Transmission of breast cancer by a single multiorgan donor to 4 transplant recipients

Matser, Yvette A. H.; Terpstra, Matty L.; Nadalin, Silvio; Nossent, George; Boer, Jan de; Bemmel, Barbara C. van; Eeden, Susanne van; Budde, Klemens; Brakemeier, Susanne; Bemelman, Fréderike J.

doi:10.1111/ajt.14766

Cited by 39 publications

(28 citation statements)

References 15 publications

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“…Cancer cells do not usually transmit between individuals. No human examples of transmissible cancers are known apart from rare iatrogenic cases during surgery and transplantation or materno-fetal transmission ( Isoda et al., 2009 , Matser et al., 2018 , Metzger and Goff, 2016 ). Accordingly, horizontal transmission is not considered a hallmark of cancer ( Hanahan and Weinberg, 2011 ).…”

Section: Introductionmentioning

confidence: 99%

The ERBB-STAT3 Axis Drives Tasmanian Devil Facial Tumor Disease

et al. 2019

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SummaryThe marsupial Tasmanian devil (Sarcophilus harrisii) faces extinction due to transmissible devil facial tumor disease (DFTD). To unveil the molecular underpinnings of this transmissible cancer, we combined pharmacological screens with an integrated systems-biology characterization. Sensitivity to inhibitors of ERBB tyrosine kinases correlated with their overexpression. Proteomic and DNA methylation analyses revealed tumor-specific signatures linked to the evolutionary conserved oncogenic STAT3. ERBB inhibition blocked phosphorylation of STAT3 and arrested cancer cells. Pharmacological blockade of ERBB or STAT3 prevented tumor growth in xenograft models and restored MHC class I expression. This link between the hyperactive ERBB-STAT3 axis and major histocompatibility complex class I-mediated tumor immunosurveillance provides mechanistic insights into horizontal transmissibility and puts forward a dual chemo-immunotherapeutic strategy to save Tasmanian devils from DFTD.Video Abstract

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Section: Introductionmentioning

confidence: 99%

The ERBB-STAT3 Axis Drives Tasmanian Devil Facial Tumor Disease

et al. 2019

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“…Previous study suggested that timely removal of allograft might be bene cial to prevent the development of metastasis 2 . In order to prevent transmission, it should be considered in all recipients after noti cation of cancer transmission in one recipient from a multiorgan donor.…”

Section: Discussionmentioning

confidence: 99%

“…The persistent organ shortage requires the maximum utilization of all available donors, including those with tumors, that may lead to donor-derived malignancy [1][2][3] . There is a consensus that whether to use donor organs with tumors depends on risk levels of tumor transmission.…”

Section: Introductionmentioning

confidence: 99%

Transmission of Synovial Sarcoma from A Single Multiorgan Donor to Three Transplant Recipients: Cases Report and Literature Review

Zhang

Tian

Yang

et al. 2020

Preprint

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Background Donor-derived malignancy is sometimes unidentified at the time of transplantation, resulting in unanticipated donor-derived malignancy, which becomes a notable problem since the increasing use of marginal donors. Case presentation We first report three cases of donor-derived synovial sarcoma from a single multiorgan donor in China. The donor was died of respiratory failure caused by an intrathoracic tumor, which was diagnosed as a benign tumor at the time of donation. All of the three recipients developed synovial sarcoma within 3 months to 13 months after transplantation, proven to be donor-derived. Liver transplant recipient died of tumor metastasis. Two kidney transplant recipients survived from metastases by comprehensive therapy, including the first use of Anlotinib, exhibiting an effective anti-tumor activity.Conclusions This report highlights the importance of detailed donor assessment, close follow-up and timely treatment, as well as the need for establishing a post-transplant surveillance system for donor-derived transmission events. Whether to use organs from a donor with initial diagnosis of benign tumor needs to be cautious. Malignant potential of tumors needs to be excluded before transplantation, otherwise, the organs should be discarded.

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“…Pommier et al [171] have recently reported that patients and mice with pancreatic ductal adenocarcinoma contained single quiescent DTCs lacking MHC-I expression, which enabled them to escape immunity and establish latent metastases. Four cases of breast cancer transmission to immunosuppressed transplant recipients from a single, clinically healthy donor have been recently described [172] . The latency time to metastasis formation ranged from 16 months to 6 years, and transmissions did not occur in a patient that discontinued immunosuppression.…”

Section: Immunological Dormancy: Active Control By the Immune Systemmentioning

confidence: 99%

“…The latency time to metastasis formation ranged from 16 months to 6 years, and transmissions did not occur in a patient that discontinued immunosuppression. This unintentional situation suggested that donor tissues harbored DTCs, which persisted in a latent state because of immune control, while the immunosuppression of the recipient allowed the DTCs to resume growth [172] . Once cells have escaped immunosurveillance it is unlikely that they can re-enter a second state of immunological dormancy, because the mechanisms that eluded immunosurveillance are generally part of the genetic or epigenetic tumor clonal evolution and therefore irreversible [59,91] .…”

Section: Immunological Dormancy: Active Control By the Immune Systemmentioning

confidence: 99%

Chemotherapy-induced immunological breast cancer dormancy: a new function for old drugs?

Peyvandi¹,

Lan²,

Lorusso³

et al. 2019

JCMT

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Breast cancer remains the main cause of cancer-related mortality for women worldwide. Main cause of death is the development of therapy-resistant metastases. Relapses occur with a bimodal temporal distribution, with a first peak at 1-2 years after initial therapy and a second peak 2-3 years later. This discontinuous growth kinetics is consistent with the notion that disseminated cancer cells can remain dormant over a prolonged period of time before resuming growth. How cancer cells enter, sustain and exit dormancy, are unanswered questions with relevance to cancer biology, monitoring and therapy. Investigating mechanisms of breast cancer dormancy remains challenging, as in patients the condition is elusive and experimentally there are only a few models that recapitulate the clinical condition. Thus, developing new models to identify clinically relevant mechanisms and candidate therapeutic targets may open new avenues for novel therapies to induce and prolong dormancy. We have observed that cells surviving chemotherapy can enter a state of immunological dormancy. Using this model, we identified IRF-7/Interferon type I/IFNRA as signaling axis essential for this effect. Here we will review concepts and recent developments in cancer metastasis and dormancy with emphasis on breast cancer, and elaborate strategies to exploit them therapeutically.

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Transmission of breast cancer by a single multiorgan donor to 4 transplant recipients

Cited by 39 publications

References 15 publications

The ERBB-STAT3 Axis Drives Tasmanian Devil Facial Tumor Disease

The ERBB-STAT3 Axis Drives Tasmanian Devil Facial Tumor Disease

Transmission of Synovial Sarcoma from A Single Multiorgan Donor to Three Transplant Recipients: Cases Report and Literature Review

Chemotherapy-induced immunological breast cancer dormancy: a new function for old drugs?

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