Breast cancer risk is elevated for defined fraction of lesions. Except for patients with a strong family history of breast cancer, where the risk is two-fold, nonproliferative lesions have no increased risk. Proliferative lesions also have approximately a 2-fold risk. In particular, atypical hyperplasia is associated with an increased risk of developing breast cancer. Atypical lobular hyperplasia is associated with the greatest risk, approximately 5-fold and especially high relative risk of developing premenopausal breast cancer. Atypical ductal hyperplasia is associated with 2.4-fold risk. In contrast, a New England Journal of Medicine article states that for women with a strong familial history of breast cancer, the risk of future breast cancer is roughly doubled, independent of histological status. The article further states "The relative risk of breast cancer for the cohort was 1.56 (95 percent confidence interval, 1.45 to 1.68), and this increased risk persisted for at least 25 years after biopsy. The relative risk associated with atypia was 4.24 (95 percent confidence interval, 3.26 to 5.41), as compared with a relative risk of 1.88 (95 percent confidence interval, 1.66 to 2.12) for proliferative changes without atypia and of 1.27 (95 percent confidence interval, 1.15 to 1.41) for nonproliferative lesions. The strength of the family history of breast cancer, available for 4808 women, was a risk factor that was independent of histologic findings. No increased risk was found among women with no family history and nonproliferative findings. In the first 10 years after the initial biopsy, an excess of cancers occurred in the same breast, especially in women with atypia."

It is not well understood whether the lesions are precursors of breast cancer or only indication of increased risk, for most types of lesions the chance of developing breast cancer is nearly the same in the affected and unaffected breast (side) indicating only coincidence of risk factors. For atypical lobular hyperplasia there is high incidence of ipsilateral breast cancers indicating a possible direct carcinogenetic link.

The average age at time of EIN diagnosis is approximately 52 years, compared to approximately 61 years for carcinoma. The timeframe and likelihood of EIN progression to cancer, however, is not constant amongst all women. Some cases of EIN are first detected as residual premalignant disease in women who already have carcinoma, whereas other EIN lesions disappear entirely and never lead to cancer. For this reason, treatment benefits and risks must be individualized for each patient under the guidance of an experienced physician.

Risk factors for development of EIN and the endometrioid type of endometrial carcinoma include exposure to estrogens without opposing progestins, obesity, diabetes, and rare hereditary conditions such as hereditary nonpolyposis colorectal cancer. Protective factors include use of combined oral contraceptive pills (low dose estrogen and progestin), and prior use of a contraceptive intrauterine device.

Endometrial polyps usually occur in women in their 40s and 50s. Endometrial polyps occur in up to 10% of women. It is estimated that they are present in 25% of women with abnormal vaginal bleeding.

Endometrial hyperplasia is a condition of excessive proliferation of the cells of the endometrium, or inner lining of the uterus.

Most cases of endometrial hyperplasia result from high levels of estrogens, combined with insufficient levels of the progesterone-like hormones which ordinarily counteract estrogen's proliferative effects on this tissue. This may occur in a number of settings, including obesity, polycystic ovary syndrome, estrogen producing tumours (e.g. granulosa cell tumour) and certain formulations of estrogen replacement therapy. Endometrial hyperplasia is a significant risk factor for the development or even co-existence of endometrial cancer, so careful monitoring and treatment of women with this disorder is essential.

Endometrial polyps are usually benign although some may be precancerous or cancerous. About 0.5% of endometrial polyps contain adenocarcinoma cells. Polyps can increase the risk of miscarriage in women undergoing IVF treatment. If they develop near the fallopian tubes, they may lead to difficulty in becoming pregnant. Although treatments such as hysteroscopy usually cure the polyp concerned, recurrence of endometrial polyps is frequent. Untreated, small polyps may regress on their own.

Most of the risk factors for endometrial cancer involve high levels of estrogens. An estimated 40% of cases are thought to be related to obesity. In obesity, the excess of adipose tissue increases conversion of androstenedione into estrone, an estrogen. Higher levels of estrone in the blood causes less or no ovulation and exposes the endometrium to continuously high levels of estrogens. Obesity also causes less estrogen to be removed from the blood. Polycystic ovary syndrome (PCOS), which also causes irregular or no ovulation, is associated with higher rates of endometrial cancer for the same reasons as obesity. Specifically, obesity, type II diabetes, and insulin resistance are risk factors for Type I endometrial cancer. Obesity increases the risk for endometrial cancer by 300–400%.

Estrogen replacement therapy during menopause when not balanced (or "opposed") with progestin is another risk factor. Higher doses or longer periods of estrogen therapy have higher risks of endometrial cancer. Women of lower weight are at greater risk from unopposed estrogen. A longer period of fertility—either from an early first menstrual period or late menopause—is also a risk factor. Unopposed estrogen raises an individual's risk of endometrial cancer by 2–10 fold, depending on weight and length of therapy. In trans men who take testosterone and have not had a hysterectomy, the conversion of testosterone into estrogen via androstenedione may lead to a higher risk of endometrial cancer.

Some therapies for other forms of cancer increase the lifetime risk of endometrial cancer, which is a baseline 2–3%. Tamoxifen, a drug used to treat estrogen-positive breast cancers, has been associated with endometrial cancer in approximately 0.1% of users, particularly older women, but the benefits for survival from tamoxifen generally outweigh the risk of endometrial cancer. A one to two-year course of tamoxifen approximately doubles the risk of endometrial cancer, and a five-year course of therapy quadruples that risk. Raloxifene, a similar drug, did not raise the risk of endometrial cancer. Previously having ovarian cancer is a risk factor for endometrial cancer, as is having had previous radiotherapy to the pelvis. Specifically, ovarian granulosa cell tumors and thecomas are tumors associated with endometrial cancer.

Low immune function has also been implicated in endometrial cancer. High blood pressure is also a risk factor, but this may be because of its association with obesity. Sitting regularly for prolonged periods is associated with higher mortality from endometrial cancer. The risk is not negated by regular exercise, though it is lowered.

The estimated figures for the prevalence of fibrocystic breast changes in women over lifetime vary widely in the literature, with estimates ranging from about 30 to 60 % over about 50 to 60 % to about 60 to 75% of all women.

The condition is most common among women between 30 and 50 years of age.

EIN lesions have been discovered by a combination of molecular, histologic, and clinical outcome studies beginning in the 1990s which provide a multifaceted characterization of this disease. They are a subset of a larger mixed group of lesions previously called "endometrial hyperplasia". The EIN diagnostic schema is intended to replace the previous "endometrial hyperplasia" classification as defined by the World Health Organization in 1994, which have been separated into benign (benign endometrial hyperplasia) and premalignant (EIN) classes in accordance with their behavior and clinical management.

EIN should not be confused with an unrelated entity, serous intraepithelial carcinoma ("serous EIC"), which is an early stage of a different tumor type known as papillary serous adenocarcinoma that also occurs in the same location within the uterus.

Vaginal adenosis is characterised by the presence of metaplastic cervical or endometrial epithelium within the vaginal wall, considered as derived from Müllerian epithelium islets in later life. In women who were exposed to certain chemicals, vaginal adenosis may arise in up to 90%. Since these contraceptives were discontinued, incidence has dropped dramatically. Risk is however still present in subsequent generations due to recent exposure.

It is thought steroid hormones play a stimulatory growth in adenosis formation. Vaginal adenosis is also often observed in adenocarcinoma patients.

Uterine sarcoma are rare, out of all malignancies of the uterine body only about 4% will be uterine sarcomas. Generally, the cause of the lesion is not known, however patients with a history of pelvic radiation are at higher risk. Most tumors occur after menopause.

Women who take long-term tamoxifen are at higher risk.

LCIS (lobular neoplasia is considered pre-cancerous) is an indicator (marker) identifying women with an increased risk of developing invasive breast cancer. This risk extends more than 20 years. Most of the risk relates to subsequent invasive ductal carcinoma rather than to invasive lobular carcinoma.

While older studies have shown that the increased risk is equal for both breasts, a more recent study suggests that the ipsilateral (same side) breast may be at greater risk.

The relative risk of breast cancer based on a median follow-up of 8 years, in a case control study of US registered nurses, is 3.7.

Treatment of endometrial hyperplasia is individualized, and may include hormonal therapy, such as cyclic or continuous progestin therapy, or hysterectomy.

Vaginal adenosis is a benign abnormality in the vagina, commonly thought to be caused by intrauterine and neonatal exposure of diethylstilbestrol and other progestagens and nonsteroidal estrogens, however it has also been observed in otherwise healthy women and has been considered at times idiopathic or congenital. Postpubertal lesions have also been observed to grow . It has a rather common incidence, of about 10% of adult women.

The treatment of hyperplasia would consist upon "which"; in the case of benign prostate hyperplasia the combination of alpha-1-receptor blockers and 5-alpha-reductase inhibitors are effective.

In breast pathology, pseudoangiomatous stromal hyperplasia, commonly abbreviated PASH, is an overgrowth of myofibroblastic cells and has an appearance similar to fibroadenomatoid changes.

The diagnostic significance is currently uncertain, but it appears to be benign. There have been cases of PASH diagnosed where the tumors co-exist with breast cancer. Other cases have made screening for breast cancer difficult and in some cases impossible due to the number and density of the existing PASH tumors. These cases have resulted in the necessity of a mastectomy and double mastectomy.

Some of the more commonly known clinical forms of hyperplasia, or conditions leading to hyperplasia, are:

- Benign prostatic hyperplasia, also known as prostate enlargement.

- Cushing's disease – Physiopathology of hyperplasia of adrenal cortex due to increased circulating level of ACTH (adrenocorticotropic hormone).

- Congenital adrenal hyperplasia – Inherited disorder of gland (adrenal).

- Endometrial hyperplasia – Hyperproliferation of the endometrium, usually in response to unopposed estrogen stimulation in the setting of polycystic ovary syndrome or exogenous administration of hormones. Atypical endometrial hyperplasia may represent an early neoplastic process which can lead to endometrial adenocarcinoma. The development of endometrial adenocarcinoma from endometrial hyperplasia is a typical example of how the effects of pathologic hyperplasia can lead to neoplasia, and females who exhibit hyperplasia of the endometrium are indeed more likely to develop cancer of these cells.

- Hemihyperplasia when only half (or one side) of the body is affected, sometimes generating limbs of different lengths.

- Hyperplasia of the breast – "Hyperplastic" lesions of the breast include "usual ductal hyperplasia", a focal expansion of the number of cells in a terminal breast duct, and "atypical ductal hyperplasia", in which a more abnormal pattern of growth is seen, and which is associated with an increased risk of developing breast cancer.

- Intimal hyperplasia – The thickening of the tunica intima of a blood vessel as a complication of a reconstruction procedure or endarterectomy. Intimal hyperplasia is the universal response of a vessel to injury and is an important reason of late bypass graft failure, particularly in vein and synthetic vascular grafts.

- Focal epithelial hyperplasia (also known as Heck's disease) – This is a wart-like growth in the mucous tissues of the mouth or, rarely, throat that is caused by certain sub-types of the human papillomavirus (HPV). Heck's disease has not been known to cause cancer.

- Sebaceous hyperplasia – In this condition, small yellowish growths develop on the skin, usually on the face. This condition is neither contagious nor dangerous.

- Compensatory liver hyperplasia – The liver undergoes cellular division after acute injury, resulting in new cells that restore liver function back to baseline. Approximately 75% of the liver can be acutely damaged or resected with seemingly full regeneration through hepatocyte division, i.e., hyperplasia. This is what makes living-donor liver transplants possible.

The rate at which breast cancer (ductal carcinoma in situ "or" invasive mammary carcinoma (all breast cancer except DCIS and LCIS)) is found at the time of a surgical (excisional) biopsy, following the diagnosis of ADH on a core (needle) biopsy varies considerably from hospital-to-hospital (range 4-54%). In two large studies, the conversion of an ADH on core biopsy to breast cancer on surgical excision, known as "up-grading", is approximately 30%.

The management of PASH is controversial. Excision may be indicated in enlarging masses or lesions with atypical features.

Uterine cancer resulted in about 58,000 deaths in 2010 up from 45,000 in 1990.

Uterine cancer is the fourth most common cancer in women in the UK (around 8,500 women were diagnosed with the disease in 2011), and it is the tenth most common cause of cancer death in women (around 2,000 people died in 2012).

PIN was historically subdivided into different stages, based on the level of cell atypia. PIN was formerly classified as PIN 1, 2 or 3, in order of increasing cell irregularities. Nowadays, PIN 1 is referred to as low grade PIN, and PIN 2 and PIN 3 are grouped together as high grade PIN. Only high grade PIN has been shown to be a risk factor for prostate cancer. Because low grade PIN has no significance and does not require repeat biopsies or treatment, it is not mentioned in pathology reports. As such, PIN has become synonymous with high grade PIN.

There are several reasons why PIN is the most likely prostate cancer precursor. PIN is more common in men with prostate cancer. High grade PIN can be found in 85 to 100% of radical prostatectomy specimens, nearby or even in connection with prostate cancer. It tends to occur in the peripheral zone of the prostate. With age, it becomes increasingly multifocal, like prostate cancer. Molecular analysis has shown that high grade PIN and prostate cancer share many genetic abnormalities. This has been confirmed in a transgenic mouse model.

The risk for men with high grade PIN of being diagnosed with prostate cancer after repeat biopsy has decreased since the introduction of biopsies at more than six locations (traditional sextant biopsies).

The terms uterine cancer and womb cancer may refer to any of several different types of cancer which occur in the uterus, namely:

- Endometrial cancer:

- Cervical cancer arises from the transformation zone of the cervix, the lower portion of the uterus and connects to the upper aspect of the vagina.

- Uterine sarcomas: sarcomas of the myometrium, or muscular layer of the uterus, are most commonly leiomyosarcomas.

- Gestational trophoblastic disease relates to neoplastic processes originating from tissue of a pregnancy that often is located in the uterus.

LCIS may be treated with close clinical follow-up and mammographic screening, tamoxifen or related hormone controlling drugs to reduce the risk of developing cancer, or bilateral prophylactic mastectomy. Some surgeons consider bilateral prophylactic mastectomy to be overly aggressive treatment except for certain high-risk cases.