bims-lifras Biomed News
on Li-Fraumeni syndrome
Issue of 2021‒09‒05
fourteen papers selected by
Joanna Zawacka-Pankau
Karolinska Institutet
  1. Hereditary pancreatic cancer.
  2. TP53 mutational hot spots for Li-Fraumeni syndrome in Asian populations.
  3. Germline DDX41 mutations cause ineffective hematopoiesis and myelodysplasia.
  4. Letter to the Editor: "Family history and pathogenic/likely pathogenic germline variants in prostate cancer patients".
  5. Germline GPR161 Mutations Are Associated With Infant Medulloblastoma.
  6. Hereditary leiomyomatosis and renal cell cancer (HLRCC): Case series and review of the literature.
  7. Germline Mutations in African American Men with Prostate Cancer: Incidence, Implications and Diagnostic Disparities.
  8. Uterine leiomyomas in hereditary leiomyomatosis and renal cell cancer (HLRCC) syndrome can be identified through distinct clinical characteristics and typical morphology.
  9. Germline variants in DNA repair genes, including BRCA1/2, may cause familial myeloproliferative neoplasms.
  10. Paired somatic-germline testing of 15 polyposis and colorectal cancer-predisposing genes highlights the role of APC mosaicism in de novo familial adenomatous polyposis.
  11. Genetic predisposition to male breast cancer in Poland.
  12. Prevalence of mutations in BRCA and homologous recombination repair genes and real-world standard of care of Asian patients with HER2-negative metastatic breast cancer starting first-line systemic cytotoxic chemotherapy: subgroup analysis of the global BREAKOUT study.
  13. Adenoma and colorectal cancer risks in Lynch syndrome, Lynch-like syndrome, and familial colorectal cancer type X.
  14. Association of Unbalanced Translocation der(1;7) with Germline GATA2 Mutations.
  1. Int J Clin Oncol. 2021 Sep 02.
    Hereditary pancreatic cancer.
    Kodai Abe, Minoru Kitago, Yuko Kitagawa, Akira Hirasawa.
      Pancreatic cancer is associated with both family and hereditary cancer syndromes. Multigene panel testing for pancreatic cancer detected the germline variants BRCA1/2, PALB2, ATM, TP53, MLH1, STK11/LKB1, APC, CDKN2A, and SPINK1/PRSS1 as high-risk genes. A latest genome-wide association study revealed the common, but low-risk germline variants in pancreatic cancer patients. Active pancreatic surveillance using magnetic resonance imaging and endoscopic ultrasound is recommended for high-risk individuals who have a family history of pancreatic cancer or harbor these germline pathogenic variants to improve the detection rate and prognosis of pancreatic cancer. Since poly-ADP-ribose polymerase (PARP) inhibitor has been shown to be effective in improving the prognosis of BRCA-positive pancreatic cancer as well as hereditary breast and ovarian cancer syndrome, PARP inhibitor therapy is currently being applied as precision medicine to pancreatic cancer patients harboring the BRCA1/2 germline variant. This review highlights the importance of surveillance for germline pathogenic variants in pancreatic cancer and is expected to lead to improvements in the diagnosis and prevention of pancreatic cancer as well as facilitate the development of effective therapeutic strategies and precision medicine.
    Keywords:  Cancer predisposition gene; Familial pancreatic cancer; Hereditary pancreatic cancer; Multigene panel testing; Surveillance
    DOI:  https://doi.org/10.1007/s10147-021-02015-6
  2. Trop Med Int Health. 2021 Sep 03.
    TP53 mutational hot spots for Li-Fraumeni syndrome in Asian populations.
    Luca Lo Piccolo, Salinee Jantrapirom, Sutpirat Moonmuang, Pimpisa Teeyakasem, Arnat Pasena, Pathacha Suksakit, Pimlak Charoenkwan, Dumnoensun Pruksakorn, Nut Koonrungsesomboon.
      OBJECTIVE: Germline mutations of the TP53 tumor suppressor gene are the only known cause of the hereditary autosomal disorder called Li-Fraumeni syndrome (LFS). However, little information is available about TP53 pathogenic variants in Asian LFS patients, making it difficult to provide precise genetic counseling with regard to long-term cancer risk. We conducted a systematic review to gather relevant case-control studies exploring the association between TP53 polymorphisms and the incidence of cancer belonging to the LFS spectrum in Asian populations.METHOD: Systematic review and meta-analysis. The odds ratio was used as a summary effect measure to quantify the strength of the association between TP53 polymorphisms and cancer risk by means of random-effects meta-analysis.
    RESULTS: 16 studies were included in this systematic review, with 13 studies (involving 10,645 cases and 28,288 controls) that enabled meta-analysis. The majority of the studies focused on a single nucleotide variation at codon 72 in exon 4 (c.215C>G, p.Arg72Pro, rs1042522). Therefore, we tested either dominant, co-dominant, recessive, or heterozygous models, and found that the p.Arg72Pro was not significantly associated with increased cancer risk in any of the models.
    CONCLUSION: We found the number of studies on cancers belonging to the LFS spectrum in Asia is very small. Thus, at the present time a meta-analysis approach is somewhat useful to identify germline TP53 mutations as potential markers of hereditary cancer associated with LFS in Asian populations.
    Keywords:   TP53 ; Asian populations; Li-Fraumeni syndrome; genetic variants; hereditary cancer; markers
    DOI:  https://doi.org/10.1111/tmi.13673
  3. Cell Stem Cell. 2021 Aug 27. pii: S1934-5909(21)00341-6. [Epub ahead of print]
    Germline DDX41 mutations cause ineffective hematopoiesis and myelodysplasia.
    Timothy M Chlon, Emily Stepanchick, Courtney E Hershberger, Noah J Daniels, Kathleen M Hueneman, Ashley Kuenzi Davis, Kwangmin Choi, Yi Zheng, Carmelo Gurnari, Torsten Haferlach, Richard A Padgett, Jaroslaw P Maciejewski, Daniel T Starczynowski.
      DDX41 mutations are the most common germline alterations in adult myelodysplastic syndromes (MDSs). The majority of affected individuals harbor germline monoallelic frameshift DDX41 mutations and subsequently acquire somatic mutations in their other DDX41 allele, typically missense R525H. Hematopoietic progenitor cells (HPCs) with biallelic frameshift and R525H mutations undergo cell cycle arrest and apoptosis, causing bone marrow failure in mice. Mechanistically, DDX41 is essential for small nucleolar RNA (snoRNA) processing, ribosome assembly, and protein synthesis. Although monoallelic DDX41 mutations do not affect hematopoiesis in young mice, a subset of aged mice develops features of MDS. Biallelic mutations in DDX41 are observed at a low frequency in non-dominant hematopoietic stem cell clones in bone marrow (BM) from individuals with MDS. Mice chimeric for monoallelic DDX41 mutant BM cells and a minor population of biallelic mutant BM cells develop hematopoietic defects at a younger age, suggesting that biallelic DDX41 mutant cells are disease modifying in the context of monoallelic DDX41 mutant BM.
    Keywords:  BM failure; DDX41; myelodysplastic syndrome; protein synthesis; ribosome biogenesis; snoRNA
    DOI:  https://doi.org/10.1016/j.stem.2021.08.004
  4. Prostate. 2021 Aug 31.
    Letter to the Editor: "Family history and pathogenic/likely pathogenic germline variants in prostate cancer patients".
    Elisa M Ledet, Oliver Sartor.
      
    DOI:  https://doi.org/10.1002/pros.24221
  5. Cancer Discov. 2019 Dec;9(12): 1645
    Germline GPR161 Mutations Are Associated With Infant Medulloblastoma.
      Germline mutations in GPR161, encoding a Sonic Hedgehog regulator, predispose to medulloblastoma.
    DOI:  https://doi.org/10.1158/2159-8290.CD-RW2019-162
  6. Urol Oncol. 2021 Aug 27. pii: S1078-1439(21)00344-6. [Epub ahead of print]
    Hereditary leiomyomatosis and renal cell cancer (HLRCC): Case series and review of the literature.
    Yanfei Yu, Mengmeng Zheng, Weijie Zhu, Fuqiang Zhao, Bao Guan, Qi Shen, Feng Yang, Qun He, Xuesong Li.
      BACKGROUND: Hereditary leiomyomatosis and renal cell cancer (HLRCC) is an autosomal dominant syndrome caused by heterozygous pathogenic germline variants in the fumarate hydratase (FH) gene. It is characterized by cutaneous and uterine leiomyomas and an increased risk of developing renal cell carcinoma (RCC). HLRCC-related RCC tends to be aggressive. To date, only a few publications have described HLRCC-related RCC, and the clinical, morphological and molecular aspects of HLRCC-related RCC need to be further studied.METHODS: We retrospectively analyzed the clinical and pathological data of 3 patients with HLRCC recently diagnosed. Immunohistochemistry and Whole-exome sequencing was performed on 3 patients. The function of the DNA variant was predicted in silico.
    RESULTS: We reported 3 patients from unrelated Chinese families, with HLRCC-related RCC and identified 3 different germline FH mutations (2 missense and 1 nonsense). A novel missense mutation of FH gene (c.454A>G, p.N152D) was predicted to be probably pathogenic and deleterious by multiple protein function predicting software. This study indicated that the novel mutation may be responsible for the occurrence of HLRCC-related RCC. 100% (2/2) female RCC patients had uterine fibroids. No cutaneous manifestations were identified.
    CONCLUSION: We indicate that germline screening should be encouraged in early-onset patients. Clinicopathological data, such as family history and immunohistochemical results can provide valuable clinical information for the differential diagnosis of HLRCC-associated RCC in advance.
    Keywords:  Fumarate hydratase; Hereditary leiomyomatosis and renal cell carcinoma (HLRCC); Immunohistochemistry; Missense mutation
    DOI:  https://doi.org/10.1016/j.urolonc.2021.07.026
  7. Urology. 2021 Aug 25. pii: S0090-4295(21)00796-2. [Epub ahead of print]
    Germline Mutations in African American Men with Prostate Cancer: Incidence, Implications and Diagnostic Disparities.
    Kelly K Bree, Patrick J Hensley, Curtis A Pettaway.
      Recent data suggests that African American men (AAM) with prostate cancer (PCa) exhibit genetic alterations in highly penetrant germline genes, as well as low penetrant single nucleotide polymorphisms. The importance of germline variants of uncertain significance (VUS) remain poorly elucidated and given the elevated rates of VUS in AAM compared to Caucasians with PCa, further studies are needed to facilitate potential reclassification of VUS. Ongoing efforts to include AAM in genomics research is of paramount importance in order to ensure applicability of discoveries across diverse populations and potentially reduce PCa disparities as we embark on the era of precision medicine.
    Keywords:  African American; germline DNA testing; polygenic risk score; prostate cancer; single nucleotide polymorphisms
    DOI:  https://doi.org/10.1016/j.urology.2021.08.017
  8. Acta Obstet Gynecol Scand. 2021 Sep 03.
    Uterine leiomyomas in hereditary leiomyomatosis and renal cell cancer (HLRCC) syndrome can be identified through distinct clinical characteristics and typical morphology.
    Outi Uimari, Anne Ahtikoski, Kati Kämpjärvi, Ralf Butzow, Ilkka Y Järvelä, Markku Ryynänen, Lauri A Aaltonen, Pia Vahteristo, Outi Kuismin.
      INTRODUCTION: Hereditary leiomyomatosis and renal cell cancer (HLRCC) constitute a tumor susceptibility syndrome caused by germline mutations in the fumarate hydratase (FH) gene. The most common features are leiomyomas of the uterus and the skin. The syndrome includes a predisposition to early-onset, aggressive renal cell cancer. It is important to identify women with HLRCC among other uterine leiomyoma patients in order to direct them to genetic counseling and to identify other affected family members.MATERIAL AND METHODS: We conducted a nationwide historical study to identify typical clinical characteristics, uterine leiomyoma morphology, and immunohistochemistry for diagnosing HLRCC. The study included 20 women with a known FH germline mutation and 77 women with sporadic uterine leiomyomas. The patient records of all women were reviewed to obtain clinical details regarding their leiomyomas. Uterine leiomyoma tissue specimens from 43 HLRCC-related leiomyomas and 42 sporadic leiomyomas were collected and prepared for histology analysis. A morphologic description was performed on hematoxylin & eosin-stained tissue slides, and immunohistochemical analysis was carried out for CD34, Bcl-2, and p53 stainings.
    RESULTS: The women with HLRCC were diagnosed with uterine leiomyomas at a young age compared with the sporadic leiomyoma group (mean 33.8 years vs. 45.4 years, P < 0.0001), and their leiomyomas occurred as multiples compared with the sporadic leiomyoma group (more than four tumors 88.9% vs. 30.8%, P < 0.0001). Congruently, these women underwent surgical treatment at younger age compared with the sporadic leiomyoma group (mean 37.3 years vs. 48.3 years, P < 0.0001). HLRCC leiomyomas had denser microvasculature highlighted by CD34 immunostaining when compared with the sporadic leiomyoma group (112.6 mean count/high-power field, SD 20.8 vs. 37.4 mean count/high-power field, SD 21.0 P < 0.0001) and stronger anti-apoptotic protein Bcl-2 immunostaining when compared with the sporadic leiomyoma group (weak 4.7%, moderate 44.2%, strong 51.2% vs. 26.2%, 52.4%, 21.4%, respectively, P = 0.003). No differences were observed in p53 staining.
    CONCLUSIONS: Women with HLRCC may be identified through the distinct clinical characteristics: symptomatic and numerous leioymyomas at young age, and morphologic features of FH-mutant leiomyomas, aided by Bcl-2 and CD34 immunohistochemistry. Further, distinguishing individuals with a germline FH mutation enables proper genetic counseling and regular renal monitoring.
    Keywords:  Bcl-2; CD34; HLRCC; fumarate hydratase; hereditary leiomyomatosis and renal cell cancer; uterine leiomyoma
    DOI:  https://doi.org/10.1111/aogs.14248
  9. Blood Adv. 2021 Sep 14. 5(17): 3373-3376
    Germline variants in DNA repair genes, including BRCA1/2, may cause familial myeloproliferative neoplasms.
    Miriam Elbracht, Robert Meyer, Kim Kricheldorf, Deniz Gezer, Eggermann Thomas, Beate Betz, Ingo Kurth, Lino L Teichmann, Tim H Brümmendorf, Ulrich Germing, Susanne Isfort, Steffen Koschmieder.
      The molecular causes of myeloproliferative neoplasms (MPNs) have not yet been fully elucidated. Approximately 7% to 8% of the patients carry predisposing genetic germline variants that lead to driver mutations, which enhance JAK-STAT signaling. To identify additional predisposing genetic germline variants, we performed whole-exome sequencing in 5 families, each with parent-child or sibling pairs affected by MPNs and carrying the somatic JAK2 V617F mutation. In 4 families, we detected rare germline variants in known tumor predisposition genes of the DNA repair pathway, including the highly penetrant BRCA1 and BRCA2 genes. The identification of an underlying hereditary tumor predisposition is of major relevance for the individual patients as well as for their families in the context of therapeutic options and preventive care. Two patients with essential thrombocythemia or polycythemia vera experienced progression to acute myeloid leukemia, which may suggest a high risk of leukemic transformation in these familial MPNs. Our study demonstrates the relevance of genetic germline diagnostics in elucidating the causes of MPNs and suggests novel therapeutic options (eg, PARP inhibitors) in MPNs. Furthermore, we uncover a broader tumor spectrum upon the detection of a germline mutation in genes of the DNA repair pathway.
    DOI:  https://doi.org/10.1182/bloodadvances.2021004811
  10. J Mol Diagn. 2021 Aug 25. pii: S1525-1578(21)00260-9. [Epub ahead of print]
    Paired somatic-germline testing of 15 polyposis and colorectal cancer-predisposing genes highlights the role of APC mosaicism in de novo familial adenomatous polyposis.
    Paula Rofes, Sara González, Matilde Navarro, José Marcos Moreno-Cabrera, Ares Solanes, Esther Darder, Estela Carrasco, Sílvia Iglesias, Mónica Salinas, Carolina Gómez, Àngela Velasco, Noemí Tuset, Mar Varela, Gemma Llort, Teresa Ramon Y Cajal, Èlia Grau, Núria Dueñas, Napoleón de la Ossa Merlano, Xavier Matías-Guiu, Bárbara Rivera, Judith Balmaña, Marta Pineda, Joan Brunet, Gabriel Capellá, Jesús Del Valle, Conxi Lázaro.
      Familial adenomatous polyposis (FAP) is an autosomal dominant syndrome responsible for 1% of colorectal cancers. Up to 90% of classical FAP are caused by inactivating mutations in APC, and mosaicism has been previously reported in 20% of de novo cases, usually linked to milder phenotypic manifestations. To explore the prevalence of mosaicism in 11 unsolved cases of classical FAP and to evaluate the diagnostic yield of somatic testing. Paired samples of colorectal polyps, tumors and/or mucosa were analyzed using a custom NGS panel targeting 15 polyposis and colorectal cancer-predisposing genes. Whenever possible, the extension of mosaicism to blood or sperm was also examined. Out of 11 patients with classical adenomatous polyposis, a mosaic pathogenic variant in APC was identified in seven (64%). No other altered genes were identified. In 2/7 (29%) mosaicism was found restricted to colonic tissues, while in 5/7 (71%) it was extended to the blood. Germline affectation was confirmed in one patient. We report the first analysis at a somatic level of 15 genes associated with colorectal cancer susceptibility, which highlights the role of APC mosaicism in classical FAP etiology. The results further reinforce the importance of testing target tissues when blood test results are negative.
    DOI:  https://doi.org/10.1016/j.jmoldx.2021.07.024
  11. BMC Cancer. 2021 Aug 30. 21(1): 975
    Genetic predisposition to male breast cancer in Poland.
    Marek Szwiec, Joanna Tomiczek-Szwiec, Wojciech Kluźniak, Dominika Wokołorczyk, Karolina Osowiecka, Robert Sibilski, Małgorzata Wachowiak, Jacek Gronwald, Helena Gronwald, Jan Lubiński, Cezary Cybulski, Steven A Narod, Tomasz Huzarski.
      BACKGROUND: Breast cancer in men accounts for fewer than 1 % of all breast cancer cases diagnosed in men and women. Genes which predispose to male breast cancer include BRCA1 and BRCA2. The role of other genes is less clear. In Poland, 20 founder mutations in BRCA1, BRCA2, CHEK2, PALB2, NBN, RECQL are responsible for the majority of hereditary breast cancer cases in women, but the utility this genes panel has not been tested in men.METHODS: We estimated the prevalence of 20 alleles in six genes (BRCA1, BRCA2, CHEK2, PALB2, NBN, RECQL) in 165 Polish male breast cancer patients. We compared the frequency of selected variants in male breast cancer cases and controls.
    RESULTS: One of the 20 mutations was seen in 22 of 165 cases (13.3%). Only one BRCA1 mutation and two BRCA2 mutations were found. We observed statistically significant associations for PALB2 and CHEK2 truncating mutations. A PALB2 mutation was detected in four cases (OR = 11.66; p < 0.001). A CHEK2 truncating mutation was detected in five cases (OR = 2.93;p = 0.02).
    CONCLUSION: In conclusion, we recommend that a molecular test for BRCA1, BRCA2, PALB2 and CHEK2 recurrent mutations should be offered to male breast cancer patients in Poland.
    Keywords:  BRCA1; BRCA2; CHEK2; Male breast cancer; Mutation; NBN; PALB2; RECQL
    DOI:  https://doi.org/10.1186/s12885-021-08718-3
  12. Breast Cancer. 2021 Aug 31.
    Prevalence of mutations in BRCA and homologous recombination repair genes and real-world standard of care of Asian patients with HER2-negative metastatic breast cancer starting first-line systemic cytotoxic chemotherapy: subgroup analysis of the global BREAKOUT study.
    Su-Jin Koh, Shozo Ohsumi, Masato Takahashi, Eisuke Fukuma, Kyung Hae Jung, Takanori Ishida, Ming-Shen Dai, Chuan-Hsun Chang, Tapashi Dalvi, Graham Walker, James Bennett, Joyce O'Shaughnessy, Judith Balmaña.
      BACKGROUND: The multinational BREAKOUT study (NCT03078036) sought to determine the prevalence of germline BRCA1/2 (gBRCA1/2) and somatic BRCA1/2 (sBRCA1/2) mutations and mutations in other homologous recombination repair (HRR) genes in women with HER2-negative metastatic breast cancer (MBC) starting first-line chemotherapy.METHODS: Genetic testing for gBRCA, sBRCA, and HRR gene mutations was performed in patients who started first-line chemotherapy for MBC in the last 90 days (341 patients across 14 countries) who were not selected based on risk factors for gBRCA mutations. We report data from the Asian cohort, which included patients in Japan (7 sites), South Korea (10 sites), and Taiwan (8 sites).
    RESULTS: Of 116 patients screened, 104 patients were enrolled in the Asian cohort. The median age was 53.0 (range 25-87) years. gBRCA1/2, gBRCA1, and gBRCA2 mutations were detected in 10.6% (11/104), 5.8% (6/104), and 4.8% (5/104) of patients, respectively; none had mutations in both gBRCA1 and gBRCA2. gBRCA1/2 mutations were detected in 10.0% (6/60) and 11.6% (5/43) of patients with hormone receptor-positive and triple-negative MBC, respectively. HRR gene mutations were tested in 48 patients without gBRCA mutations, and 5 (10.4%) had at least one HRR mutation in sBRCA, ATM, PALB2, and CHEK2.
    CONCLUSION: We report for the first time the prevalence of gBRCA and HRR mutations in an Asian cohort of patients with HER2-negative MBC. Our results suggest that BRCA mutation testing is valuable to determine appropriate treatment options for patients with hormone receptor-positive or triple-negative MBC.
    STUDY REGISTRATION: NCT03078036.
    Keywords:  BRCA; Germline mutations; HER2-negative metastatic breast cancer; Homologous recombination repair; Somatic mutations
    DOI:  https://doi.org/10.1007/s12282-021-01283-4
  13. Int J Cancer. 2021 Sep 01.
    Adenoma and colorectal cancer risks in Lynch syndrome, Lynch-like syndrome, and familial colorectal cancer type X.
    Karolin Bucksch, Silke Zachariae, Aysel Ahadova, Stefan Aretz, Reinhard Büttner, Heike Görgens, Elke Holinski-Feder, Robert Hüneburg, Matthias Kloor, Magnus von Knebel Doeberitz, Swetlana Ladigan-Badura, Gabriela Moeslein, Monika Morak, Jacob Nattermann, Huu Phuc Nguyen, Claudia Perne, Silke Redler, Ariane Schmetz, Verena Steinke-Lange, Harald Surowy, Deepak B Vangala, Jürgen Weitz, Markus Loeffler, Christoph Engel, .
      Lynch syndrome (LS), Lynch-like syndrome (LLS), and familial colorectal cancer type X (FCCX) are different entities of familial cancer predisposition leading to an increased risk of colorectal cancer (CRC). The aim of this prospective study was to characterize and to compare the risks for adenoma and CRC in these three risk groups. Data was taken from the registry of the German Consortium for Familial Intestinal Cancer. Patients were prospectively followed up in an intensified colonoscopic surveillance programme that included annual examinations. Cumulative risks for adenoma and CRC were calculated separately for LS, LLS, and FCCX, and then for males and females. Multivariate Cox regression was used to analyse the independent contributions of risk group, mismatch repair gene (within LS), sex, and previous adenoma. The study population comprised 1448 individuals (103 FCCX, 481 LLS and 864 LS). The risks were similar for colorectal adenomas, but different for first and metachronous CRC between the three risk groups. CRC risk was highest in LS, followed by LLS, and lowest in FCCX. Male sex and a prevalent adenoma in the index colonoscopy were associated with a higher risk for incident adenoma and CRC. In patients with LS, CRC risks were particularly higher in female MSH2 than MLH1 carriers. This study may support the development of risk-adapted surveillance policies in LS, LLS and FCCX. This article is protected by copyright. All rights reserved.
    Keywords:  Cancer risk; Familial colorectal cancer type X; Lynch syndrome; Lynch-like syndrome; Prospective study
    DOI:  https://doi.org/10.1002/ijc.33790
  14. Blood. 2021 Sep 01. pii: blood.2021012781. [Epub ahead of print]
    Association of Unbalanced Translocation der(1;7) with Germline GATA2 Mutations.
    Emilia J Kozyra, Gudrun Gohring, Dennis D Hickstein, Katherine R Calvo, Courtney D DiNardo, Michael Dworzak, Valerie de Haas, Jan Stary, Henrik Hasle, Akiko Shimamura, Mark D Fleming, Hiroto Inaba, Sara Lewis, Amy P Hsu, Steven M Holland, Danielle E Arnold, Cristina Mecucci, Sioban B Keel, Alison A Bertuch, Kiran Tawana, Shlomit Barzilai-Birenboim, Shinsuke Hirabayashi, Masahiro Onozawa, Shaohua Lei, Helena Alaiz, Hajnalka Andrikovics, David Betts, H Berna Beverloo, Jochen Buechner, Martin Čermák, Jose Cervera, Olga Haus, Kirsi Jahnukainen, Kalliopi Manola, Karin Nebral, Francesco Pasquali, Joelle Tchinda, Dominik Turkiewicz, Nadine Van Roy, Zuzana Zemanova, Victor B Pastor, Brigitte Strahm, Peter Nöllke, Charlotte M Niemeyer, Brigitte Schlegelberger, Ayami Yoshimi, Marcin W Wlodarski.
      
    DOI:  https://doi.org/10.1182/blood.2021012781
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