title: Pregnancy and lactation after breast cancer elevate plasma prolactin, do not shorten and may prolong survival.
abstract: The affliction of breast cancer is doubled for young patients wishing to have a child. Because estrogens can cause breast cancer and its elevation during pregnancy, clinical advice historically restricted pregnancy to at least 5 years post-diagnosis. Opposing evidence gradually relaxed this. Furthermore, in the last decade it was clarified that overall, post-treatment pregnancy and breast-feeding do not shorten survival. Despite this evidence and patients such as S.B. (deceased) and remarkable L.H. (five children, starting immediately after treatment for node-positive breast cancer), much opposition and restrictive advice remain: additional therapy preferred over pregnancy. In healthy women, pregnancy reduces (cause unknown) the risk of breast cancer and lactation may reduce it. These are accompanied by highly elevated plasma prolactin (PRL) over many months (pregnancy, 15-25 x daily mean 10 ng/ml; lactation, up to 30 x daily mean). PRL concentration too increases in other natural and non-biological conditions, also apparently without increasing breast cancer incidence. Nevertheless, firm and implied support for early pregnancy (and lactation) post-diagnosis and treatment may face a new issue. Over a decade, some studies have claimed epidemiological evidence that a relatively minute PRL elevation (from zero to 0.6-0.8 ng/ml) over mean level increases the risk of breast cancer (i.e. it is a carcinogen) and that this supports (and is supported by) a similar view from some laboratory research. This two-pronged mutuality could create further anxiety and unjustified advice dashing the wish for a child. Is this justified? Epidemiology on PRL and breast cancer risk in the eighties/nineties was contradictory and inconclusive; in the last decade, it was also biologically implausible. 'Positive' laboratory results targeting a 'tamoxifen for PRL' have over-shadowed confounding, negative (often called 'inconsistent') laboratory evidence. Increasingly evident complexity of conflicting biochemical, hormonal, cellular and tissue interactions, confused further by failure of molecular genetics to confirm PRL as a carcinogen, make this target more a mirage than an oasis. While recognizing the value of laboratory research primarily for facts, future progress will be most sound and rapid from observation starting with the human entity, not with its parts. Molecular genetics makes this possible and will be the epicentre of breast cancer research. Meanwhile, young breast cancer patients after initial treatment and eager for a child can today reasonably benefit from advice based on phenomena evolved over eons: pregnancy, lactation and accompanying highly-elevated PRL will not increase risk of recurrence and will in some cases prolong survival.
authors.affiliation: Human Molecular Genetics and Pharmacogenetics, Migal Biotechnology Institute, Galilee, POB 831, Kiryat Shmona 11016, Israel.
authors.forename: Dani
authors.initials: D
authors.lastname: Bercovich
authors.forename: Geoffrey
authors.initials: G
authors.lastname: Goodman
mesh_terms: D001943:Breast Neoplasms / Q000097:blood / Q000503:physiopathology*; D005260:Female; D006801:Humans; D007774:Lactation; D011247:Pregnancy; D011388:Prolactin / Q000097:blood*; D016019:Survival Analysis
chemical_list: D011388:Prolactin