Atypical Lobular Hyperplasia of the Breast: Understanding Your Pathology Report

by Jason Wasserman MD PhD FRCPC
July 3, 2026

Atypical lobular hyperplasia (ALH) is a non-cancerous change in the breast in which the number of epithelial cells lining the small glands (called acini) inside the lobules is increased, and the cells look mildly abnormal. Although the cells are abnormal, they are not abnormal enough, or extensive enough, to be called cancer. Instead, atypical lobular hyperplasia is considered a marker that a person has an increased risk of developing breast cancer in the future. Together with lobular carcinoma in situ (LCIS), it is part of a group of changes called lobular neoplasia. This article will help you understand the findings in your pathology report, what each term means, and why it matters for your care.

Is atypical lobular hyperplasia a type of cancer?

No. Atypical lobular hyperplasia is not breast cancer, and the abnormal cells cannot spread to other parts of the body. It is best understood as a marker that a person is at somewhat higher risk of developing breast cancer in the future. The increased risk applies to both breasts, not only the breast where atypical lobular hyperplasia was found. Most people with this finding never develop breast cancer.

What causes atypical lobular hyperplasia?

Atypical lobular hyperplasia develops when cells lining the lobules of the breast lose a protein called e-cadherin, which normally helps cells stick together. This loss is usually caused by a change in the gene CDH1 in breast cells themselves and is not inherited. Because the cells no longer stick together, they grow as loose, single cells. Like most breast changes, atypical lobular hyperplasia is influenced by lifetime exposure to the hormone estrogen, and a family history of breast cancer may also contribute.

What are the symptoms of atypical lobular hyperplasia?

Atypical lobular hyperplasia does not cause any symptoms. It usually cannot be felt as a lump and does not reliably show up on a mammogram. For this reason, it is almost always found incidentally, meaning it is discovered when breast tissue is examined under the microscope for another reason.

How is the diagnosis made?

The diagnosis of atypical lobular hyperplasia is made after a pathologist examines breast tissue under the microscope. The tissue usually comes from a core needle biopsy or from a larger surgical sample removed for another reason. Under the microscope, the small glands within a lobule are partly filled with cells that look very similar to one another (monomorphic) and do not stick together (discohesive). Unlike normal lobules, the glands contain extra cells but are not greatly expanded.

To confirm the diagnosis, the pathologist may perform a test called immunohistochemistry (IHC) for e-cadherin, a protein that normally helps breast cells stick together. In atypical lobular hyperplasia, cells lose e-cadherin, so the test is negative (with little or no staining). This loss is the hallmark that separates lobular changes from ductal changes, in which e-cadherin is kept.

What is the difference between atypical lobular hyperplasia and lobular carcinoma in situ?

Atypical lobular hyperplasia and lobular carcinoma in situ (LCIS) are made up of the same type of cells, and both lose e-cadherin. The difference is one of amount and extent: in atypical lobular hyperplasia, the abnormal cells only partially fill the small glands of the lobule, whereas in LCIS, the cells fill and expand more of the glands. Because they lie on the same spectrum, the two are grouped together under the term lobular neoplasia. LCIS carries a somewhat higher risk of future breast cancer than atypical lobular hyperplasia.

What is the risk of developing breast cancer?

Atypical lobular hyperplasia is best thought of as a risk marker. Having it raises the chance of developing breast cancer in either breast to about 4 to 5 times that of the general population. Despite this, the overall risk remains modest, and most people with atypical lobular hyperplasia never develop breast cancer. A strong personal or family history of breast cancer adds to the overall level of risk. Importantly, the increased risk applies to both breasts, which is why follow-up looks at the breast tissue on both sides rather than only the area where atypical lobular hyperplasia was found.

What happens after this diagnosis?

Because atypical lobular hyperplasia is a risk marker rather than a cancer, the goals after diagnosis are to make sure no more advanced change is present and to lower the future risk of breast cancer. Care is often coordinated with a breast surgeon and, when appropriate, a medical oncologist. The pathology findings guide which options the team discusses, rather than dictating a single path.

Surveillance — When atypical lobular hyperplasia is found on its own and the biopsy result matches the imaging, close follow-up with regular clinical examinations and imaging is often recommended rather than surgery, because the chance of finding a hidden cancer is low.
Surgical excision — Removing the area may be recommended when the biopsy result does not match the imaging, when another atypical or higher-risk change is present in the same sample, or when the finding is more extensive than expected.
Risk-reducing medication — Medications that block or lower estrogen, such as tamoxifen, raloxifene, or an aromatase inhibitor, can substantially lower the risk of developing breast cancer and may be discussed.
Genetic counseling — Considered when there is a strong family history of breast cancer.

Questions to ask your doctor

Was my atypical lobular hyperplasia found on a needle biopsy, and do I need surgery to remove the area, or is close follow-up enough?
Did the biopsy result match my imaging findings?
Were any other atypical or higher-risk changes found in the same sample?
How much does this finding increase my risk of developing breast cancer?
Does the increased risk apply to both breasts?
What surveillance schedule and imaging do you recommend?
Would a risk-reducing medication such as tamoxifen or an aromatase inhibitor be appropriate for me?
Should I be referred for genetic counseling based on my personal or family history?
What is the difference between my diagnosis and lobular carcinoma in situ?
What signs or symptoms should prompt me to contact you between visits?