E-ISSN: 1309-0380
Transplacental cancer transmission: a comprehensive review focusing on mechanisms, challenges, and maternal-fetal outcomes
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30 July 2025

Transplacental cancer transmission: a comprehensive review focusing on mechanisms, challenges, and maternal-fetal outcomes

J Turk Ger Gynecol Assoc. Published online 30 July 2025.
Mishu Mangla 1
Seetu Palo 2
Naina Kumar 2
1. Department of Obstetrics and Gynaecology, All India Institute of Medical Sciences, Bibinagar, India
2. Department of Pathology and Laboratory Medicine, All India Institute of Medical Sciences, Bibinagar, India
No information available.
No information available
Received Date: 02.01.2025
Accepted Date: 08.05.2025
E-Pub Date: 30.07.2025
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Abstract

The phenomenon of transplacental transmission of cancer, where cancer cells pass from a pregnant mother to her fetus is an extremely rare occurrence. This phenomenon has significant implications for maternal and fetal health, challenging our understanding of cancer biology and maternal-fetal interactions. The literature on transplacental cancer transmission is sparse, consisting mainly of case reports, small cohort studies, and reviews. Examples of cancers that have been transmitted in this way include melanoma, choriocarcinoma, leukaemia, and lymphoma. Understanding this phenomenon is important because it has direct clinical implications for managing pregnant women with cancer and the infant, raises questions about the placental barrier and immune interactions between mother and fetus, and offers insights that could influence cancer biology and treatment strategies. This review aims to evaluate existing data, identify and synthesize evidence on transplacental cancer transmission cases, evaluate cancer types involved, their transmission mechanisms, and clinical outcomes for both mothers and infants. A comprehensive electronic search of databases was conducted for relevant case reports and series, using specific keywords related to vertical and transplacental transmission of cancer. The review elucidates comprehensive information from the reports to understand how cancer transmission occurred and was confirmed as vertical transmission, aiming to enhance knowledge in this critical area of maternal-fetal medicine.

Keywords:
Cancer, choriocarcinoma, melanoma, transplacental transmission, vertical transmission

Introduction

Transplacental transmission of cancer, also known as vertical transmission, is an exceedingly rare but intriguing phenomenon where cancer cells cross the placental barrier from a pregnant mother to her fetus. Although, about 1 in 1,000 live births involves a mother who has cancer, maternal transmission of cancer to offspring is exceedingly rare, estimated at approximately 1 in every 500,000 infants born to mothers with cancer (1, 2). This mode of transmission has profound implications for both maternal and fetal health, challenging our understanding of cancer biology and maternal-fetal interactions. It presents a unique conundrum, combining elements of oncology, immunology, and obstetrics. Given the rarity and complexity of transplacental transmission of cancer, the existing literature is sparse and comprised of case reports, small cohort studies and reviews; types of cancer include melanoma, leukaemia, and lymphoma being transmitted from mother to fetus. Understanding the transplacental transmission of cancer is important for several reasons. Firstly, it has direct clinical implications for the management of pregnant women with cancer, influencing decisions regarding treatment and monitoring. Secondly, it raises fundamental questions about the nature of the placental barrier, the immune interactions between mother and fetus, and the unique environment that allows for transmitting malignant cells. Thirdly, insights gained from studying this rare event may have broader implications for cancer biology and treatment along with strategies to prevent metastasis and improve outcomes for patients with cancer. This review sought to critically analyze existing data, identify and consolidate evidence on transplacental cancer transmission, examine the types of cancers involved, their transmission mechanisms, and the clinical impact on both mothers and infants. By consolidating comprehensive data from these rare case scenarios, this review offers a novel perspective on previously overlooked patterns, proposing new insights into transplacental transmission pathways, maternal-fetal interactions, and potential diagnostic as well as therapeutic advances in this rare phenomenon.

Methodology

An electronic search of Scopus, PubMed, Embase and other databases was conducted for case reports and case series of suspected, probable and confirmed mother-to-child transmission or vertical transmission of cancer, published in English from inception until July 2024. The electronic search strategy used keywords such as “vertical transmission” and “transplacental transmission”, “mother to child transmission” and “cancer”, “carcinoma” and “transplacental transfer”, and “metastasis to the fetus” “mother to baby”; “mother and baby”. We analysed the titles and abstracts of all case reports identified by the initial search. The reference lists of relevant reports were also explored. Two reviewers double-checked the data to avoid duplication. Case reports with placental metastasis only, without metastasis to the fetus, were excluded. Review articles, original articles, clinical trials, conference abstracts, editorials, poorly described cases, and articles in language other than English language or commentary were also excluded. The article selection and screening process details are presented in the Preferred Reporting Items for Systematic Reviews and Meta-analysis flowchart (Figure 1). Of the eligible articles, information pertaining to author and year of publication, age of the patient at the time of presentation, the type of primary cancer in the mother and its stage if available, primary site in the mother, gestational age at the time of delivery, age at diagnosis, presenting clinical features, and sites of metastasis for the baby, and the outcome of the case in the form maternal and fetal/neonatal/infant outcome was extracted. An attempt was made to extract all the possible information mentioned in the report regarding how the cancer transmission occurred and how it was confirmed to be “vertical transmission”. By systematically reviewing the literature, we hope to enhance the understanding of transplacental cancer transmission and provide a foundation for informed clinical practice and future research directions in this important area of maternal-fetal medicine.

Overview of published cases of transplacental cancer transmission

A summary of all probable and confirmed cases of transplacental cancer transmission reported in the literature to date are summarised in Table 1: all cases of choriocarcinoma (3-23), Table 2: all cases of malignant melanoma (24-40) and Table 3: other cancers, including leukaemia, lymphomas, lung cancers and cervical cancers (41-51). Choriocarcinoma is the most common tumor showing mother-to-child transmission. In a previous systematic review, conducted by one of the authors of this article, the 12-month overall survival rate for mothers was 71.8%±10.7%, while for infants, it was 22.2%±9.8% (52). The median time to diagnose gestational trophoblastic neoplasia in mothers was six weeks post-partum. For infants, the median age at presentation was 1.75 weeks [interquartile range (IQR): 0.1 to 6.75 weeks], and the median age at diagnosis was 5.00 weeks (IQR: 3.55 to 8 weeks). However, the diagnosis of vertical transmission was not confirmed in most cases (16/20). It was not clear whether the infant’s tumor was primary or secondary to maternal choriocarcinoma. Another diagnostic dilemma with choriocarcinoma is whether it has arisen from the present pregnancy or hydatiform mole in a previous pregnancy or from previous abortions where histopathology was not done, as they could have been molar pregnancy of choriocarcinoma, and this is usually not clear (52).

Malignant melanoma was found to be the second most common tumor, showing transplacental transmission after gestational choriocarcinoma. After analyzing the existing literature, we found that the tumor might have a higher incidence in male fetuses, with a male-to-female ratio of 2:1. However, in two cases where the tumor metastasis led to intrauterine fetal demise, the sex was not mentioned. All infants presented during infancy with cutaneous metastasis. The mastoid cavity and external auditory meatus were other favoured sites, followed by brain, lung, liver, testicles and adrenal glands. Interestingly, in two cases, auto-regression of the tumour was noted (28, 32). In 4/14 cases, vertical transmission was confirmed because the placenta was grossly and microscopically involved. In 5/14 cases, karyotypically female cells in a male baby were presumed to be of maternal origin, or genetically identical mutations in both tumours were confirmatory. The prognosis was very poor, both for the mother and the baby. Most (9/14, 64.3%) of the babies died, while in one case, the details were not available. For mothers, if vertical transmission had occurred, the result was invariably fatal when outcome was reported; 13/14 mothers died, while in one patient, the details were not available.

There are three cases of cervical cancer reported to be transmitted vertically (47, 48). In all three cases, the authors stressed mother-to-infant vaginal transmission through aspiration of tumour-contaminated vaginal fluids during birth. In the case described by Herskovic et al. (47), the authors acknowledged that the spread could have been hematogenous transplacental or through direct inoculation or transbronchial spread. In the cases reported by Arakawa et al. (48), the transmission was evidenced by the fact that the tumors in both male children lacked the Y chromosome and shared multiple somatic mutations, an human papilloma virus genome, and single nuclear polymorphic (SNP) alleles with their mothers’ tumors. In addition, the peri-bronchial growth pattern of the tumors in both children suggested that they originated from mother-to-infant transmission via aspiration of tumor-contaminated vaginal fluids during birth. Maternal tumor cells were likely present in the amniotic fluid, cervical secretions, or blood and were aspirated by the infants during vaginal delivery.

We found six reported cases of haemato-lymphoid malignancies that have been reported to be transmitted from mother to child trans-placentally (41-46). Transplacental transmission of cancer appears to have a predisposition for male fetuses. In cases of leukaemia and lymphoma, 5 out of 6 reported instances involved male fetuses, with the remaining one case involving a female fetus (46). Similarly, in lung cancer, 2 out of 3 cases involved male fetuses (with the sex of the baby in the third case not reported). For cervical cancer also, 2 out of 3 cases, involved male fetuses (with the sex of the baby in the third case not reported). The confirmation in these cases (where done) is either by gross/microscopic involvement of the placenta, of the finding of XX genotype in cancer cells of the male fetus, which is presumed to be of maternal origin or by identical mutations found in maternal and fetal tumors.

Mechanisms of transplacental cancer transmission, engraftment and survival

Unlike vertical transmission of infectious agents, cancer cells typically cannot cross the placental barrier due to robust immune surveillance and the placental membrane’s selective permeability (Figure 2). However, certain conditions can allow this rare transmission, leading to significant clinical and research implications. Several hypotheses explain how cancer cells might breach the placental barrier and establish themselves in the fetus (Figure 3)  including the following.

Immune tolerance

In pregnancy, immune tolerance, the immune system’s ability to recognize and not attack the own body’s cells, is critical (53). The mother’s immune system must tolerate the fetus, which expresses maternal and paternal antigens, to avoid attacking it as foreign tissue. This tolerance is mediated by various mechanisms, including the action of regulatory T cells, placental hormones, and other immunomodulatory factors that help maintain a healthy pregnancy (54).

Vertical cancer cell transmission occurs during the perinatal period, a time when the fetus is still developing immunity. Thymic development begins around week 8 of human gestation, and initial fetal T cells populate the periphery by weeks 12-14 of gestation (55). If cancer cells are transmitted before this period, they may not be recognized as foreign antigens, potentially evading an immune response, resulting in their engraftment or growth. Moreover, maintaining pregnancy requires tolerance to self-in and non-inherited maternal antigens, primarily regulated by regulatory T cells. Intrauterine hypoxia or placental hormones may influence maternal tolerance by modulating T-cell function. Taken together, fetal immune immaturity/tolerance could play a role in facilitating the engraftment and survival of maternal-derived cancer cells within the body. However, the specific mechanistic evidence for fetal cancer immune tolerance remains to be demonstrated conclusively (56-60).

Bi-directional transplacental cell trafficking (feto-maternal micro-chimerism)

It is well-documented that normal blood cells migrate between mother and fetus and vice versa, leading to micro chimerism. Micro-chimerism refers to a small population of cells originating from another individual, making them genetically distinct from the host individual’s cells (61, 62). During pregnancy, there are two types of feto-maternal micro-chimerism: fetal micro-chimerism (FMc) and maternal micro-chimerism (MMc). FMc occurs when fetal cells persist in maternal tissues, while MMc involves the presence and maintenance of maternal cells in fetal tissues (63-65). It is, therefore, quite plausible that maternal cancer cells can sometimes take advantage of this mechanism of micro chimerism, leading to carcinogenesis in the infant (1).

Immune evasion: How cancer cells escape immunity

Cancer cells can escape the immune system through various mechanisms, enabling them to survive, proliferate, and spread within the body (Figure 4) (66). Tumour cells gradually develop mechanisms to evade immune surveillance, a process known as “cancer immunoediting,” to avoid elimination by immune cells with antitumor properties. Cancer cells can exploit immune checkpoints, regulatory pathways in the immune system that prevent excessive immune responses. For instance, they may overexpress proteins like PD-L1 (Programmed Death-Ligand 1), which binds to PD-1 receptors on T cells, leading to T cell inactivation and immune evasion (67, 68). Tumor microenvironment might further dampen the immune response by recruitment of regulatory T cells (Tregs) and myeloid-derived suppressor cells that inhibit other immune cells and elaboration of immunosuppressive cytokines like transforming growth factor-beta and interleukin 10 (IL-10).

Tumor cells can downregulate the expression of major histocompatibility complex molecules on their surface, essential for presenting tumor antigens to T cells (69). This prevents the immune system from recognizing and attacking the cancer cells. Immune evasion through the loss of heterozygosity of HLA genes has also been proposed (70). Loss or mutation of molecules involved in the antigen-processing machinery can also impair antigen presentation. Cancer cells can develop resistance to apoptosis, which allows them to survive despite immune attacks (71). Cancer cells can secrete various substances that inhibit immune cell function, such as indoleamine 2,3-dioxygenase, which depletes tryptophan and suppresses T-cell activity.

Placental microscopic trauma

Trophoblasts, chorionic villi, and capillary endothelium separate the fetal and maternal circulations (Figure 2). Along with the fetal immune system, the placental barrier prevents the spread and allografting of maternal tumors into the fetus. Despite this protection, the transmission of neoplastic and non-neoplastic maternal cells to the fetus does occur during pregnancy. Suppose the separation between the fetal and maternal blood systems is breached, maternal intravascular tumour cells can cross the placenta and reach the fetal liver through the umbilical vein or the fetal lungs via the ductus venosus (49).

Several obstetric conditions can cause microscopic damage to the placenta, affecting its structure and function. Preeclampsia and placental fetal growth restriction can lead to placental infarcts, intervillous fibrin deposition, and increased syncytial knots, resulting in reduced placental perfusion and placental insufficiency. Gestational diabetes leads to villous immaturity, and villous hyperplasia. There can also be increased deposition of glycogen in the placental tissue. Placental abruption can cause haemorrhage into the placental tissue, leading to infarcts, necrosis, and fibrin deposition. Maternal infections, such as chorioamnionitis, may cause inflammatory changes in the placenta, including villitis and funisitis, leading to damage and sometimes necrosis of the placental tissue. Each of these conditions may compromise placental ability to effectively control cell and nutrient traffic across the placental membrane, potentially leading to adverse pregnancy outcomes (49, 50).

Placental receptor similarity and reduced placental function

Tumor cells may exploit receptors on placental cells to gain entry into fetal circulation, mimicking the way nutrients and other substances pass through. Also, given the similarities between tumor cells and trophoblastic cells in biological processes, there is substantial evidence that maternal tumour-induced effects could impact placental function (72). Studies have indicated that the presence of maternal cancer or certain tumor factors, such as proinflammatory cytokines IL-6, interferon-gamma (IFN-γ), and tumour necrosis factor, can impair the placental integrity and function (73, 74). These factors may play a role in the vertical transfer of cancer clones. However, more research is needed on how the damage caused by cancer cells in the placenta facilitates transplacental cancer spread.

Diagnostic confirmation of vertical transmission

Modern genetic tools, such as DNA sequencing and genomic profiling, can compare the genetic material of maternal and fetal tumors, providing concrete evidence of the origin of the cancer. Next-generation sequencing (NGS) can be used to look for mutations in the tumor that are present in the maternal DNA but absent in the patient’s germline DNA, which can help determine if the cancer was inherited from the mother. Since mitochondrial DNA (mtDNA) is inherited maternally, analyzing mtDNA from the tumor and comparing it to the maternal mtDNA can provide additional clues. SNP arrays can be used to compare genetic variations between the tumor, patient’s germline or maternal DNA, which can further help identify the source of the cancer (75-77).

Most of the studies have used karyotyping or fluorescent in situ hybridisation (FISH) techniques, as the absence of Y chromosome in the cancer tissue, in a male fetus, provides indirect evidence that the tumor originated from the mother. Involvement of placenta by the tumor, on gross and microscopic examination, particularly the presence of villous invasion, also implies that the transmission occurred through the placenta. Arakawa et al. (48) recently reported two intriguing cases of perinatal transmission of maternal cervical cancer to the infant, subsequently developing into lung cancer. FISH analysis revealed the absence of the Y chromosome in tumor in the male babies and upon sequencing, both the tumors in the mothers and babies showed shared genomic tumor characteristics, which substantiates mother-to-infant vaginal transmission through aspiration of tumor cell-contaminated vaginal fluids during birth.

Treatment considerations: Why is an understanding of transplacental cancer transmission essential?

Clinicians must distinguish whether the tumor in the newborn is a primary disease or a metastasis from the mother as treatment protocols differ drastically between congenital cancers and those acquired through transmission. Vertical transmission of metastases could be viewed as a “haploidentical transplant” (78). In this scenario, the newborn’s already functional immune system might reject non-inherited maternal antigens. Consequently, administering modified or reduced therapeutic regimens could be justified, allowing the newborn’s immune system time to develop effective responses. The possibility of transplacental cancer transmission also brings forth ethical dilemmas. Decisions regarding the continuation of pregnancy, the timing of delivery, and the treatment options for both mother and child are complex and emotionally charged. Counselling and psychological support for affected families are critical components of care.

Due to the rarity of infant melanoma, infants and children have not been included in the majority of clinical trials for treatment, resulting in a lack of specialized treatment standards for this population. Consequently, current treatment strategies for melanoma in this age group are derived from adult treatment protocols. Surgery remains the primary treatment for melanoma in both children and adults. For pediatric patients with more advanced disease, biologic therapies are more commonly used than chemotherapy or radiation therapy (79). Since BRAF mutations are present in approximately 50% of melanoma patients, BRAF inhibitors like Vemurafenib and Dabrafenib, and other specific inhibitors like Trametinib, which targets other components of the MAPK signal transduction pathway, such as MEK1 and MEK2, provide an effective therapeutic option for patients with this mutation. Another treatment approach involves modulating the host’s immune system to target melanoma. Immunotherapy drugs, such as Ipilimumab, use monoclonal antibodies to suppress CTLA-4, enhancing the immune system’s response to tumor cells. Agents like IL-2 activate the immune system to attack malignant cells. High-dose interferon alfa-2b has shown promising results in children with melanoma with an acceptable risk-benefit profile. In addition, anti-PD1 antibodies, such as Pembrolizumab and Nivolumab, have the potential to improve prognosis with long-lasting effects (80, 81). One such case with successful treatment with nivolumab therapy has been reported by Arakawa et al (48).

As with other germ cell tumors, the management of choriocarcinoma in infants and children involves a comprehensive approach with multi-agent neoadjuvant chemotherapy, reassessment after 2-4 cycles, surgical removal of persistent disease, and adjuvant chemotherapy. This complex therapy aims to control the metastatic nature of the disease and prevent relapse. Upfront chemotherapy is particularly crucial for children with multi-systemic involvement who are not candidates for immediate surgery. The excellent survival rates observed in this review reinforce the effectiveness of these treatment principles, which are well-established and readily available (82, 83). In most current protocols, treatment is stratified based on an initial risk assessment that includes age, site, histology, stage, completeness of resection, and tumor markers alpha1-fetoprotein and human chorionic gonadotropin (β-HCG). Using these modern protocols, overall cure rates exceed 80%. Moreover, previously high-risk groups can now expect a favourable prognosis with risk-adapted treatment, while an increasing number of low-risk patients are managed expectantly or with significantly reduced chemotherapy (82).

Conclusion

Transplacental transmission of cancer, while rare, poses significant medical and ethical challenges. It underscores the complexity of the placental barrier and the interactions between maternal and fetal health. Advances in genetic diagnostics and a deeper understanding of immune mechanisms hold promise for better management and outcomes for both mothers and their children. NGS of paired tumors (both mother and baby) and normal tissue samples might be a valuable method for diagnosing cancer transmitted from mothers to infants and for understanding how common this transmission is. Furthermore, analysing the HLA haplotype of cancer cells and peripheral normal lymphocytes may offer insights into the risk of maternal-to-fetus transmission. Continued research and interdisciplinary collaboration are essential in unravelling the mysteries of this unique cancer transmission pathway.

Author Contributions: Design: M.M., N.K., Analysis or Interpretation: M.M., S.P., Literature Search: S.P., Writing: M.M., S.P., N.K., Critical Review: M.M., S.P., N.K.
Conflict of Interest: No conflict of interest is declared by the authors.
Financial Disclosure: The authors declared that this study received no financial support.

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