bims-lifras Biomed News
on Li-Fraumeni syndrome
Issue of 2021‒10‒31
ten papers selected by
Joanna Zawacka-Pankau
Karolinska Institutet


  1. JAMA Oncol. 2021 Oct 28.
      Importance: Li-Fraumeni syndrome is a cancer predisposition syndrome that is associated with a high, lifelong risk of a broad spectrum of cancers that is caused by pathogenic TP53 germline variants. A definition that reflects the broad phenotypic spectrum that has evolved since the gene discovery is lacking, and mechanisms leading to phenotypic differences remain largely unknown.Objective: To define the phenotypic spectrum of Li-Fraumeni syndrome and conduct phenotype-genotype associations across the phenotypic spectrum.
    Design, Setting, and Participants: We analyzed and classified the germline variant data set of the International Agency for Research on Cancer TP53 database that contains data on a cohort of 3034 persons from 1282 families reported in the scientific literature since 1990. We defined the term Li-Fraumeni spectrum to encompass (1) phenotypic Li-Fraumeni syndrome, defined by the absence of a pathogenic/likely pathogenic TP53 variant in persons/families meeting clinical Li-Fraumeni syndrome criteria; (2) Li-Fraumeni syndrome, defined by the presence of a pathogenic/likely pathogenic TP53 variant in persons/families meeting Li-Fraumeni syndrome testing criteria; (3) attenuated Li-Fraumeni syndrome, defined by the presence of a pathogenic/likely pathogenic TP53 variant in a person/family with cancer who does not meet Li-Fraumeni syndrome testing criteria; and (4) incidental Li-Fraumeni syndrome, defined by the presence of a pathogenic/likely pathogenic TP53 variant in a person/family without a history of cancer. Data analysis occurred from November 2020 to March 2021.
    Main Outcomes and Measures: Differences in variant distribution and cancer characteristics in patients with a germline TP53 variant who met vs did not meet Li-Fraumeni syndrome testing criteria.
    Results: Tumor spectra showed significant differences, with more early adrenal (n = 166, 6.5% vs n = 0), brain (n = 360, 14.17% vs n = 57, 7.46%), connective tissue (n = 303, 11.92% vs n = 56, 7.33%), and bone tumors (n = 279, 10.98% vs n = 3, 0.39%) in patients who met Li-Fraumeni syndrome genetic testing criteria (n = 2139). Carriers who did not meet Li-Fraumeni syndrome genetic testing criteria (n = 678) had more breast (n = 292, 38.22% vs n = 700, 27.55%) and other cancers, 45% of them occurring after age 45 years. Hotspot variants were present in both groups. Several variants were exclusively found in patients with Li-Fraumeni syndrome, while others where exclusively found in patients with attenuated Li-Fraumeni syndrome. In patients who met Li-Fraumeni syndrome genetic testing criteria, most TP53 variants were classified as pathogenic/likely pathogenic (1757 of 2139, 82.2%), whereas 40.4% (404 of 678) of TP53 variants identified in patients who did not meet the Li-Fraumeni syndrome genetic testing criteria were classified as variants of uncertain significance, conflicting results, likely benign, benign, or unknown.
    Conclusions and Relevance: The findings of this cohort study suggest that this new classification, Li-Fraumeni spectrum, is a step toward understanding the factors that lead to phenotypic differences and may serve as a model for other cancer predisposition syndromes.
    DOI:  https://doi.org/10.1001/jamaoncol.2021.4398
  2. Eur Urol. 2021 Oct 25. pii: S0302-2838(21)02059-5. [Epub ahead of print]
      BACKGROUND: Identification of germline mutations in DNA repair genes has significant implications for the personalized treatment of individuals with prostate cancer (PrCa).OBJECTIVE: To determine DNA repair genes associated with localized PrCa in a diverse academic biobank and to determine genetic testing burden.
    DESIGN, SETTING, AND PARTICIPANTS: A cross-sectional study of 2391 localized PrCa patients was carried out.
    OUTCOME MEASUREMENTS AND STATISTICAL ANALYSIS: Genetic ancestry and mutation rates (excluding somatic interference) in 17 DNA repair genes were determined in 1588 localized PrCa patients and 3273 cancer-free males. Burden testing within individuals of genetically determined European (EUR) and African (AFR) ancestry was performed between biobank PrCa cases and cancer-free biobank and gnomAD males.
    RESULTS AND LIMITATIONS: AFR individuals with localized PrCa had lower DNA repair gene mutation rates than EUR individuals (1.4% vs 4.0%, p = 0.02). Mutation rates in localized PrCa patients were similar to those in biobank and gnomAD controls (EUR: 4.0% vs 2.8%, p = 0.15, vs 3.1%, p = 0.04; AFR: 1.4% vs 1.8%, p = 0.8, vs 2.1%, p = 0.5). Gene-based rare variant association testing revealed that only BRCA2 mutations were significantly enriched compared with gnomAD controls of EUR ancestry (1.0% vs 0.28%, p = 0.03). Of the participants, 21% and 11% met high-risk and very-high-risk criteria; of them, 3.7% and 6.2% had any germline genetic mutation and 1.0% and 2.5% had a BRCA2 mutation, respectively. Limitations of this study include an analysis of a relatively small, single-institution cohort.
    CONCLUSIONS: DNA repair gene germline mutation rates are low in an academic biobank cohort of localized PrCa patients, particularly among individuals of AFR genetic ancestry. Mutation rates in genes with published evidence of association with PrCa exceed 2.5% only in high-risk, very-high-risk localized, and node-positive PrCa patients. These findings highlight the importance of risk stratification in localized PrCa patients to identify appropriate patients for germline genetic testing.
    PATIENT SUMMARY: In the majority of patients who develop localized prostate cancer, germline genetic testing is unlikely to reveal an inherited DNA repair mutation, regardless of race. High-risk features increase the possibility of a germline DNA repair mutation.
    Keywords:  BRCA2; Genetic association study; Germline genetics; Inherited genes; Localized prostate cancer
    DOI:  https://doi.org/10.1016/j.eururo.2021.09.029
  3. Pancreas. 2021 Sep 01. 50(8): 1123-1130
      ABSTRACT: CDKN2A is cell cycle negative regulator, and the role of CDKN2A in the development of pancreatic ductal adenocarcinoma, which continues to be a lethal cancer, is well-established. Somatic loss of CDKN2A is considered one of the major drivers of pancreatic tumorigenesis. CDKN2A gene is one of the pancreatic cancer susceptibility gene; in addition to melanoma, pathogenic germline CDKN2A variants have been identified in up to 3.3% patients with pancreatic ductal adenocarcinoma depending on family history of disease. Carriers of a known pathogenic germline CDKN2A variant have up to a 12.3-fold increased risk of developing pancreatic cancer. Recently, several studies have demonstrated the benefit of clinical surveillance in patients with pathogenic germline CDKN2A variants. Therefore, identification of patients with a pathogenic germline CDKN2A variant is important for screening of at-risk relatives for pancreatic cancer. It has the potential to lead to the detection of early, potentially curable pancreatic cancer and precursor neoplasms, and reduce mortality. Furthermore, patients with a germline pathogenic CDKN2A variant and somatic loss of CDKN2A may benefit in the future from treatment with targeted therapies, such as a CDK4/6 inhibitor.
    DOI:  https://doi.org/10.1097/MPA.0000000000001888
  4. Hered Cancer Clin Pract. 2021 Oct 28. 19(1): 46
      Multiple primary cancers, defined as three or more primary tumours, are rare, and there are few genetic studies concerning them. There is a need for increased knowledge on the heritability of multiple primary cancers and genotype-phenotype correlations. We have performed whole-genome/exome sequencing (WGS/WES) in ten individuals with three or more primary tumours, with no previous findings on standard clinical genetic investigations. In one individual with a clinical diagnosis of MEN1, a likely pathogenic cryptic splice site variant was detected in the MEN1 gene. The variant (c.654C > A) is synonymous but we showed in a cDNA analysis that it affects splicing and leads to a frameshift, with the theoretical new amino acid sequence p.(Gly219Glufs*13). In one individual with metachronous colorectal cancers, ovarian cancer, endometrial cancer and chronic lymphocytic leukaemia, we found a likely pathogenic variant in the MLH1 gene (c.27G > A), and two risk factor variants in the genes CHEK2 and HOXB13. The MLH1 variant is synonymous but has previously been shown to be associated to constitutional low-grade hypermethylation of the MLH1 promoter, and segregates with disease in families with colorectal and endometrial cancer. No pathogenic single nucleotide or structural variants were detected in the remaining eight individuals in the study. The pathogenic variants found by WGS/WES were in genes already sequenced by Sanger sequencing and WES in the clinic, without any findings. We conclude that, in individuals with an unequivocal clinical diagnosis of a specific hereditary cancer syndrome, where standard clinical testing failed to detect a causative variant, re-analysis may lead to a diagnosis.
    Keywords:  Hereditary cancer; MEN1; MLH1; Multiple primary; Re-analysis; WES; WGS
    DOI:  https://doi.org/10.1186/s13053-021-00203-z
  5. Int J Radiat Oncol Biol Phys. 2021 Nov 01. pii: S0360-3016(21)01650-3. [Epub ahead of print]111(3S): e227
      PURPOSE/OBJECTIVE(S): There is mixed and limited scientific evidence regarding radiotherapy (RT) tolerance in carriers of a pathogenic, germline ATM variant. The ASTRO-ASCO-SSO guidelines on management of hereditary breast cancer suggest offering RT to these patients if clinically indicated. We investigate RT toxicity for carriers of either a pathogenic ATM variant, or variant of unknown significance (VUS), in ATM.MATERIALS/METHODS: Patients with a breast cancer history who had hereditary genetic testing and were found to carry either a pathogenic variant or VUS in ATM were identified. For those who received RT at our institution, toxicity metrics were recorded including dermatitis (scored per CTCAE version 4.0), moist desquamation, and cosmetic outcome (scored per Harvard scale). Fisher's exact test for count data was performed to compare toxicity between the two cohorts. Wilcoxon rank-sum testing was performed to assess for differences in cohort patient characteristics.
    RESULTS: Forty-four carriers of a pathogenic ATM variant, and 163 carriers of an ATM VUS, were identified. Fifteen pathogenic and 56 VUS patients, respectively, received RT at our institution and had available toxicity records. The cohorts did not statistically differ in race, medical comorbidities, clinical or pathologic T-stage, hormone receptor status, receipt of chemotherapy, fractionation schedule, or receipt of a boost. No patients had a known collagen vascular disease. 77% of patients (55/71) had breast conservation. 62% received whole breast RT, 7% received chest wall RT, 4.2% received partial breast RT, and 26.8% received whole breast or chest wall RT with regional nodal RT. 58% received conventionally-fractionated RT, and 38% received hypofractionated RT. Median toxicity follow up was 11.6 months. 29% (4/15) of pathogenic carriers and 26.4% (14/56) of VUS carriers developed moist desquamation (P = 0.7). The rates of grade 2+ acute dermatitis were 71% in pathogenic carriers and 57% in VUS carriers (P = 0.4). 100% of pathogenic carriers and 91% of VUS carriers had a good/excellent cosmetic outcome at first follow up (P > 0.9). No patients with a pathogenic variant had a fair or poor cosmetic outcome at last follow up.
    CONCLUSION: RT is well tolerated in carriers of a pathogenic ATM variant, with rates of grade 2+ dermatitis and moist desquamation comparable to a matched VUS cohort. High rates of good or excellent cosmetic outcome were seen following treatment. Further analyses including an ATM wild type cohort and continued detailed toxicity documentation/analysis is on-going to elucidate longer term morbidity.
    DOI:  https://doi.org/10.1016/j.ijrobp.2021.07.780
  6. Gynecol Oncol. 2021 Oct 23. pii: S0090-8258(21)01516-X. [Epub ahead of print]
      BACKGROUND: Histology restricted genetic predisposition testing of ovarian carcinoma patients is a topic of debate as the prevalence of BRCA1/2 pathogenic variants (PVs) in various histological subtypes is ambiguous. Our primary aim was to investigate the proportion of germline BRCA1/2 PVs per histological subtype. Additionally, we evaluated (i) proportion of somatic BRCA1/2 PVs and (ii) proportion of germline PVs in other ovarian carcinoma risk genes.METHODS: PubMed, EMBASE and Web of Science were systematically searched and we included all studies reporting germline BRCA1/2 PVs per histological subtype. Pooled proportions were calculated using a random-effects meta-analysis model. Subsets of studies were used for secondary analyses.
    RESULTS: Twenty-eight studies were identified. The overall estimated proportion of germline BRCA1/2 PVs was 16.8% (95% CI 14.6 to 19.2). Presence differed substantially among patients with varying histological subtypes of OC; proportions being highest in high-grade serous (22.2%, 95% CI 19.6 to 25.0) and lowest in clear cell (3.0%, 95% CI 1.6 to 5.6) and mucinous (2.5%, 95% CI 0.6 to 9.6) carcinomas. Somatic BRCA1/2 PVs were present with total estimated proportion of 6.0% (95% CI 5.0 to 7.3), based on a smaller subset of studies. Germline PVs in BRIP1, RAD51C, RAD51D, PALB2, and ATM were present in approximately 3%, based on a subset of nine studies.
    CONCLUSION: Germline BRCA1/2 PVs are most frequently identified in high-grade serous ovarian carcinoma patients, but are also detected in patients having ovarian carcinomas of other histological subtypes. Limiting genetic predisposition testing to high-grade serous ovarian carcinoma patients will likely be insufficient to identify all patients with a germline PV.
    Keywords:  BRCA; Epithelial ovarian cancer; Genetic testing; Histology; Probability
    DOI:  https://doi.org/10.1016/j.ygyno.2021.10.072
  7. Cancer Genet. 2021 Oct 04. pii: S2210-7762(21)00212-X. [Epub ahead of print]258-259 101-109
      Fanconi anemia (FA) is the most common inherited bone marrow failure syndrome and a cancer predisposition disorder. Cancers in FA include acute leukemia and solid tumors; the most frequent solid tumor is head and neck squamous cell carcinoma. FA is a primarily autosomal recessive disorder. Several of the genes in which biallelic pathogenic variants cause FA are also autosomal monoallelic cancer predisposition genes e.g. FANCD1 (BRCA2) and FANCN (PALB2). We observed that patients with FA due to biallelic or homozygous pathogenic variants in FANCD1 and FANCN have a unique cancer association. We curated published cases plus our NCI cohort cases, including 71 patients in the FANCD1 group (94 cancers and 69 variants) and 16 patients in the FANCN group (23 cancers and 20 variants). Only patients in FANCD1 and FANCN groups had one or more of these tumors: brain tumors (primarily medulloblastoma), Wilms tumor and neuroblastoma; this is a genotype-specific cancer combination of tumors of embryonal origin. Acute leukemias, seen in all FA genotypes, also occurred in FANCD1 and FANCN group patients at young ages. In silico predictions of pathogenicity for FANCD1 variants were compared with results from a mouse embryonic stem cell-based functional assay. Patients with two null FANCD1 variants did not have an increased frequency of cancer nor earlier onset of cancer compared with those with hypomorphic variants. Patients with FA and these specific cancers should consider genetic testing focused on FANCD1 and FANCN, and patients with these genotypes may consider ongoing surveillance for these specific cancers.
    Keywords:  Brain tumor; Cancer predisposition; Fanconi anemia; Genetic testing; Neuroblastoma; Wilms tumor
    DOI:  https://doi.org/10.1016/j.cancergen.2021.10.001
  8. J Hepatobiliary Pancreat Sci. 2021 Oct 24.
      BACKGROUND/PURPOSE: Pancreatic and biliary tract cancers are one of the Lynch syndrome-associated malignancies. There are few reports describing the patients' background and clinical characteristics.METHODS: We retrospectively reviewed the medical records of patients with Lynch syndrome-associated pancreatic or biliary tract malignant tumors at National Cancer Center Hospital between March 1992 and October 2019.
    RESULTS: Fourteen patients were included. They had a history of multiple cancers and a family history of cancer. For the six patients with pancreatic malignant tumor, the median age was 63 years. The primary tumor site of 5/6 patients with pancreatic cancer was the body or tail. Only one patient had pancreatic head cancer. The median overall survival was 68 (range, 17-198) months. For the eight patients with biliary tract malignant tumor, the median age was 65.5 years. The primary tumor site of 5/8 patients was the intrahepatic bile duct, whereas the primary site of 2/8 was the hilar bile duct. The median overall survival was 62 (range, 3-183) months.
    CONCLUSIONS: This study brought out several observations on tumor location, late development, and favorable long-term outcomes. Additional studies are needed to identify the characteristics.
    Keywords:  Biliary tract cancer; Hereditary cancer; History of cancer; Lynch syndrome; Pancreatic cancer
    DOI:  https://doi.org/10.1002/jhbp.1063
  9. Int J Hematol. 2021 Oct 26.
      Shwachman-Diamond syndrome (SDS) is an autosomal recessive inherited disorder characterized by bone marrow failure, exocrine pancreatic dysfunction, and skeletal abnormalities. SDS is typically caused by a pathogenic mutation in the Shwachman-Bodian-Diamond Syndrome (SBDS) gene. Patients with SDS have an increased risk of developing acute myeloid leukemia (AML) and myelodysplastic syndromes. We identified germline biallelic SBDS mutations (p.K62X and p.I167M) in a 50-year-old AML patient who had never experienced the typical symptoms of SDS. The K62X mutation is one of the most common pathogenic mutations, whereas the significance of the I167M mutation was unclear. Based on cellular experiments, we concluded that the I167M mutation contributed to the development of AML, and chemotherapy including topoisomerase inhibitors, which induce DNA double-strand breaks, may have been toxic to this patient. Our experience indicates that some asymptomatic Shwachman-Bodian-Diamond syndrome mutations contribute to the development of leukemia, and that careful treatment selection may be warranted for patients harboring these mutations.
    Keywords:  Acute myeloid leukemia; DNA double-strand break repair; Shwachman–Diamond syndrome
    DOI:  https://doi.org/10.1007/s12185-021-03251-2
  10. Front Oncol. 2021 ;11 662055
      Mutated germline alleles in the DNA damage repair (DDR) genes "breast cancer gene 1" (BRCA1) and BRCA2 have originally been identified as major susceptibility genes in breast and ovarian cancers. With the establishment and approval of more cost-effective gene sequencing methods, germline and somatic BRCA mutations have been detected in several cancers. Since the approval of poly (ADP)-ribose polymerase inhibitors (PARPi) for BRCA-mutated cancers, BRCA mutations gained rising therapeutic implications. The impact and significance of BRCA mutations have been evaluated extensively in the last decades. Moreover, other genes involved in the DDR pathway, such as ATM, ATR, or CHK1, have emerged as potential new treatment targets, as inhibitors of these proteins are currently under clinical investigation. This review gives a concise overview on the emerging clinical implications of mutations in the DDR genes in gastrointestinal cancers with a focus on BRCA mutations.
    Keywords:  BRCA; DNA damage repair; PARP inhibitors (PARPi); gastrointenstinal cancer; molecular profiling; precision oncology
    DOI:  https://doi.org/10.3389/fonc.2021.662055