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Abortion–breast cancer hypothesis

notion that abortion increases breast cancer risk

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Record originEnglish Wikipedia
Text licenseCC BY-SA 4.0
Source revisionMay 28, 2026
Entity authorityQ4668515 ↗
Source-derived summary

The abortion–breast cancer hypothesis posits that having an induced abortion can increase the risk of getting breast cancer. This hypothesis is at odds with mainstream scientific opinion and is rejected by major medical professional organizations; despite this, it continues to be widely propagated as pseudoscience, typically in service of an anti-abortion agenda.

In early pregnancy, hormone levels increase, leading to breast growth. The hypothesis proposes that if this process is altered by an abortion, then more immature cells could be left behind, and that these immature cells could increase the risk of breast cancer over time.

The abortion–breast cancer hypothesis has been the subject of extensive scientific inquiry, and the scientific community has concluded that abortion does not cause breast cancer; and that breast cancer should not be a concern for women who are having a miscarriage or considering having an abortion. This consensus is supported by major medical bodies, including the World Health Organization, the U.S. National Cancer Institute, the American Cancer Society, the American Congress of Obstetricians and Gynecologists, the Royal College of Obstetricians and Gynaecologists, the German Cancer Research Center, and the Canadian Cancer Society.

Some anti-abortion activists have continued to advance a discredited causal link between abortion and breast cancer. In the United States, they have advanced state legislation that in several states requires health care providers to present abortion as a cause of breast cancer when counseling women who are seeking abortion. This political intervention culminated when the George W. Bush administration altered the National Cancer Institute website to suggest that abortion might cause breast cancer. In response to public concern over this intervention, the NCI convened a 2003 workshop bringing together over 100 experts on the issue.

Editorial summary

This brief starts where responsible research should: with the source description of “Abortion–breast cancer hypothesis” as notion that abortion increases breast cancer risk. Everything that follows is an evidence route, not borrowed authority.

Editorial reviewA dependable orientation record for establishing vocabulary, names and a first evidence trail. The current lead gives the account dated anchors—2003—that can be checked directly. The selected authority fields contribute no independent date. The account is most persuasive where Abortion, breast and cancer can be independently traced.
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Why this record matters

The subject matters to the general reference register because the source frames it as notion that abortion increases breast cancer risk. Its deeper value depends on whether names, dates, institutions and citations support that framing.

Evidence profile

The citation trail is more important than the brevity of the summary: it shows where individual claims can be examined in context. The source revision retrieved here is dated May 28, 2026. The linked authority identifier is Q4668515. None of the 0 selected statements returned an explicit reference. The first chronological checks are 2003.

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Overview language is designed for orientation and should not be treated as a substitute for the evidence cited beneath it. The source lead contains qualifying language; that uncertainty should survive quotation, summary and reuse. Authority statements aid reconciliation but still require their own references, qualifiers and ranks to be checked.

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This entry incorporates text from “Abortion–breast cancer hypothesis” on English Wikipedia. Contributors are listed in the page history. Text is available under the Creative Commons Attribution-ShareAlike 4.0 License. Selected authority identifiers and statements are retrieved from Wikidata under CC0; their references and qualifiers remain part of the verification path.