Uterine cancer is a malignancy that originates in the tissues of the uterus. The most common form is endometrial cancer, which starts in the endometrium, the inner lining of the uterus. Biologically, men cannot develop uterine cancer because they do not possess a uterus, making the disease exclusively specific to biological females.
Anatomical Differences Between Biological Sexes
The inability for men to develop uterine cancer stems from fundamental differences in reproductive anatomy established during embryonic development. All human embryos initially possess two sets of primitive ducts: the Müllerian ducts and the Wolffian ducts. In females, the Müllerian ducts persist and develop into the internal reproductive organs, including the fallopian tubes, cervix, and the uterus.
In a male embryo, the SRY gene on the Y chromosome triggers the production of Anti-Müllerian Hormone (AMH) by the testes, causing the Müllerian ducts to regress. Simultaneously, testosterone stimulates the Wolffian ducts to develop into the male reproductive tract, such as the epididymis, seminal vesicles, and vas deferens. This regression means that biological males lack the uterine tissue, specifically the endometrium, where over 90% of uterine cancers originate.
Common Misconceptions and Related Male Cancers
The question of whether men can get uterine cancer often arises from a desire to understand sex-specific cancers that share common biological drivers. The closest analogy in men is prostate cancer, which is the most common non-skin cancer in men and is highly dependent on male sex hormones. Like endometrial cancer’s link to estrogen, prostate cancer’s growth is often driven by androgens, making both conditions hormone-sensitive malignancies.
While the organs are different, they both involve uncontrolled cell growth in a gland or lining of the reproductive tract. Other cancers are sometimes grouped with uterine cancer because of shared symptoms or anatomical location. For instance, some symptoms of advanced uterine cancer, such as changes in urination or pelvic pain, can overlap with cancers that affect the male urinary tract, such as bladder cancer or ureteral cancers.
Shared Hormonal and Genetic Risk Factors
Men and women share underlying systemic risk factors that can predispose them to different, yet biologically related, cancers. The influence of hormones is a major area of overlap, particularly concerning excess body weight. Adipose tissue, or body fat, is metabolically active and produces hormones, including estrogen, by converting androgens through an enzyme called aromatase.
In women, this excess estrogen, particularly after menopause when the ovaries stop producing hormones, can cause the cells in the endometrium to grow too much, significantly increasing the risk of endometrial cancer. In men, this same hormonal environment, characterized by obesity and metabolic syndrome, elevates the risk for several cancers, including aggressive prostate cancer and colorectal cancer. High levels of insulin and insulin-like growth factor-1 (IGF-1) associated with obesity also drive cell proliferation in both sexes, increasing the overall cancer risk.
Genetic predisposition is another significant shared risk factor, exemplified by Lynch Syndrome, also known as hereditary non-polyposis colorectal cancer (HNPCC). This inherited condition involves a mutation in mismatch repair genes, which significantly increases the lifetime risk of several cancers in both men and women. For women with Lynch Syndrome, the lifetime risk of developing endometrial cancer can be as high as 40% to 60%, making it the most common non-colorectal cancer they face.
Men with Lynch Syndrome do not face a uterine cancer risk, but they have a substantially elevated risk of colorectal cancer, with a lifetime risk between 60% and 80%, and an increased risk of prostate, gastric, and urinary tract cancers. The syndrome demonstrates how a single genetic defect can manifest as different, organ-specific cancers in men and women, linking them through a common underlying mechanism of DNA repair failure.