscles.

NACT (Neoadjuvant Chemotherapy)

Chemotherapy given before surgery to shrink the tumour. Allows real-time assessment of response and may convert an inoperable cancer to operable.

OFS (Ovarian Function Suppression)

Shutting down ovarian estrogen production via medication (GnRH agonists), radiation, or surgical removal (oophorectomy). Used in premenopausal high-risk patients.

pCR (Pathological Complete Response)

No residual invasive cancer found in the breast (and ideally the nodes) at surgery after NACT. A strong positive prognostic sign.

SBRT (Stereotactic Body Radiation Therapy)

Very high-dose, precisely targeted radiation delivered in a small number of fractions (1–5). Used for oligo-metastatic sites and spine metastases.

SLNB (Sentinel Lymph Node Biopsy)

Surgical technique to identify and remove only the first lymph node draining the tumour site. If negative, no further axillary dissection is needed.

SERM (Selective Estrogen Receptor Modulator)

A drug (e.g., Tamoxifen) that acts as an estrogen receptor agonist in some tissues (bone) and antagonist in others (breast). Tamoxifen blocks the ER in breast cells.

TNBC (Triple-Negative Breast Cancer)

Cancer negative for ER, PR, and HER2. Cannot benefit from hormone or HER2-targeted therapy. Chemotherapy is the mainstay of systemic treatment.

Trastuzumab (Herceptin)

A monoclonal antibody targeting the HER2 receptor. Standard treatment for HER2-positive breast cancer in both early and metastatic settings.