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Anemia de Fanconi
ORPHA:84CID-10 · D61.0CID-11 · 3A70.0DOENÇA RARA

A anemia de Fanconi (AF) é um distúrbio hereditário de reparo do DNA caracterizado por pancitopenia progressiva com insuficiência da medula óssea, malformações congênitas variáveis ​​e predisposição para desenvolver tumores hematológicos ou sólidos.

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Introdução

O que você precisa saber de cara

📋

A anemia de Fanconi (AF) é um distúrbio hereditário de reparo do DNA caracterizado por pancitopenia progressiva com insuficiência da medula óssea, malformações congênitas variáveis ​​e predisposição para desenvolver tumores hematológicos ou sólidos.

Pesquisas ativas
19 ensaios
147 total registrados no ClinicalTrials.gov
Publicações científicas
3.990 artigos
Último publicado: 2026 Apr 15
Medicamentos
2 registrados
FLUDARABINE PHOSPHATE, METFORMIN

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Escala de raridade

CLASSIFICAÇÃO ORPHANET · BRASIL 2024
1-9 / 100 000
Ultra-rara
<1/50k
Muito rara
1/20k
Rara
1/10k
Pouco freq.
1/5k
Incomum
1/2k
Prevalência
3.3
Specific population
Início
Childhood
🏥
SUS: Sem cobertura SUSScore: 0%
CID-10: D61.0
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Sinais e sintomas

O que aparece no corpo e com que frequência cada sintoma acontece

Partes do corpo afetadas

🦴
Ossos e articulações
28 sintomas
😀
Face
20 sintomas
🫘
Rins
18 sintomas
📏
Crescimento
15 sintomas
👁️
Olhos
14 sintomas
❤️
Coração
12 sintomas

+ 97 sintomas em outras categorias

Características mais comuns

90%prev.
Anormalidade do membro superior
Muito frequente (99-80%)
90%prev.
Aplasia/Hipoplasia do rádio
Muito frequente (99-80%)
90%prev.
Anormalidade do sangue e tecidos hematopoiéticos
Muito frequente (99-80%)
90%prev.
Anemia
Muito frequente (99-80%)
90%prev.
Baixa estatura
Muito frequente (99-80%)
90%prev.
Morfologia anormal do polegar
Muito frequente (99-80%)
251sintomas
Muito frequente (13)
Frequente (10)
Ocasional (83)
Sem dados (145)

Os sintomas variam de pessoa para pessoa. Abaixo estão as 251 características clínicas mais associadas, ordenadas por frequência.

Anormalidade do membro superiorAbnormality of the upper limb
Muito frequente (99-80%)90%
Aplasia/Hipoplasia do rádioAplasia/Hypoplasia of the radius
Muito frequente (99-80%)90%
Anormalidade do sangue e tecidos hematopoiéticosAbnormality of blood and blood-forming tissues
Muito frequente (99-80%)90%
Anemia
Muito frequente (99-80%)90%
Baixa estaturaShort stature
Muito frequente (99-80%)90%

Linha do tempo da pesquisa

Publicações por ano — veja quando o interesse científico cresceu
Anos de pesquisa1desde 2026
Total histórico3.990PubMed
Últimos 10 anos200publicações
Pico2025128 papers
Linha do tempo
2026Hoje · 2026🧪 1975Primeiro ensaio clínico📈 2025Ano de pico
Publicações por ano (últimos 10 anos)

Encontrou um erro ou informação desatualizada? Sugira uma correção →

Genética e causas

O que está alterado no DNA e como passa nas famílias

Genes associados

23 genes identificados com associação a esta condição. Padrão de herança: Autosomal recessive, X-linked recessive.

BRIP1Fanconi anemia group J proteinDisease-causing germline mutation(s) inTolerante
FUNÇÃO

DNA-dependent ATPase and 5'-3' DNA helicase required for the maintenance of chromosomal stability (PubMed:11301010, PubMed:14983014, PubMed:16116421, PubMed:16153896, PubMed:17596542, PubMed:36608669). Acts late in the Fanconi anemia pathway, after FANCD2 ubiquitination (PubMed:14983014, PubMed:16153896). Involved in the repair of DNA double-strand breaks by homologous recombination in a manner that depends on its association with BRCA1 (PubMed:14983014, PubMed:16153896). Involved in the repair

LOCALIZAÇÃO

NucleusCytoplasm

VIAS BIOLÓGICAS (1)
Cytosolic iron-sulfur cluster assembly
MECANISMO DE DOENÇA

Breast cancer

A common malignancy originating from breast epithelial tissue. Breast neoplasms can be distinguished by their histologic pattern. Invasive ductal carcinoma is by far the most common type. Breast cancer is etiologically and genetically heterogeneous. Important genetic factors have been indicated by familial occurrence and bilateral involvement. Mutations at more than one locus can be involved in different families or even in the same case.

OUTRAS DOENÇAS (4)
Fanconi anemia complementation group JFanconi anemiahereditary breast ovarian cancer syndromehereditary breast carcinoma
HGNC:20473UniProt:Q9BX63
FAAP100Fanconi anemia core complex-associated protein 100Disease-causing germline mutation(s) (loss of function) inTolerante
FUNÇÃO

Plays a role in Fanconi anemia-associated DNA damage response network. Regulates FANCD2 monoubiquitination and the stability of the FA core complex. Induces chromosomal instability as well as hypersensitivity to DNA cross-linking agents, when repressed

LOCALIZAÇÃO

Nucleus

VIAS BIOLÓGICAS (1)
PKR-mediated signaling
MECANISMO DE DOENÇA

Fanconi anemia, complementation group X

A form of Fanconi anemia, a disorder affecting all bone marrow elements and resulting in anemia, leukopenia and thrombopenia. It is associated with cardiac, renal and limb malformations, dermal pigmentary changes, and a predisposition to the development of malignancies. At the cellular level it is associated with hypersensitivity to DNA-damaging agents, chromosomal instability (increased chromosome breakage) and defective DNA repair. FANCX is an autosomal recessive form characterized by multiple pregnancy losses and offspring presenting with severe developmental and hematologic abnormalities leading to death in utero or in early life.

EXPRESSÃO TECIDUAL(Ubíquo)
Cerebelo
59.1 TPM
Cérebro - Hemisfério cerebelar
57.9 TPM
Baço
43.1 TPM
Tireoide
35.6 TPM
Fallopian Tube
30.2 TPM
OUTRAS DOENÇAS (1)
Fanconi anemia
HGNC:26171UniProt:Q0VG06
FANCLE3 ubiquitin-protein ligase FANCLDisease-causing germline mutation(s) inTolerante
FUNÇÃO

Ubiquitin ligase protein that mediates monoubiquitination of FANCD2 in the presence of UBE2T, a key step in the DNA damage pathway (PubMed:12973351, PubMed:16916645, PubMed:17938197, PubMed:19111657, PubMed:24389026). Also mediates monoubiquitination of FANCI (PubMed:19589784). May stimulate the ubiquitin release from UBE2W. May be required for proper primordial germ cell proliferation in the embryonic stage, whereas it is probably not needed for spermatogonial proliferation after birth

LOCALIZAÇÃO

CytoplasmNucleus

VIAS BIOLÓGICAS (1)
PKR-mediated signaling
MECANISMO DE DOENÇA

Fanconi anemia complementation group L

A disorder affecting all bone marrow elements and resulting in anemia, leukopenia and thrombopenia. It is associated with cardiac, renal and limb malformations, dermal pigmentary changes, and a predisposition to the development of malignancies. At the cellular level it is associated with hypersensitivity to DNA-damaging agents, chromosomal instability (increased chromosome breakage) and defective DNA repair.

EXPRESSÃO TECIDUAL(Ubíquo)
Pituitária
51.5 TPM
Linfócitos
44.1 TPM
Glândula adrenal
32.0 TPM
Testículo
28.2 TPM
Útero
27.3 TPM
OUTRAS DOENÇAS (2)
Fanconi anemia complementation group LFanconi anemia
HGNC:20748UniProt:Q9NW38
FANCBFanconi anemia group B proteinDisease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

DNA repair protein required for FANCD2 ubiquitination

LOCALIZAÇÃO

Nucleus

VIAS BIOLÓGICAS (1)
PKR-mediated signaling
MECANISMO DE DOENÇA

Fanconi anemia complementation group B

A disorder affecting all bone marrow elements and resulting in anemia, leukopenia and thrombopenia. It is associated with cardiac, renal and limb malformations, dermal pigmentary changes, and a predisposition to the development of malignancies. At the cellular level it is associated with hypersensitivity to DNA-damaging agents, chromosomal instability (increased chromosome breakage) and defective DNA repair. Some severe FANCB cases manifest features of VACTERL syndrome with hydrocephalus.

EXPRESSÃO TECIDUAL(Tecido-específico)
Linfócitos
5.5 TPM
Fibroblastos
3.2 TPM
Nervo tibial
1.5 TPM
Baço
0.8 TPM
Esôfago - Mucosa
0.7 TPM
OUTRAS DOENÇAS (3)
Fanconi anemia complementation group BVACTERL with hydrocephalusFanconi anemia
HGNC:3583UniProt:Q8NB91
FANCEFanconi anemia group E proteinDisease-causing germline mutation(s) inTolerante
FUNÇÃO

As part of the Fanconi anemia (FA) complex functions in DNA cross-links repair. Required for the nuclear accumulation of FANCC and provides a critical bridge between the FA complex and FANCD2

LOCALIZAÇÃO

Nucleus

VIAS BIOLÓGICAS (1)
PKR-mediated signaling
MECANISMO DE DOENÇA

Fanconi anemia complementation group E

A disorder affecting all bone marrow elements and resulting in anemia, leukopenia and thrombopenia. It is associated with cardiac, renal and limb malformations, dermal pigmentary changes, and a predisposition to the development of malignancies. At the cellular level it is associated with hypersensitivity to DNA-damaging agents, chromosomal instability (increased chromosome breakage) and defective DNA repair.

EXPRESSÃO TECIDUAL(Ubíquo)
Skin Sun Exposed Lower leg
24.3 TPM
Skin Not Sun Exposed Suprapubic
24.1 TPM
Testículo
22.8 TPM
Artéria tibial
21.1 TPM
Vagina
16.6 TPM
OUTRAS DOENÇAS (2)
Fanconi anemia complementation group EFanconi anemia
HGNC:3586UniProt:Q9HB96
FANCD2Fanconi anemia group D2 proteinDisease-causing germline mutation(s) inTolerante
FUNÇÃO

Required for maintenance of chromosomal stability (PubMed:11239453, PubMed:14517836). Promotes accurate and efficient pairing of homologs during meiosis (PubMed:14517836). Involved in the repair of DNA double-strand breaks, both by homologous recombination and single-strand annealing (PubMed:15671039, PubMed:15650050, PubMed:30335751, PubMed:36385258). The FANCI-FANCD2 complex binds and scans double-stranded DNA (dsDNA) for DNA damage; this complex stalls at DNA junctions between double-stranded

LOCALIZAÇÃO

Nucleus

VIAS BIOLÓGICAS (2)
TP53 Regulates Transcription of DNA Repair GenesFanconi Anemia Pathway
MECANISMO DE DOENÇA

Fanconi anemia complementation group D2

A disorder affecting all bone marrow elements and resulting in anemia, leukopenia and thrombopenia. It is associated with cardiac, renal and limb malformations, dermal pigmentary changes, and a predisposition to the development of malignancies. At the cellular level it is associated with hypersensitivity to DNA-damaging agents, chromosomal instability (increased chromosome breakage) and defective DNA repair.

EXPRESSÃO TECIDUAL(Ubíquo)
Linfócitos
29.3 TPM
Testículo
22.2 TPM
Baço
7.5 TPM
Intestino delgado
4.5 TPM
Fibroblastos
4.1 TPM
OUTRAS DOENÇAS (2)
Fanconi anemia complementation group D2Fanconi anemia
HGNC:3585UniProt:Q9BXW9
RFWD3E3 ubiquitin-protein ligase RFWD3Disease-causing germline mutation(s) inTolerante
FUNÇÃO

E3 ubiquitin-protein ligase required for the repair of DNA interstrand cross-links (ICL) in response to DNA damage (PubMed:21504906, PubMed:21558276, PubMed:26474068, PubMed:28575657, PubMed:28575658, PubMed:33321094). Plays a key role in RPA-mediated DNA damage signaling and repair (PubMed:21504906, PubMed:21558276, PubMed:26474068, PubMed:28575657, PubMed:28575658, PubMed:28691929). Acts by mediating ubiquitination of the RPA complex (RPA1, RPA2 and RPA3 subunits) and RAD51 at stalled replicat

LOCALIZAÇÃO

NucleusNucleus, PML bodyCytoplasm

MECANISMO DE DOENÇA

Fanconi anemia, complementation group W

A form of Fanconi anemia, a disorder affecting all bone marrow elements and resulting in anemia, leukopenia and thrombopenia. It is associated with cardiac, renal and limb malformations, dermal pigmentary changes, and a predisposition to the development of malignancies. At the cellular level it is associated with hypersensitivity to DNA-damaging agents, chromosomal instability (increased chromosome breakage) and defective DNA repair.

EXPRESSÃO TECIDUAL(Ubíquo)
Linfócitos
41.9 TPM
Testículo
37.6 TPM
Fibroblastos
18.6 TPM
Skin Sun Exposed Lower leg
15.7 TPM
Skin Not Sun Exposed Suprapubic
14.7 TPM
OUTRAS DOENÇAS (2)
Fanconi anemia, complementation group WFanconi anemia
HGNC:25539UniProt:Q6PCD5
ERCC4DNA repair endonuclease XPFDisease-causing germline mutation(s) inTolerante
FUNÇÃO

Catalytic component of a structure-specific DNA repair endonuclease responsible for the 5-prime incision during DNA repair, and which is essential for nucleotide excision repair (NER) and interstrand cross-link (ICL) repair

LOCALIZAÇÃO

NucleusChromosome

VIAS BIOLÓGICAS (5)
HDR through Single Strand Annealing (SSA)Dual incision in TC-NERDual Incision in GG-NERFormation of Incision Complex in GG-NERFanconi Anemia Pathway
MECANISMO DE DOENÇA

Xeroderma pigmentosum complementation group F

An autosomal recessive pigmentary skin disorder characterized by solar hypersensitivity of the skin, high predisposition for developing cancers on areas exposed to sunlight and, in some cases, neurological abnormalities. The skin develops marked freckling and other pigmentation abnormalities. XP-F patients show a mild phenotype.

EXPRESSÃO TECIDUAL(Ubíquo)
Testículo
13.8 TPM
Fibroblastos
6.2 TPM
Linfócitos
5.4 TPM
Cervix Endocervix
5.1 TPM
Fallopian Tube
5.1 TPM
OUTRAS DOENÇAS (7)
Fanconi anemia complementation group Qxeroderma pigmentosum group FXFE progeroid syndromexeroderma pigmentosum
HGNC:3436UniProt:Q92889
SLX4Structure-specific endonuclease subunit SLX4Disease-causing germline mutation(s) inTolerante
FUNÇÃO

Regulatory subunit that interacts with and increases the activity of different structure-specific endonucleases. Has several distinct roles in protecting genome stability by resolving diverse forms of deleterious DNA structures originating from replication and recombination intermediates and from DNA damage. Component of the SLX1-SLX4 structure-specific endonuclease that resolves DNA secondary structures generated during DNA repair and recombination. Has endonuclease activity towards branched DN

LOCALIZAÇÃO

Nucleus

VIAS BIOLÓGICAS (2)
Resolution of D-loop Structures through Holliday Junction IntermediatesFanconi Anemia Pathway
MECANISMO DE DOENÇA

Fanconi anemia complementation group P

A disorder affecting all bone marrow elements and resulting in anemia, leukopenia and thrombopenia. It is associated with cardiac, renal and limb malformations, dermal pigmentary changes, and a predisposition to the development of malignancies. At the cellular level it is associated with hypersensitivity to DNA-damaging agents, chromosomal instability (increased chromosome breakage) and defective DNA repair. Some individuals affected by Fanconi anemia of complementation group P have skeletal anomalies.

EXPRESSÃO TECIDUAL(Ubíquo)
Cerebelo
28.6 TPM
Testículo
27.2 TPM
Cérebro - Hemisfério cerebelar
24.9 TPM
Linfócitos
12.8 TPM
Pituitária
8.1 TPM
OUTRAS DOENÇAS (2)
Fanconi anemia complementation group PFanconi anemia
HGNC:23845UniProt:Q8IY92
FANCFFanconi anemia group F proteinDisease-causing germline mutation(s) inDesconhecido
FUNÇÃO

DNA repair protein that may operate in a postreplication repair or a cell cycle checkpoint function. May be implicated in interstrand DNA cross-link repair and in the maintenance of normal chromosome stability (By similarity)

LOCALIZAÇÃO

Nucleus

VIAS BIOLÓGICAS (1)
PKR-mediated signaling
MECANISMO DE DOENÇA

Fanconi anemia complementation group F

A disorder affecting all bone marrow elements and resulting in anemia, leukopenia and thrombopenia. It is associated with cardiac, renal and limb malformations, dermal pigmentary changes, and a predisposition to the development of malignancies. At the cellular level it is associated with hypersensitivity to DNA-damaging agents, chromosomal instability (increased chromosome breakage) and defective DNA repair.

EXPRESSÃO TECIDUAL(Ubíquo)
Linfócitos
13.4 TPM
Testículo
12.7 TPM
Baço
8.8 TPM
Pituitária
8.5 TPM
Cervix Endocervix
7.5 TPM
OUTRAS DOENÇAS (2)
Fanconi anemia complementation group FFanconi anemia
HGNC:3587UniProt:Q9NPI8
RAD51CDNA repair protein RAD51 homolog 3Disease-causing germline mutation(s) inTolerante
FUNÇÃO

Essential for the homologous recombination (HR) pathway of DNA repair. Involved in the homologous recombination repair (HRR) pathway of double-stranded DNA breaks arising during DNA replication or induced by DNA-damaging agents. Part of the RAD51 paralog protein complexes BCDX2 and CX3 which act at different stages of the BRCA1-BRCA2-dependent HR pathway. Upon DNA damage, BCDX2 seems to act downstream of BRCA2 recruitment and upstream of RAD51 recruitment; CX3 seems to act downstream of RAD51 re

LOCALIZAÇÃO

NucleusCytoplasmCytoplasm, perinuclear regionMitochondrion

VIAS BIOLÓGICAS (10)
Resolution of D-loop Structures through Holliday Junction IntermediatesHDR through Homologous Recombination (HRR)Resolution of D-loop Structures through Synthesis-Dependent Strand Annealing (SDSA)Homologous DNA Pairing and Strand ExchangePresynaptic phase of homologous DNA pairing and strand exchange
MECANISMO DE DOENÇA

Fanconi anemia complementation group O

A disorder affecting all bone marrow elements and resulting in anemia, leukopenia and thrombopenia. It is associated with cardiac, renal and limb malformations, dermal pigmentary changes, and a predisposition to the development of malignancies. At the cellular level it is associated with hypersensitivity to DNA-damaging agents, chromosomal instability (increased chromosome breakage) and defective DNA repair.

EXPRESSÃO TECIDUAL(Ubíquo)
Testículo
13.8 TPM
Linfócitos
11.8 TPM
Cérebro - Hemisfério cerebelar
8.9 TPM
Brain Frontal Cortex BA9
8.0 TPM
Artéria tibial
7.3 TPM
OUTRAS DOENÇAS (4)
Fanconi anemia complementation group Ohereditary breast ovarian cancer syndromeFanconi anemiabreast-ovarian cancer, familial, susceptibility to, 3
HGNC:9820UniProt:O43502
FANCAFanconi anemia group A proteinDisease-causing germline mutation(s) inTolerante
FUNÇÃO

DNA repair protein that may operate in a postreplication repair or a cell cycle checkpoint function. May be involved in interstrand DNA cross-link repair and in the maintenance of normal chromosome stability

LOCALIZAÇÃO

NucleusCytoplasm

VIAS BIOLÓGICAS (1)
PKR-mediated signaling
MECANISMO DE DOENÇA

Fanconi anemia, complementation group A

A disorder affecting all bone marrow elements and resulting in anemia, leukopenia and thrombopenia. It is associated with cardiac, renal and limb malformations, dermal pigmentary changes, and a predisposition to the development of malignancies. At the cellular level it is associated with hypersensitivity to DNA-damaging agents, chromosomal instability (increased chromosome breakage) and defective DNA repair.

EXPRESSÃO TECIDUAL(Tecido-específico)
Testículo
25.2 TPM
Linfócitos
22.3 TPM
Fibroblastos
6.8 TPM
Baço
4.8 TPM
Cerebelo
4.7 TPM
OUTRAS DOENÇAS (2)
Fanconi anemia complementation group AFanconi anemia
HGNC:3582UniProt:O15360
BRCA2Breast cancer type 2 susceptibility proteinDisease-causing germline mutation(s) inTolerante
FUNÇÃO

Involved in double-strand break repair and/or homologous recombination. Binds RAD51 and potentiates recombinational DNA repair by promoting assembly of RAD51 onto single-stranded DNA (ssDNA). Acts by targeting RAD51 to ssDNA over double-stranded DNA, enabling RAD51 to displace replication protein-A (RPA) from ssDNA and stabilizing RAD51-ssDNA filaments by blocking ATP hydrolysis. Part of a PALB2-scaffolded HR complex containing RAD51C and which is thought to play a role in DNA repair by HR. May

LOCALIZAÇÃO

NucleusCytoplasm, cytoskeleton, microtubule organizing center, centrosome

VIAS BIOLÓGICAS (3)
Presynaptic phase of homologous DNA pairing and strand exchangeHDR through MMEJ (alt-NHEJ)Meiotic recombination
MECANISMO DE DOENÇA

Breast cancer

A common malignancy originating from breast epithelial tissue. Breast neoplasms can be distinguished by their histologic pattern. Invasive ductal carcinoma is by far the most common type. Breast cancer is etiologically and genetically heterogeneous. Important genetic factors have been indicated by familial occurrence and bilateral involvement. Mutations at more than one locus can be involved in different families or even in the same case.

OUTRAS DOENÇAS (17)
Wilms tumor 1Fanconi anemia complementation group D1breast-ovarian cancer, familial, susceptibility to, 2BRCA2-related cancer predisposition
HGNC:1101UniProt:P51587
FANCCFanconi anemia group C proteinDisease-causing germline mutation(s) inTolerante
FUNÇÃO

DNA repair protein that may operate in a postreplication repair or a cell cycle checkpoint function. May be implicated in interstrand DNA cross-link repair and in the maintenance of normal chromosome stability. Upon IFNG induction, may facilitate STAT1 activation by recruiting STAT1 to IFNGR1

LOCALIZAÇÃO

NucleusCytoplasm

VIAS BIOLÓGICAS (1)
PKR-mediated signaling
MECANISMO DE DOENÇA

Fanconi anemia complementation group C

A disorder affecting all bone marrow elements and resulting in anemia, leukopenia and thrombopenia. It is associated with cardiac, renal and limb malformations, dermal pigmentary changes, and a predisposition to the development of malignancies. At the cellular level it is associated with hypersensitivity to DNA-damaging agents, chromosomal instability (increased chromosome breakage) and defective DNA repair.

EXPRESSÃO TECIDUAL(Ubíquo)
Testículo
14.6 TPM
Cerebelo
12.3 TPM
Cérebro - Hemisfério cerebelar
12.2 TPM
Fígado
8.8 TPM
Cervix Endocervix
5.9 TPM
OUTRAS DOENÇAS (2)
Fanconi anemia complementation group CFanconi anemia
HGNC:3584UniProt:Q00597
BRCA1Breast cancer type 1 susceptibility proteinDisease-causing germline mutation(s) (loss of function) inTolerante
FUNÇÃO

E3 ubiquitin-protein ligase that specifically mediates the formation of 'Lys-6'-linked polyubiquitin chains and plays a central role in DNA repair by facilitating cellular responses to DNA damage (PubMed:10500182, PubMed:12887909, PubMed:12890688, PubMed:14976165, PubMed:16818604, PubMed:17525340, PubMed:19261748). It is unclear whether it also mediates the formation of other types of polyubiquitin chains (PubMed:12890688). The BRCA1-BARD1 heterodimer coordinates a diverse range of cellular path

LOCALIZAÇÃO

NucleusChromosomeCytoplasm

VIAS BIOLÓGICAS (10)
Recruitment and ATM-mediated phosphorylation of repair and signaling proteins at DNA double strand breaksMetalloprotease DUBsTP53 Regulates Transcription of DNA Repair GenesTranscriptional Regulation by E2F6Meiotic synapsis
MECANISMO DE DOENÇA

Breast cancer

A common malignancy originating from breast epithelial tissue. Breast neoplasms can be distinguished by their histologic pattern. Invasive ductal carcinoma is by far the most common type. Breast cancer is etiologically and genetically heterogeneous. Important genetic factors have been indicated by familial occurrence and bilateral involvement. Mutations at more than one locus can be involved in different families or even in the same case.

OUTRAS DOENÇAS (12)
Fanconi anemia, complementation group Sbreast-ovarian cancer, familial, susceptibility to, 1BRCA1-related cancer predispositionprostate cancer, hereditary
HGNC:1100UniProt:P38398
FANCGFanconi anemia group G proteinDisease-causing germline mutation(s) inTolerante
FUNÇÃO

DNA repair protein that may operate in a postreplication repair or a cell cycle checkpoint function. May be implicated in interstrand DNA cross-link repair and in the maintenance of normal chromosome stability. Candidate tumor suppressor gene

LOCALIZAÇÃO

NucleusCytoplasm

VIAS BIOLÓGICAS (1)
PKR-mediated signaling
MECANISMO DE DOENÇA

Fanconi anemia complementation group G

A disorder affecting all bone marrow elements and resulting in anemia, leukopenia and thrombopenia. It is associated with cardiac, renal and limb malformations, dermal pigmentary changes, and a predisposition to the development of malignancies. At the cellular level it is associated with hypersensitivity to DNA-damaging agents, chromosomal instability (increased chromosome breakage) and defective DNA repair.

EXPRESSÃO TECIDUAL(Ubíquo)
Linfócitos
34.6 TPM
Cerebelo
29.3 TPM
Cérebro - Hemisfério cerebelar
29.1 TPM
Testículo
25.7 TPM
Cervix Endocervix
18.5 TPM
OUTRAS DOENÇAS (2)
Fanconi anemia complementation group GFanconi anemia
HGNC:3588UniProt:O15287
MAD2L2Mitotic spindle assembly checkpoint protein MAD2BDisease-causing germline mutation(s) inTolerante
FUNÇÃO

Adapter protein able to interact with different proteins and involved in different biological processes (PubMed:11459825, PubMed:11459826, PubMed:17296730, PubMed:17719540, PubMed:19443654, PubMed:29656893). Mediates the interaction between the error-prone DNA polymerase zeta catalytic subunit REV3L and the inserter polymerase REV1, thereby mediating the second polymerase switching in translesion DNA synthesis (PubMed:20164194, PubMed:23143872). Translesion DNA synthesis releases the replication

LOCALIZAÇÃO

NucleusCytoplasm, cytoskeleton, spindleCytoplasmChromosome

VIAS BIOLÓGICAS (3)
Translesion synthesis by POLKTranslesion synthesis by REV1Translesion synthesis by POLI
MECANISMO DE DOENÇA

Fanconi anemia, complementation group V

A disorder affecting all bone marrow elements and resulting in anemia, leukopenia and thrombopenia. It is associated with cardiac, renal and limb malformations, dermal pigmentary changes, and a predisposition to the development of malignancies. At the cellular level it is associated with hypersensitivity to DNA-damaging agents, chromosomal instability (increased chromosome breakage) and defective DNA repair.

EXPRESSÃO TECIDUAL(Ubíquo)
Testículo
68.8 TPM
Linfócitos
35.5 TPM
Fibroblastos
34.8 TPM
Nervo tibial
29.1 TPM
Cérebro - Hemisfério cerebelar
28.0 TPM
OUTRAS DOENÇAS (2)
Fanconi anemia complementation group VFanconi anemia
HGNC:6764UniProt:Q9UI95
RAD51DNA repair protein RAD51 homolog 1Disease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

Plays an important role in homologous strand exchange, a key step in DNA repair through homologous recombination (HR) (PubMed:12205100, PubMed:18417535, PubMed:20231364, PubMed:20348101, PubMed:22325354, PubMed:23509288, PubMed:23754376, PubMed:26681308, PubMed:28575658, PubMed:32640219). Binds to single-stranded DNA in an ATP-dependent manner to form nucleoprotein filaments which are essential for the homology search and strand exchange (PubMed:12205100, PubMed:18417535, PubMed:15226506, PubMed

LOCALIZAÇÃO

NucleusCytoplasmCytoplasm, perinuclear regionMitochondrion matrixChromosomeCytoplasm, cytoskeleton, microtubule organizing center, centrosome

VIAS BIOLÓGICAS (4)
Presynaptic phase of homologous DNA pairing and strand exchangeHDR through Single Strand Annealing (SSA)Transcriptional Regulation by E2F6Meiotic recombination
MECANISMO DE DOENÇA

Breast cancer

A common malignancy originating from breast epithelial tissue. Breast neoplasms can be distinguished by their histologic pattern. Invasive ductal carcinoma is by far the most common type. Breast cancer is etiologically and genetically heterogeneous. Important genetic factors have been indicated by familial occurrence and bilateral involvement. Mutations at more than one locus can be involved in different families or even in the same case.

EXPRESSÃO TECIDUAL(Tecido-específico)
Linfócitos
26.5 TPM
Testículo
24.1 TPM
Fibroblastos
6.8 TPM
Esôfago - Mucosa
4.0 TPM
Cólon transverso
2.3 TPM
OUTRAS DOENÇAS (6)
Fanconi anemia complementation group Rmirror movements 2familial congenital mirror movementshereditary breast ovarian cancer syndrome
HGNC:9817UniProt:Q06609
XRCC2DNA repair protein XRCC2Disease-causing germline mutation(s) inTolerante
FUNÇÃO

Involved in the homologous recombination repair (HRR) pathway of double-stranded DNA, thought to repair chromosomal fragmentation, translocations and deletions. Part of the RAD51 paralog protein complex BCDX2 which acts in the BRCA1-BRCA2-dependent HR pathway. Upon DNA damage, BCDX2 acts downstream of BRCA2 recruitment and upstream of RAD51 recruitment. BCDX2 binds predominantly to the intersection of the four duplex arms of the Holliday junction and to junction of replication forks. The BCDX2 c

LOCALIZAÇÃO

NucleusCytoplasm, cytoskeleton, microtubule organizing center, centrosome

VIAS BIOLÓGICAS (9)
Resolution of D-loop Structures through Holliday Junction IntermediatesHDR through Homologous Recombination (HRR)Resolution of D-loop Structures through Synthesis-Dependent Strand Annealing (SDSA)Homologous DNA Pairing and Strand ExchangePresynaptic phase of homologous DNA pairing and strand exchange
MECANISMO DE DOENÇA

Fanconi anemia, complementation group U

A disorder affecting all bone marrow elements and resulting in anemia, leukopenia and thrombopenia. It is associated with cardiac, renal and limb malformations, dermal pigmentary changes, and a predisposition to the development of malignancies. At the cellular level it is associated with hypersensitivity to DNA-damaging agents, chromosomal instability (increased chromosome breakage) and defective DNA repair.

EXPRESSÃO TECIDUAL(Tecido-específico)
Linfócitos
13.0 TPM
Testículo
6.4 TPM
Fibroblastos
3.1 TPM
Esôfago - Mucosa
1.5 TPM
Intestino delgado
1.0 TPM
OUTRAS DOENÇAS (6)
premature ovarian failure 17Fanconi anemia complementation group Uspermatogenic failure 50hereditary breast carcinoma
HGNC:12829UniProt:O43543
PALB2Partner and localizer of BRCA2Disease-causing germline mutation(s) inTolerante
FUNÇÃO

Plays a critical role in homologous recombination repair (HRR) through its ability to recruit BRCA2 and RAD51 to DNA breaks (PubMed:16793542, PubMed:19369211, PubMed:19423707, PubMed:22941656, PubMed:24141787, PubMed:28319063). Strongly stimulates the DNA strand-invasion activity of RAD51, stabilizes the nucleoprotein filament against a disruptive BRC3-BRC4 polypeptide and helps RAD51 to overcome the suppressive effect of replication protein A (RPA) (PubMed:20871615). Functionally cooperates wit

LOCALIZAÇÃO

Nucleus

VIAS BIOLÓGICAS (6)
Resolution of D-loop Structures through Holliday Junction IntermediatesHDR through Homologous Recombination (HRR)Resolution of D-loop Structures through Synthesis-Dependent Strand Annealing (SDSA)Homologous DNA Pairing and Strand ExchangeImpaired BRCA2 binding to PALB2
MECANISMO DE DOENÇA

Breast cancer

A common malignancy originating from breast epithelial tissue. Breast neoplasms can be distinguished by their histologic pattern. Invasive ductal carcinoma is by far the most common type. Breast cancer is etiologically and genetically heterogeneous. Important genetic factors have been indicated by familial occurrence and bilateral involvement. Mutations at more than one locus can be involved in different families or even in the same case.

EXPRESSÃO TECIDUAL(Ubíquo)
Linfócitos
13.6 TPM
Testículo
10.3 TPM
Fibroblastos
10.2 TPM
Cérebro - Hemisfério cerebelar
8.7 TPM
Cerebelo
8.4 TPM
OUTRAS DOENÇAS (9)
Fanconi anemia complementation group NPALB2-related cancer predispositionchordomahereditary breast carcinoma
HGNC:26144UniProt:Q86YC2
FANCMFanconi anemia group M proteinDisease-causing germline mutation(s) inTolerante
FUNÇÃO

DNA-dependent ATPase component of the Fanconi anemia (FA) core complex (PubMed:16116422). Required for the normal activation of the FA pathway, leading to monoubiquitination of the FANCI-FANCD2 complex in response to DNA damage, cellular resistance to DNA cross-linking drugs, and prevention of chromosomal breakage (PubMed:16116422, PubMed:19423727, PubMed:20347428, PubMed:20347429, PubMed:29231814). In complex with CENPS and CENPX, binds double-stranded DNA (dsDNA), fork-structured DNA (fsDNA) a

LOCALIZAÇÃO

Nucleus

VIAS BIOLÓGICAS (1)
PKR-mediated signaling
MECANISMO DE DOENÇA

Spermatogenic failure 28

An autosomal recessive infertility disorder caused by spermatogenesis defects that result in oligoasthenospermia or non-obstructive azoospermia.

EXPRESSÃO TECIDUAL(Ubíquo)
Testículo
9.4 TPM
Linfócitos
6.7 TPM
Ovário
3.2 TPM
Cervix Ectocervix
3.1 TPM
Útero
2.8 TPM
OUTRAS DOENÇAS (4)
premature ovarian failure 15spermatogenic failure 28Fanconi anemiaobsolete male infertility with azoospermia or oligozoospermia due to single gene mutation
HGNC:23168UniProt:Q8IYD8
UBE2TUbiquitin-conjugating enzyme E2 TDisease-causing germline mutation(s) inTolerante
FUNÇÃO

Accepts ubiquitin from the E1 complex and catalyzes its covalent attachment to other proteins. Catalyzes monoubiquitination. Involved in mitomycin-C (MMC)-induced DNA repair. Acts as a specific E2 ubiquitin-conjugating enzyme for the Fanconi anemia complex by associating with E3 ubiquitin-protein ligase FANCL and catalyzing monoubiquitination of FANCD2, a key step in the DNA damage pathway (PubMed:16916645, PubMed:17938197, PubMed:19111657, PubMed:19589784, PubMed:28437106). Also mediates monoub

LOCALIZAÇÃO

Nucleus

VIAS BIOLÓGICAS (2)
Fanconi Anemia PathwaySynthesis of active ubiquitin: roles of E1 and E2 enzymes
MECANISMO DE DOENÇA

Fanconi anemia complementation group T

A disorder affecting all bone marrow elements and resulting in anemia, leukopenia and thrombopenia. It is associated with cardiac, renal and limb malformations, dermal pigmentary changes, and a predisposition to the development of malignancies. At the cellular level it is associated with hypersensitivity to DNA-damaging agents, chromosomal instability (increased chromosome breakage) and defective DNA repair.

EXPRESSÃO TECIDUAL(Ubíquo)
Linfócitos
92.9 TPM
Testículo
42.7 TPM
Fibroblastos
29.0 TPM
Brain Frontal Cortex BA9
18.6 TPM
Brain Nucleus accumbens basal ganglia
13.8 TPM
OUTRAS DOENÇAS (2)
Fanconi anemia complementation group TFanconi anemia
HGNC:25009UniProt:Q9NPD8
FANCIFanconi anemia group I proteinDisease-causing germline mutation(s) inTolerante
FUNÇÃO

Plays an essential role in the repair of DNA double-strand breaks by homologous recombination and in the repair of interstrand DNA cross-links (ICLs) by promoting FANCD2 monoubiquitination by FANCL and participating in recruitment to DNA repair sites (PubMed:17412408, PubMed:17460694, PubMed:17452773, PubMed:19111657, PubMed:36385258). The FANCI-FANCD2 complex binds and scans double-stranded DNA (dsDNA) for DNA damage; this complex stalls at DNA junctions between double-stranded DNA and single-s

LOCALIZAÇÃO

NucleusCytoplasm

VIAS BIOLÓGICAS (2)
TP53 Regulates Transcription of DNA Repair GenesFanconi Anemia Pathway
MECANISMO DE DOENÇA

Fanconi anemia complementation group I

A disorder affecting all bone marrow elements and resulting in anemia, leukopenia and thrombopenia. It is associated with cardiac, renal and limb malformations, dermal pigmentary changes, and a predisposition to the development of malignancies. At the cellular level it is associated with hypersensitivity to DNA-damaging agents, chromosomal instability (increased chromosome breakage) and defective DNA repair.

EXPRESSÃO TECIDUAL(Ubíquo)
Linfócitos
62.0 TPM
Testículo
42.1 TPM
Fibroblastos
14.0 TPM
Esôfago - Mucosa
9.7 TPM
Skin Sun Exposed Lower leg
7.5 TPM
OUTRAS DOENÇAS (2)
Fanconi anemia complementation group IFanconi anemia
HGNC:25568UniProt:Q9NVI1

Medicamentos e terapias

FLUDARABINE PHOSPHATEPhase 2

Mecanismo: DNA polymerase (alpha/delta/epsilon) inhibitor

METFORMINPhase 2

Mecanismo: Mitochondrial complex I (NADH dehydrogenase) inhibitor

Ver mais no OpenTargets

Variantes genéticas (ClinVar)

5,436 variantes patogênicas registradas no ClinVar.

🧬 BRIP1: NM_032043.3(BRIP1):c.2920del (p.Leu974fs) ()
🧬 BRIP1: NM_032043.3(BRIP1):c.1511del (p.Ile504fs) ()
🧬 BRIP1: NM_032043.3(BRIP1):c.942T>A (p.His314Gln) ()
🧬 BRIP1: NM_032043.3(BRIP1):c.1340+8G>A ()
🧬 BRIP1: NM_032043.3(BRIP1):c.1243C>T (p.Leu415Phe) ()
Ver todas no ClinVar

Classificação de variantes (ClinVar)

Distribuição de 28,126 variantes classificadas pelo ClinVar.

9844
18282
VUS (35.0%)
Benigna (65.0%)
VARIANTES MAIS SIGNIFICATIVAS
FANCA: NM_000135.4(FANCA):c.2918G>C (p.Cys973Ser) [Uncertain significance]
FANCF: NM_022725.4(FANCF):c.125G>A (p.Arg42His) [Uncertain significance]
FANCB: NM_001018113.3(FANCB):c.1677G>C (p.Lys559Asn) [Uncertain significance]
FANCL: NM_018062.4(FANCL):c.578C>G (p.Ala193Gly) [Uncertain significance]
FANCD2: NM_001018115.3(FANCD2):c.2169A>G (p.Lys723=) [Uncertain significance]

Vias biológicas (Reactome)

41 vias biológicas associadas aos genes desta condição.

Cytosolic iron-sulfur cluster assembly HDR through Single Strand Annealing (SSA) HDR through Homologous Recombination (HRR) Resolution of D-loop Structures through Synthesis-Dependent Strand Annealing (SDSA) Resolution of D-loop Structures through Holliday Junction Intermediates Homologous DNA Pairing and Strand Exchange Processing of DNA double-strand break ends Presynaptic phase of homologous DNA pairing and strand exchange Regulation of TP53 Activity through Phosphorylation G2/M DNA damage checkpoint Defective homologous recombination repair (HRR) due to BRCA1 loss of function Defective HDR through Homologous Recombination Repair (HRR) due to PALB2 loss of BRCA1 binding function Defective HDR through Homologous Recombination Repair (HRR) due to PALB2 loss of BRCA2/RAD51/RAD51C binding function Impaired BRCA2 binding to RAD51 Impaired BRCA2 binding to PALB2 Fanconi Anemia Pathway PKR-mediated signaling TP53 Regulates Transcription of DNA Repair Genes Formation of Incision Complex in GG-NER Dual Incision in GG-NER Dual incision in TC-NER Meiotic recombination Factors involved in megakaryocyte development and platelet production HDR through MMEJ (alt-NHEJ) Impaired BRCA2 translocation to the nucleus Impaired BRCA2 binding to SEM1 (DSS1) Meiotic synapsis SUMOylation of DNA damage response and repair proteins Metalloprotease DUBs Recruitment and ATM-mediated phosphorylation of repair and signaling proteins at DNA double strand breaks Nonhomologous End-Joining (NHEJ) Neddylation Transcriptional Regulation by E2F6 Defective DNA double strand break response due to BRCA1 loss of function Defective DNA double strand break response due to BARD1 loss of function KEAP1-NFE2L2 pathway Regulation of MITF-M-dependent genes involved in DNA replication, damage repair and senescence Translesion synthesis by REV1 Translesion synthesis by POLK Translesion synthesis by POLI Synthesis of active ubiquitin: roles of E1 and E2 enzymes

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Publicações mais relevantes

Timeline de publicações
2.003 papers (10 anos)

Mostrando amostra de 200 publicações de um total de 2.003

#1

Metabolite-induced DNA damage drives stochastic stem cell loss and clonal hematopoiesis.

Cell stem cell2026 Mar 23

DNA damage and mutations in hematopoietic stem cells (HSCs) enable clonal hematopoiesis (CH). Such damage occurs across a lifetime, but its origins remain unknown. Here, we demonstrate that endogenous formaldehyde causes HSC attrition and subsequently CH. We generated conditional mouse models lacking formaldehyde detoxification and Fanconi anemia (FA) DNA repair in blood. Formaldehyde protection was crucial for embryonic HSC emergence and throughout life. Despite severe deficiencies in HSCs, these mice produced blood for many months. To determine what enables this, we employed an unbiased method for detecting clones, which exploits somatic variant data. This revealed initial polyclonal hematopoiesis that diminishes to monoclonal hematopoiesis, devoid of known genetic selection. Furthermore, in FA children, we find the same transition to monoclonal hematopoiesis. Therefore, DNA damage-induced attrition down to the last functional cell can be a driving force for CH, representing an alternative route to CH other than purely by fitness-enhancing selection.

#2

Deficiencies in the Fanconi anemia or homologous recombination pathway enhance the antitumor effects of the hypoxia-activated prodrug CP-506.

Molecular therapy. Oncology2026 Mar 19

The novel hypoxia-activated prodrug CP-506 selectively targets the hypoxic, treatment-resistant tumor microenvironment. Given the alkylating effector metabolites of CP-506, we hypothesized that defects in interstrand crosslink (ICL) and double-strand break repair influence treatment efficacy. In vitro and in vivo isogenic cancer models proficient or deficient in the Fanconi anemia (FA), homologous recombination (HR), or non-homologous end joining (NHEJ) pathway were used to assess CP-506-induced cytotoxicity and DNA damage. Viability and clonogenic assays demonstrated enhanced sensitivity to CP-506 in FA- or HR-deficient cells compared to parental cells, which was confirmed by spheroid growth inhibition studies. In vivo, CP-506 caused greater enhancement ratios in FA- and HR-deficient xenografts versus parental controls (p < 0.0001) but not in NHEJ-deficient xenografts (p = 0.18). Mechanistically, CP-506 increased γH2AX expression (1.9- to 9.3-fold) in FA- and HR-deficient cells and xenografts, whereas NHEJ-deficient models showed a 0.5-fold reduction. Alkaline comet assays confirmed CP-506-induced ICLs and DNA strand breaks but did not explain the differential therapeutic responses among isogenic cancer cells. These data indicate that deficiencies within FA or HR, but not NHEJ or nucleotide excision repair (NER), determine CP-506 sensitivity, consistent with a synthetic-lethal interaction. Therefore, tumor hypoxia and DNA repair status are key biomarkers for stratifying patients in CP-506 clinical trials.

#3

Towards evolutionary guided precision medicine of acute myeloid leukemia and Fanconi anemia associated bone marrow failure.

Stem cells translational medicine2026 Feb 25

Carcinogenesis and acquisition of multidrug resistance within established cancers are both multistep evolutionary processes in which stem cells play a role. This perspective will briefly review two corresponding theoretical constructs under development. Efficiency of carcinogenesis (EOC) considers multistep carcinogenesis and predicts the effect of differing dynamics on the efficiency of generating a transformed founder cell. EOC has been applied to evaluation of the role of genetic instability in carcinogenesis. Dynamic precision medicine (DPM) is a method for providing personalized treatment sequences for cancer while explicitly considering intracancer subclonal heterogeneity and evolutionary dynamics (growth and evolutionary rates). It adapts therapy frequently and proactively by anticipating the kinetics of multidrug resistance prior to its detection, and prioritizing its prevention. Simulations suggest potential to substantially increase survival and cure rates across a broad range of clinical presentations. Both of these problems implicate very small subclones within stem cell and/or differentiated compartments, and evolution may occur over months to years. We describe novel experimental technologies for quantifying longitudinal dynamics of very large numbers of cells for prolonged periods, allowing detection and tracking of rare events and their evolution over time. We further highlight two potential applications. In Fanconi anemia, optimal treatment sequences for minimizing bone marrow failure while not increasing the risk of leukemia may be designed using EOC and DPM and tested in laboratory models. In refractory acute myeloid leukemia, high throughput molecular characterization and drug sensitivity screening of subclones is showing clinical promise, and may be further optimized with DPM.

#4

Beyond readthrough: ataluren restores mitochondrial function and reduces oxidative stress in FANCA-mutated cells via mTOR-DRP1 modulation.

Cell death discovery2026 Feb 28

Fanconi anemia (FA) is a rare inherited bone marrow failure syndrome characterized by genomic instability, mitochondrial dysfunction, and oxidative stress. While the therapeutic potential of ataluren, a translational readthrough-inducing drug, has been investigated in FA cells carrying nonsense mutations, its broader metabolic impact remains unclear. Here, we demonstrate that ataluren (tested at 2.5, 5, and 10 μM) modulates cellular energy metabolism and redox homeostasis in FA lymphoblasts harboring either nonsense or missense mutations in the FANCA gene. At low doses (2.5 μM for 72 h), ataluren improved the ATP/AMP ratio, enhanced oxidative phosphorylation efficiency, and reduced lipid peroxidation and oxidative DNA damage. These effects were independent of mutation type and were not associated with compensatory glycolysis, as lactate dehydrogenase activity remained unchanged. Strikingly, ataluren restored the P/O ratio under pyruvate/malate-driven respiration to near-normal values, indicating improved coupling between oxygen consumption and ATP synthesis. Mechanistically, ataluren reduced DRP1 protein levels and attenuated mTOR-S6 signaling, suggesting that mitochondrial dynamics and bioenergetic efficiency are modulated via the mTOR-DRP1 axis. Additionally, ataluren lowered IMPDH activity, contributing to reduced cell proliferation and DNA damage without impairing cellular energy status. Notably, these beneficial effects persisted under immune stimulation, where ataluren mitigated the metabolic and oxidative burden imposed by lymphocyte activation. Our findings unveil a pleiotropic role for ataluren that extends beyond its canonical readthrough activity, highlighting its potential as a metabolic modulator for FA and possibly other DNA repair-deficient disorders.

#5

Differential genetic analysis of ectrodactyly in a Fanconi anemia pedigree with FANCA mutations.

MedScience2026 Feb 14

Fanconi anemia (FA; OMIM: 227650) is a rare genetic disorder characterized by bone marrow failure, congenital anomalies, and cancer predisposition. While FANCA mutations account for most FA cases, phenotypic overlap with other disorders complicates diagnosis. This study analyzes molecular diagnostic pathways for FANCA-related FA and establishes a hereditary differential diagnosis for ectrodactyly. A Chinese FA family clinical phenotype was collected. The proband and father underwent whole-genome sequencing. Copy number variations (CNVs) in FANCA were assessed by genomic qPCR. Functional characterization of the EHMT1 variant included minigene splicing assays, RT-qPCR and Western blotting on peripheral blood samples. The proband showed pancytopenia and bone marrow hypoplasia, suggesting aplastic anemia. Sequencing analysis identified two FANCA mutations, NM_000135.4: c.154C>T and NC_000016.9: g.89865477_89895212del, which caused partial protein deletion. Subsequent pedigree analysis revealed that the affected individuals of the proband's paternal lineage, who exhibited ectrodactyly, were heterozygous for the EHMT1 c.2382 + 1750G>A variant (NM 024757.5) and showed significantly reduced EHMT1 mRNA expression, demonstrating complete genotype-phenotype co-segregation. Furthermore, Western blot revealed reduced H3K9me2 and decreased intensity of a ∼100 kDa EHMT1-reactive band in the proband's father. The newly identified g.89865477_89895212del mutation enriches the FANCA gene mutant spectrum. Additionally, the EHMT1 c.2382 + 1750G>A variant co-segregates with ectrodactyly and is accompanied by significantly reduced EHMT1 mRNA expression.

Publicações recentes

Ver todas no PubMed

📚 EuropePMC2.252 artigos no totalmostrando 198

2026

Tumor Treating Fields (TTFields), and their concomitant application with FOLFOX, are effective for the treatment of gastric cancer cells.

Frontiers in oncology
2026

Metabolite-induced DNA damage drives stochastic stem cell loss and clonal hematopoiesis.

Cell stem cell
2026

Deficiencies in the Fanconi anemia or homologous recombination pathway enhance the antitumor effects of the hypoxia-activated prodrug CP-506.

Molecular therapy. Oncology
2026

[Mutation characteristics and prognosis of patients with Fanconi anemia signaling pathway gene mutation myeloproliferative neoplasm].

Zhonghua yi xue za zhi
2026

Expanding genetic landscape of inherited bone marrow failure syndromes: Insights from the Canadian Inherited Marrow Failure Registry (CIMFR) (2001-2023).

British journal of haematology
2026

The tight bond between Fanconi anemia and aging.

Frontiers in aging
2026

Towards evolutionary guided precision medicine of acute myeloid leukemia and Fanconi anemia associated bone marrow failure.

Stem cells translational medicine
2026

Infective endocarditis in an adult male patient with tetralogy of Fallot physiology secondary to double outlet right ventricle presenting with stroke: a complex presentation with multiorgan dysfunction-a case report.

Journal of medical case reports
2026

Beyond readthrough: ataluren restores mitochondrial function and reduces oxidative stress in FANCA-mutated cells via mTOR-DRP1 modulation.

Cell death discovery
2026

Statement of Retraction: A novel role for fanconi anemia (FA) pathway effector protein FANCD2 in cell cycle progression of untransformed primary human cells.

Cell cycle (Georgetown, Tex.)
2026

Insights and modulation of RNA polymerases-dependentR-loop and dsRNA inFanconi anemia hematopoietic stem cells.

JCI insight
2026

BRIP1-mediated RINT1 acetylation and NF-κB activation promote DNA repair and immunosuppressive microenvironment in lung adenocarcinoma.

Cancer letters
2026

Differential genetic analysis of ectrodactyly in a Fanconi anemia pedigree with FANCA mutations.

MedScience
2026

Multi-omics and machine learning-based profiling of severity signatures in Mycoplasma pneumoniae infection in children.

iScience
2026

Possible link between the apparently pathogenic FANCI variant and beneficial effects in sports performance.

Frontiers in genetics
2026

Identification of shared gene signature between lung cancer and postoperative delirium by transcriptome data analysis.

Medicine
2026

A custom phenotypic profile for Fanconi anemia: Addressing gaps in existing disease annotations.

medRxiv : the preprint server for health sciences
2026

RAD51C-XRCC3 complex regulates FANCM-mediated R-loop resolution to safeguard genome integrity.

Science advances
2026

BRCA1/2, PALB2 mutations and first-line CDK4/6 inhibitor efficacy in HR+ metastatic breast cancer.

Breast (Edinburgh, Scotland)
2026

Attitudes Toward Prenatal Interventions in the Fanconi Anemia Community.

Prenatal diagnosis
2026

Discovering Hereditary Risk Through Surveillance: A Prospective Genetic Analysis of Individuals With Familial Pancreatic Cancer.

United European gastroenterology journal
2026

Genetic Syndromes Associated With Congenital Upper Limb Differences.

The Journal of hand surgery
2026

Targeting FANCD2 to overcome enzalutamide resistance in prostate cancer.

Cancer &amp; metabolism
2026

Expression of Concern: Rad18 E3 ubiquitin ligase activity mediates Fanconi anemia pathway activation and cell survival following DNA Topoisomerase 1 inhibition.

Cell cycle (Georgetown, Tex.)
2026

Ultrarare Variants in DNA Damage Repair and Mitochondrial Genes in Pediatric Acute-Onset Neuropsychiatric Syndrome and Acute Behavioral Regression in Neurodevelopmental Disorders.

Developmental neuroscience
2026

FANCD2 restrains fork progression and prevents fragility at early origins upon re-replication.

Nature communications
2026

[Homologous recombination repair gene variants in hormone-sensitive prostate cancer].

Zhonghua bing li xue za zhi = Chinese journal of pathology
2026

Patients with Fanconi Anemia Have an Increased Incidence of Diabetes Mellitus After Allogeneic Stem Cell Transplantation.

Hematology/oncology and stem cell therapy
2026

Insights into the host response to 'dormant' Mycobacterium tuberculosis utilizing 'Vitamin C-induced dormant Mtb' THP-1 cell infection model.

BMC genomics
2026

Fanconi anaemia as a human model of accelerated epigenetic and immune ageing.

Ageing research reviews
2026

Hematologic malignancies in pediatric patients with RUNX1-Familial Platelet Disorder with Associated Myeloid Malignancy.

Blood advances
2026

TBCRC 048 (Olaparib Expanded) Expansion Cohorts: Phase II Study of Olaparib Monotherapy for Patients With Metastatic Breast Cancer With Germline Mutations in PALB2 or Somatic Mutations in BRCA1 or BRCA2.

Journal of clinical oncology : official journal of the American Society of Clinical Oncology
2025

Clinical and Prognostic Relevance of BRIP1 Expression in Colorectal Cancer: Evidence from TCGA and Korean Cohorts.

Medicina (Kaunas, Lithuania)
2026

The Genetic and Molecular Analyses of Rare Candidate Germline BRIP1/FANCJ Variants Implicated in Hereditary Breast and Ovarian Cancers.

International journal of molecular sciences
2026

Subsequent Neoplasms After Umbilical Cord Blood Transplantation in the Japanese and European Populations.

Transplantation and cellular therapy
2026

A Rare Case of Co-occurring Fanconi Anemia and Primary Ciliary Dyskinesia.

Turkish journal of haematology : official journal of Turkish Society of Haematology
2026

Advances in stem cell transplantation for Fanconi anemia.

Expert review of hematology
2026

Activation of GLP-1R ameliorates microglial pyroptosis after spinal cord injury by restoring FANCC expression.

Brain, behavior, and immunity
2026

Genotype-phenotype characteristics and disease progression of FAN1-related karyomegalic tubulointerstitial nephropathy.

Kidney international
2026

Fanconi anemia complementation group C gene (FANCC) association with hereditary and sporadic renal tumors.

The oncologist
2026

Prediction of myeloid malignant cells in Fanconi anemia using machine learning.

PloS one
2026

Characterizing the molecular and clinical implications of NRG1 fusions in NSCLC through integrated RNA and DNA sequencing analysis.

European journal of medical research
2026

Site-saturation functional screens identify PALB2 missense variants associated with increased breast cancer risk.

Nature communications
2026

Pathogenic Germline PALB2 and RAD50 Variants in Patients With Relapsed Ewing Sarcoma.

Pediatric blood &amp; cancer
2025

Clinical and genetic spectrum of Fanconi anemia in Australia and New Zealand.

Genetics in medicine open
2026

Human cytomegalovirus regulates host DNA repair machinery for viral genome integrity.

Nucleic acids research
2026

The SMC5/SMC6 complex is critical for resolving R-loop-induced transcription-replication conflicts.

Nucleic acids research
2026

FANCD2 promotes wound healing through DNMT1.

Histochemistry and cell biology
2026

Targeted CRISPR knockout screening identifies known and novel chemogenomic interactions between DNA damaging agents and DNA repair genes.

NAR cancer
2026

Evaluating the Effectiveness of Early Genetic Screening for Fanconi Anemia in High-Risk Pediatric Populations.

Molecular genetics &amp; genomic medicine
2026

Genomic comparisons and the adaptive basis of brain size plasticity and chromosomal instability in the Eurasian common shrew.

Molecular biology and evolution
2026

The FANCD2-FANCI heterodimer coordinates chromatin openness and cell cycle progression throughout DNA double-strand break repair.

Cell reports
2025

Artificial Intelligence-Assisted Automated DNA Ploidy Analysis of Oral Lesions From Fanconi Anemia Patients With DNA Karyometry.

Frontiers in bioscience (Elite edition)
2026

BLM and FANCJ role in the response to G-quadruplex-dependent telomeric replicative stress.

Communications biology
2026

Characterization of Copy Number Variants in Hereditary Cancer Patients Through NGS Shows a Distinctive PALB2 Contribution to the Diagnostic Yield.

Human mutation
2026

Betulinic Acid Suppresses UBE2T Expression via MAPK/ERK Inhibition to Block FANCI and FANCD2 Monoubiquitination in Glioblastoma.

Journal of cellular and molecular medicine
2026

Oral squamous cell carcinoma risk and magnitude of association in inherited cancer predisposition syndromes: evidence from a large real-world cohort.

Oral surgery, oral medicine, oral pathology and oral radiology
2025

Molecular and immune determinants of response in locally advanced deficient DNA mismatch repair/microsatellite instability-high gastric or gastroesophageal junction adenocarcinoma treated with neoadjuvant chemoimmunotherapy.

Cell communication and signaling : CCS
2025

Complex Relationships Between Homologous Recombination Deficiency (HRD) Score and Mutational Status of Homologous Recombination Repair (HRR) Genes in Prostate Carcinomas.

International journal of molecular sciences
2025

Tracking Cytopenias in FANCA-deficient Fanconi Anemia.

medRxiv : the preprint server for health sciences
2026

Genetic insights and diagnostic challenges in inherited bone marrow failure syndromes: a comprehensive study from a low middle-income country.

Expert review of hematology
2025

PanERBB CAR T-cells: Shifting gears toward a cure for fanconi anemia head/neck cancers.

Molecular therapy. Oncology
2025

A Population-Based Assessment of Cancer Risk in Children With VACTERL.

American journal of medical genetics. Part A
2025

Pan-cancer atlas analysis of FANCB and its potential mechanism in cholangiocarcinoma.

Discover oncology
2025

Diagnosis and Management of Fanconi Anemia.

Journal of evidence-based medicine
2025

Immunosuppression-Free Kidney Transplantation after Haploidentical Hematopoietic Stem Cell Transplantation in Fanconi Anemia.

Kidney international reports
2025

Ginsenoside Rh2 Suppresses the Fanconi Anemia Pathway by Inhibiting NF-κB-Mediated FANCL Transcription in Bladder Cancer.

Dose-response : a publication of International Hormesis Society
2026

Patient-derived xenograft models of Fanconi anemia-associated head and neck cancer identify personalized therapeutic strategies.

The Journal of clinical investigation
2025

Mechanisms of Acetaldehyde-Induced Organ Injury via Impairment of Vascular Endothelial Cells.

Vascular health and risk management
2026

A nuclear-targeted activity-based sensing probe for ratiometric imaging of formaldehyde reveals endogenous epigenetic contributors to the nuclear formaldehyde pool.

Chemical science
2026

Polygenic variants in DNA repair genes are associated with neurodevelopmental disorders, regression and increased burdens of somatic variants and short tandem repeat expansions.

Genetics in medicine : official journal of the American College of Medical Genetics
2025

Molecular biomarkers of sintilimab plus lenvatinib in hepatitis-B-virus-associated hepatocellular carcinoma.

World journal of hepatology
2025

Microporous structures on mineralized collagen mediate bone restoration by promoting nucleolin secretion to induce macrophage M2 polarization.

Regenerative biomaterials
2025

TSN Disrupts Fanconi Anemia Pathway Activation Through JAK/STAT1-Mediated Transcriptional Repression of FA Core Subunits in Bladder Cancer.

Dose-response : a publication of International Hormesis Society
2025

Recent advances in understanding the molecular mechanisms of SLX4 recruitment in the replication stress response.

DNA repair
2025

Defective Microhomology-Mediated End-joining in SMARCB1-Deficient Tumors.

bioRxiv : the preprint server for biology
2025

Managing acute myeloid leukemia in the context of sickle cell anemia and suspected Fanconi anemia in Tanzania: a case report.

Journal of medical case reports
2025

Metabolic reprogramming in Fanconi anemia: Evidence of compromised glucose oxidation, enhanced ketogenesis, and metabolic inflexibility.

Science advances
2025

Synergistic inhibition of CHK1 and MUS81 to combat replication stress resistance in high-risk neuroblastoma.

Scientific reports
2025

Piperine Targets the FANCL/UBE2T Complex to Inhibit the FA Pathway and Sensitize Bladder Cancer to Cisplatin.

Dose-response : a publication of International Hormesis Society
2025

A Deadly Duet: Fanconi Anemia (FA) With Head and Neck Cancer.

Cureus
2025

The Fanconi anemia pathway repairs colibactin-induced DNA interstrand cross-links.

Nature communications
2025

Genotoxic formaldehyde and lipid aldehydes are sources of DNA damage in keratinocytes.

bioRxiv : the preprint server for biology
2025

Ferroptosis and cancer: when iron turns against tumors.

Cellular and molecular life sciences : CMLS
2025

ATM promotes reversed fork processing during DNA interstrand cross-link repair.

bioRxiv : the preprint server for biology
2025

Loss of CFIm activates YAP/TAZ and connects mRNA cleavage and polyadenylation inhibition to BRCAness.

bioRxiv : the preprint server for biology
2026

Increased Vascular Age in Patients with Fanconi Anemia after Hematopoietic Cell Transplantation: Results of a Single-Center Descriptive Analysis.

Transplantation and cellular therapy
2026

Fancl-mutant mice reveal central role of monoubiquitination in Fanconi anemia and a model for therapeutic gene editing.

Blood advances
2026

The NuRD chromatin remodeling complex contributes to repairing exogenous double-strand breaks in the Caenorhabditis elegans germline.

Genetics
2026

DNA Methylation Episignature as a Novel Diagnostic Tool for Diamond-Blackfan Anemia Syndrome.

American journal of hematology
2026

Timeless prevents senescence-associated phenotypes and enhances DNA repair to promote esophageal cancer cell growth.

Experimental cell research
2025

MCM8/9 and FANCD2 interact within a shared pathway in response to replication stress caused by DNA crosslinks.

DNA repair
2025

The crucial role of circadian synchronization in bone marrow adipose tissue mesenchymal stem cells: insights into pathogenesis in Fanconi anemia and acute myeloid leukemia.

Molecular biology reports
2026

Generation of functional noncanonical donor splice sites by +2T variants in breast cancer susceptibility genes: impact on clinical interpretation.

The Journal of pathology
2026

Cryo-electron microscopic visualization of RAD51 filament assembly and end-capping by XRCC3-RAD51C-RAD51D-XRCC2.

Science (New York, N.Y.)
2025

Loss of Fanconi anemia proteins causes a reliance on lysosomal exocytosis.

Cell death &amp; disease
2025

BACH1 promotes hepatocellular carcinoma progression by targeting PDP1 towards the PI3K-AKT-mTOR signaling activation.

Bioorganic chemistry
2025

BRCA1-, BRCA2-, and PALB2-related Fanconi anemia: Scope to expand disease phenotypic features and predict breast cancer risk in heterozygotes.

American journal of human genetics
2025

A porcine model of Fanconi anemia.

PloS one
2026

Lnk deficiency enhances translesion synthesis to alleviate replication stress and promote hematopoietic stem cell fitness.

The Journal of clinical investigation
2025

Beyond Hematologic Malignancies: Colorectal Cancer as a Solid Tumor Manifestation of Inherited Bone Marrow Failure Syndromes.

International journal of molecular sciences
2025

Red Blood Cell Antioxidant State in Fanconi Anemia: The Highlighted Roles of Pi-Class Glutathione S-Transferase and Glutathione Peroxidase.

Antioxidants (Basel, Switzerland)
2025

Lentiviral-mediated panErbB CAR-T cell therapy against head and neck squamous cell carcinomas for patients with Fanconi anemia.

Molecular therapy. Oncology
2025

Ubiquitin and SUMO pathways in DNA replication and replication-coupled repair.

Critical reviews in biochemistry and molecular biology
2025

Mutagenesis of the PALB2 WD40 domain identifies variants defective in interaction with BRCA2 and DNA repair.

The Journal of biological chemistry
2025

Infectious complications in pediatric acute lymphoblastic leukemia treatment: A comparison of ALL-IC BFM 2009 vs. modified St. Jude total XV in a single-center retrospective cohort study.

Leukemia research
2025

Outcome of immunosuppressive therapy in pediatric patients with acquired aplastic anemia.

Journal of family medicine and primary care
2025

Ending diagnostic odyssey by reanalysis of whole exome sequencing data: reclassification of suspected Fanconi anemia cases to dyskeratosis congenita and Diamond-Blackfan anemia.

Orphanet journal of rare diseases
2025

Research Communication: Prevalence of Asymptomatic Premalignant Oesophageal Lesions in Patients With Fanconi Anaemia.

Alimentary pharmacology &amp; therapeutics
2025

Areas of Uncertainty in Pancreatic Cancer Surveillance: A Survey Across the International Pancreatic Cancer Early Detection (PRECEDE) Consortium.

JCO precision oncology
2025

Management of individuals with heterozygous germline pathogenic variants in RAD51C, RAD51D, and BRIP1: A clinical practice resource of the American College of Medical Genetics and Genomics (ACMG).

Genetics in medicine : official journal of the American College of Medical Genetics
2025

Pathogenic Variants, Family History, and Cumulative Risk of Breast Cancer in US Women.

JAMA oncology
2025

Dynamics of Fanconi anemia protein D2 in association with nuclear lipid droplet formation.

Journal of cell science
2025

DNA repair helicases: from mechanistic understanding to therapeutic implications.

NAR cancer
2025

Global Neurocognitive and Emotional Dysfunction in Fanconi Anemia: A Neuropsychological Case Report of a 39-Year-Old Patient.

Case reports in neurological medicine
2025

Emergence of PALB2 Reversion Mutations as a Mechanism of Resistance to Niraparib in Breast Cancer: A Case Report.

Cancer science
2025

A case of ADH5/ALDH2 deficiency combined with 3q29 microduplication syndrome.

BMC pediatrics
2025

The TONSL-MMS22L complex and FANCM form an interdependent complex on chromatin to counter replication stress.

bioRxiv : the preprint server for biology
2025

Editor's Note: Werner Syndrome Helicase Has a Critical Role in DNA Damage Responses in the Absence of a Functional Fanconi Anemia Pathway.

Cancer research
2025

LncRNA LOXL1-AS1 promotes ovarian cancer progression by enhanced BRIP1 mRNA stability.

Medical oncology (Northwood, London, England)
2026

RAD51 -Related Fanconi Anemia: Expanding the Phenotypic Spectrum and Strong Association With VACTERL.

Clinical genetics
2025

Mechanistic insights into alcohol-induced DNA crosslink repair by Slx4-Xpf-Ercc1 nuclease complex in the Fanconi anaemia pathway.

Communications biology
2025

EXO1 as a therapeutic target for Fanconi Anaemia, ZRSR2 and BRCA1-A complex deficient cancers.

Nature communications
2025

Sellar Metastatic Follicular Thyroid Carcinoma With Novel Mutations Clinically Mimicking Pituitary Macroadenoma: Intraoperative Frozen Section Diagnosis Challenges.

Anticancer research
2025

[Hereditary genetic testing and its application in the diagnosis, treatment, and prevention of breast cancer].

Magyar onkologia
2025

LINE-1 Retroelement Activation and Neuroinflammation in Persons With Fanconi Anemia.

Pediatric blood &amp; cancer
2026

Uptake of Risk Reducing Mastectomy in Older BRCA1/2 and PALB2 Carriers Undergoing Genetic Testing after 60 Years of Age.

Annals of surgical oncology
2025

Complete remission with olaparib in BRIP1-mutated metastatic high-grade pleomorphic sarcoma: case study and literature review - an example of a genomic profiling-based tumor treatment, in a cancer type with high unmet clinical need.

Acta oncologica (Stockholm, Sweden)
2025

DNA polymerase kappa is the primary translesion synthesis polymerase for aldehyde ICLs.

Nucleic acids research
2025

Insights in bone marrow failure syndromes: take home messages from the 3rd ESH-EBMT-EHA-IPIG translational research conference.

Bone marrow transplantation
2025

Head and Neck Cancer in Fanconi Anemia: Clinical Challenges and Molecular Insights into a DNA Repair Disorder.

Cancers
2025

Specifications of the ACMG/AMP variant curation guidelines for the analysis of germline PALB2 sequence variants.

American journal of human genetics
2025

Targeting BACH1 by HPPE inhibits the Wnt/β-catenin pathway and malignant phenotype in glioblastoma cells.

Apoptosis : an international journal on programmed cell death
2025

Epithelial competition determines gene therapy potential to suppress Fanconi Anemia oral cancer risk.

PLoS computational biology
2025

Integrated single-cell and spatial transcriptomics uncover the prognostic, epigenetic, and immunological roles of FANCC in low-grade glioma.

Neurological research
2025

Heterozygous Germline Fanconi Anemia-Related Gene Mutations Increase Susceptibility to Germ Cell Tumors.

JCO precision oncology
2025

Prevalence of germline pathogenic variants in 779 patients with metastatic prostate cancer.

BJU international
2025

8-Oxoguanine Disrupts G-Quadruplex DNA Stability and Modulates FANCJ AKKQ Peptide Binding.

Molecules (Basel, Switzerland)
2025

Impact of Incidental Germline BRCA1/2 and PALB2 Alterations on EGFR Monotherapy Real-World Outcomes for Patients With Advanced Non-Small-Cell Lung Cancer.

Clinical lung cancer
2025

Insights into Fanconi Anemia Based on Molecular and Clinical Characteristics: A Multicentre Study of 13 Patients.

Children (Basel, Switzerland)
2025

Opening of a phase Ib/II study to investigate the safety and efficacy of Afatinib in patients with Fanconi anemia and unresectable locally advanced or metastatic head and neck squamous cell carcinoma.

BMC cancer
2025

Prevalence of Incidental Breast Cancer and Precursor Lesions in Carriers of Pathogenic Germline Variants Undergoing Risk-Reducing Mastectomy.

Anticancer research
2025

SLFN11, far from being limited to responding to cancer DNA damage.

Clinical and experimental medicine
2025

Case Report: Eltrombopag in mosaic and gene therapy-treated patients with Fanconi anemia.

Frontiers in pediatrics
2025

Whole exome sequencing identifies FANCM as a susceptibility gene for estrogen-receptor-negative breast cancer in Hispanic/Latina women.

Nature communications
2025

G-quadruplexes as a source of vulnerability in BRCA2-deficient granule cell progenitors and medulloblastoma.

Proceedings of the National Academy of Sciences of the United States of America
2025

Potential role of Fanconi anemia pathway in the pathogenesis of endometrial cancer (Review).

Molecular medicine reports
2025

The haplotype-resolved chromosome-level genome assembly of Spinibarbus caldwelli provides insights into environmental adaptability and disease resistance.

Comparative biochemistry and physiology. Part D, Genomics &amp; proteomics
2026

BRCA1 and BRCA2 gene expression: p53- and cell cycle-dependent repression requires RB and DREAM.

Cell death and differentiation
2025

GEN1 regulates cell proliferation, migration, apoptosis and ferroptosis in gastric cancer.

World journal of gastrointestinal oncology
2025

Homozygous FANCM Variant c.5101C>T p.(Gln1701*) in a Patient With Early Onset Breast Cancer, Chemotherapy Toxicity, and Chromosome Fragility: A Case Report.

Cancer reports (Hoboken, N.J.)
2025

Identification of hypoxia-related diagnostic biomarkers and immune signatures in diminished ovarian reserve.

Frontiers in genetics
2025

Homologous Repair-Deficient Pancreatic Cancer: Refined Targeting of DNA Damage Response is an Effective Therapeutic Strategy.

United European gastroenterology journal
2025

A rescue fanconi anemia humanized mouse model with endogenous FA mutation and high human hematopoietic stem cell chimerism.

Molecular therapy. Methods &amp; clinical development
2025

Genotype-phenotype correlations in biallelic carriers of FANCM protein truncating variants: A systematic literature review.

Mutation research. Reviews in mutation research
2025

53BP1 regulates p53-E2F7-dependent transcriptional gene repression and participates in the Fanconi anemia pathway.

Cell reports
2025

The Fanconi Anemia Pathway Inhibits mTOR Signaling and Prevents Accelerated Translation in Head and Neck Cancer Cells.

Cancers
2025

The Impact of DDR Gene Mutations on the Efficacy of Etoposide Plus Cisplatin in Grade 3 Metastatic Gastroenteropancreatic (GEP)-Neuroendocrine Carcinoma (NEC).

Cancers
2025

Emerging drivers of DNA repeat expansions.

Biochemical Society transactions
2025

MR Promotes Ferroptosis in Gastric Cancer by Regulating FANCD2 Expression Mediated by m6A Modification.

Applied biochemistry and biotechnology
2025

Comprehensive Bioinformatics Analysis Reveals Associations between the DNA Damage Response and Osteoarthritis.

Gerontology
2025

Exploration of possible association of BRIP1 pathogenic variants with central nervous system cancers in an institutional cohort.

Journal of medical genetics
2025

Oral Verruciform Xanthoma as a Manifestation of Chronic Graft-Versus-Host Disease in Fanconi Anemia: A Rare Case Report.

Special care in dentistry : official publication of the American Association of Hospital Dentists, the Academy of Dentistry for the Handicapped, and the American Society for Geriatric Dentistry
2025

Exploring the aftermath of hematopoietic cell transplantation: 18-year insights into post-transplant neoplasms.

Frontiers in oncology
2026

Pathogenic Variants in Mennonites From Southern Brazil: Implications for Preventive Measures in Public Health.

Clinical genetics
2025

CRISPR-Cas9: a prominent genome editing tool in the management of inherited blood disorders and hematological malignancies.

Current research in translational medicine
2026

"I would love to talk to someone that actually understands": Psychosocial experiences of adults with Fanconi anemia.

Journal of health psychology
2025

RBM39 silence suppresses esophageal cancer proliferation and metastasis via FANCD2 mRNA destabilization.

Cellular signalling
2025

PALB2 c.3106G>C (p.Val1036Leu) in a familial cancer setting suggesting potential pathogenicity.

BMJ case reports
2025

PALB2 and 53BP1 govern post-resection homologous recombination DNA repair.

Molecular cell
2025

Genetic landscape of Pakistani familial breast cancer patients using multigene panel testing.

International journal of cancer
2025

Comprehensive review on Fanconi anemia: insights into DNA interstrand cross-links, repair pathways, and associated tumors.

Orphanet journal of rare diseases
2025

PALB2 mutations increase oncogenic properties of breast epithelial cells by enhancing JAM3 and PARVB expression.

Biochemical and biophysical research communications
2025

Alu-mediated FANCD2 exonic deletion contributes to Fanconi anaemia.

British journal of haematology
2025

BRCA2 Pre-mRNA Differential 5' Splicing: A Rescue of Functional Protein Properties from Pathogenic Gene Variants and a Lifeline for Fanconi Anemia D1 Patients.

International journal of molecular sciences
2025

Identification of a BACH1 lung cancer signature: A novel tool for understanding BACH1 biology and identifying new inhibitors.

Redox biology
2025

NSUN5 Mediates Resistance to Doxorubicin via Up-regulation of DNA Damage Repair Proteins BRCA2 and BRIP1 in Colorectal Cancer.

The American journal of pathology
2025

Hematopoietic Stem Cell Transplant in Adult Patients with Fanconi Anemia: A Review.

Diseases (Basel, Switzerland)
2025

Enhanced sensitivity, robust p21 activation, and sustained DNA repair responses to interstrand crosslinks in elephant cells compared to humans.

Frontiers in veterinary science
2025

Novel trispecific killer engager targeting B7-H3 enhances natural killer cell antitumor activity against head and neck cancer.

Journal for immunotherapy of cancer
2025

Irradiation- and busulfan-free stem cell transplantation in Fanconi anemia using an anti-CD117 antibody: a phase 1b trial.

Nature medicine
2025

Multi-omics Characterization of Acquired Olaparib Resistance in BRCA1 and BRCA2 Mutant Breast Cancer Cell Lines.

Molecular &amp; cellular proteomics : MCP
2025

Eltrombopag for Bone Marrow Failure in Fanconi Anemia: Results From the Phase II Clinical Trial FANCREV.

European journal of haematology
2025

Skin Signals: Exploring the Intersection of Cancer Predisposition Syndromes and Dermatological Manifestations.

International journal of molecular sciences
2025

Expanding the Genomic Landscape of HBOC and Cancer Risk Among Mutation Carriers.

International journal of molecular sciences
2025

Recessive FANCM cancer syndrome with high cancer risks, chemotherapy toxicity, chromosome fragility, and gonadal failure.

Genetics in medicine : official journal of the American College of Medical Genetics
2025

Identification of FANCG as a prognostic factor for prostate cancer.

European journal of medical research
2025

Role and mechanism of RPA1 in the development and progression of glioma.

Experimental and therapeutic medicine
2025

Environmental arsenic hijacks DDX5-mediated FANCA splicing to impair R-loops resolution and drive ovarian aging.

Ecotoxicology and environmental safety
2025

RAD51 and PALB2 in precision oncology: Clinical implications for HRD associated breast and ovarian cancers (Review).

International journal of oncology
2025

[Family history of breast cancer - Genetic screening and risk-based surveillance].

Bulletin du cancer
2025

Association of TGF-β1 -509 C > T (rs1800469) polymorphism with bone marrow failure severity in Fanconi anemia subjects.

Molecular biology reports
2025

Assessing germline mutational profile and its clinicopathological associations in Triple Negative Breast Cancer.

Cancer genetics
2025

Analysis of BRCA1, BRCA2 and PALB2 related Fanconi anemia identifies scope to expand disease phenotypic features and predict breast cancer risk in heterozygotes.

medRxiv : the preprint server for health sciences
2025

Disruption of Microhomology-mediated End-joining in Ewing Sarcoma.

bioRxiv : the preprint server for biology
2025

miR-29a-3p and TGF-β Axis in Fanconi anemia: mechanisms driving metabolic dysfunction and genome stability.

Cellular and molecular life sciences : CMLS
2025

Development of translational read-through-inducing drugs as novel therapeutic options for patients with Fanconi anemia.

Cell death discovery
2025

ALDH9A1 deficiency as a source of endogenous DNA damage that requires repair by the Fanconi anemia pathway.

The Journal of cell biology
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Referências e fontes

Bases de dados externas citadas neste artigo

Publicações científicas

Artigos indexados no PubMed ligados a esta doença no grafo RarasNet — título, periódico e PMID direto da fonte, sem intermediação de IA.

  1. Metabolite-induced DNA damage drives stochastic stem cell loss and clonal hematopoiesis.
    Cell stem cell· 2026· PMID 41875892mais citado
  2. Deficiencies in the Fanconi anemia or homologous recombination pathway enhance the antitumor effects of the hypoxia-activated prodrug CP-506.
    Molecular therapy. Oncology· 2026· PMID 41859007mais citado
  3. Towards evolutionary guided precision medicine of acute myeloid leukemia and Fanconi anemia associated bone marrow failure.
    Stem cells translational medicine· 2026· PMID 41814545mais citado
  4. Beyond readthrough: ataluren restores mitochondrial function and reduces oxidative stress in FANCA-mutated cells via mTOR-DRP1 modulation.
    Cell death discovery· 2026· PMID 41764196mais citado
  5. Differential genetic analysis of ectrodactyly in a Fanconi anemia pedigree with FANCA mutations.
    MedScience· 2026· PMID 41733882mais citado
  6. Efficacy and safety of gene therapy in pediatric patients with Fanconi anemia: a systematic review.
    An Pediatr (Engl Ed)· 2026· PMID 41991439recente
  7. PRMT5 inhibition impairs Fanconi Anemia pathway-mediated homologous recombination and enhances the antitumor efficacy of Temozolomide in glioblastoma.
    Cell Death Dis· 2026· PMID 41986321recente
  8. Allogeneic CD56(+) cell-based immunotherapy in a patient with Fanconi anemia developing acute myeloid leukemia.
    J Cancer Res Clin Oncol· 2026· PMID 41920213recente
  9. The landscape and regulatory potential of eccDNAs in mammalian preimplantation embryos.
    Nat Commun· 2026· PMID 41917015recente
  10. Functional Germline DNA Repair Mutations as Predictors of Acute Radiodermatitis in Breast Cancer.
    Diagnostics (Basel)· 2026· PMID 41897566recente

Bases de dados e fontes oficiais

Identificadores e referências canônicas usadas para montar este verbete.

  1. ORPHA:84(Orphanet)
  2. MONDO:0019391(MONDO)
  3. GARD:6425(GARD (NIH))
  4. Variantes catalogadas(ClinVar)
  5. Busca completa no PubMed(PubMed)
  6. Artigo Wikipedia(Wikipedia)
  7. Q845779(Wikidata)

Dados compilados pelo RarasNet a partir de fontes abertas (Orphanet, OMIM, MONDO, PubMed/EuropePMC, ClinicalTrials.gov, DATASUS, PCDT/MS). Este conteúdo é informativo e não substitui avaliação médica.

Conteúdo mantido por Agente Raras · Médicos e pesquisadores podem colaborar

Anemia de Fanconi
Compêndio · Raras BR

Anemia de Fanconi

ORPHA:84 · MONDO:0019391
Prevalência
1-9 / 100 000
Herança
Autosomal recessive, X-linked recessive
CID-10
D61.0 · Anemia aplástica constitucional
CID-11
Ensaios
19 ativos
Medicamentos
2 registrados
Início
Childhood
Prevalência
3.3 (Specific population)
MedGen
UMLS
C0015625
Repurposing
11 candidatos
azacitidineDNA methyltransferase inhibitor
cyanocobalaminmethylmalonyl CoA mutase stimulant|vitamin B
decitabineglucocorticoid receptor agonist
+8 outros
EuropePMC
Wikidata
Wikipedia
Papers 10a
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