Epithelial ovarian tumors risk factors

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Hannan Javed, M.D.[2]

Overview

Epithelial ovarian tumors can have multiple risk factors. Genetic risk factors constitute a major proportion of all the associated risk factors.

Risk Factors

Genetic Risk Factors

BRCA Mutations and Hereditary Breast and Ovarian Cancer (HBOC)

  • Hereditary breast and ovarian cancer (HBOC) is an autosomal dominant disorder caused by mutations in BRCA1 and BRCA2 genes that are responsible for DNA repair in homologous recombination pathway.[1][2]
  • Individuals with this disorder are at risk of developing breast (lifetime risk is 30-80%) and ovarian cancer (lifetime risk is 30-50%), along with other malignancies such as pancreatic, stomach, laryngeal, fallopian tube and prostate cancer.[1][2]
  • The reason for increased susceptibility to ovarian and epithelial cancer is not fully understood but but may be explained by repression of the transcription of hormone-mediated signalling factors or production of reactive oxygen species during menstrual cycle mediating DNA damage.[2][3][4]

Mismatch Repair Genes and Lynch Syndrome

  • Lynch syndrome (LS), also known as hereditary nonpolyposis colon cancer (HNPCC), is characterized by germline mutations in DNA mismatch repair genes MLH1, MSH2, MSH6, MLH3, and PMS2.[1][5][6]
  • A simplified version of repair mechanism by mismatch repair genes products is described below:[6][7]

MutS Homologs (MSHs) Recognize the DNA Mismatch → MutS Homologs (MSHs) Recruit MutL Homologs (MLHs) → Excision of Mismatched DNA → DNA Polymerase Re-synthesizes DNA

  • Accounted for 10-15% of all ovarian cancers, this syndrome is caused by inherited mutation in one allele and then loss of second allele (secondary hit).[1][8]
  • The most common malignancies in Lynch syndrome are colorectal carcinoma and gynecological cancers, endometrial carcinoma being the most common among gynecological malignancies followed by ovarian carcinoma.[8]
  • Other malignancies that have been observed in lynch syndrome are gastric cancer, small bowel malignancies, hepatobiliary epithelial carcinoma, uroepithelial epithelial carcinoma and brain tumors.[8][9]

TP53 Mutation and Li-Fraumeni Syndrome

  • Li-Fraumeni Syndrome is an autosomal dominant disorder caused by germline mutation in TP53, the most mutated gene in human cancers. The most common of the mutations are missense mutations.[10][11]
  • TP53 encodes for a transcription factor that responds to various cell signals and is a major regulator of the cell cycle. It is involved in variety of cellular functions such as cellular proliferation and cell cycle, apoptosis, and stability & integrity of the genome.[12][11]
  • * Mutations in TP53 resulting defective or decreased p53 are not only implicated in pathogenesis but also impact prognosis, causing worse survival rate among the individuals with the mutations.[12][13]
  • These mutations are most commonly observed in epithelial ovarian cancer (47%), colorectal carcinoma (43%), head/neck cancer (42%), and esophageal cancer (41%). Breast cancer, sarcoma and brain, and adrenocortical carcinoma account for majority of the tumors encountered in Li-Fraumeni syndrome.[12][14]

PTEN Mutations and Cowden Syndrome

  • An autosomal-dominant syndrome , caused by mutations in PTEN gene, has been associated with a variety of neoplastic/non-neoplastic lesions and clinical manifestations throughout the body including:[15][16][17]
  • Epithelial ovarian cancer
  • Hamartomatous lesions of skin and organs
  • Macrocephaly
  • Breast cancer
  • Thyroid cancer
  • Endometrial cancer

RAD51 Mutations

  • RAD51 is a recombinase that binds with eight BRC repeats of BRCA2. This allows RAD51 to be recruited to double stranded DNA breaks, an essential step in homologous recombination double stranded DNA repair.[2][18][19][10]
  • Some studies have suggested risk for developing ovarian cancer in RAD51 mutations is as high as six-fold. There is also an increased risk for developing breast cancer.[10][20][21]

PALB2 Mutations

  • Partner and localizer of BRCA2 (PALB2) physically connects BRCA1 and BRCA2 through N-terminal coiled-coil domain and the C terminus. This BRCA2 interacting protein plays an essential role in DNA repair.[2][22][23]
  • The association of PALB2 with ovarian cancer has not be fully established but an increased risk for breast cancer, pancreatic cancer and ovarian cancer has been observed in some studies..[5][24][25]

CHEK2 Mutations

  • CHEK2 gene encodes for a protein called checkpoint kinase 2 (CHK2). It interacts with other regulators and tumor suppressors such as TP53 to play a role in tumor suppression through cell-cycle regulation and apoptosis.
  • There are conflicting results regarding association of CHEK2 with ovarian cancers. Some studies have suggested no association but the limitations were observed because of focus on only certain allelic mutations in CHEK2.

Mre11 Complex Alterations

  • Mre11 Complex is involved in DNA repair and comprises of meiotic recombination 11 (MRE11), RAD50 and Nijmegen breakage syndrome 1 (NBS1; also known as nibrin).
  • This complex plays an essential role in homologous recombination mediated DNA repair, non-homologous end-joining (NHEJ) and alternative non-homologous end-joining (A-NHEJ) pathways, all involved in double stranded DNA repair.
  • Some studies have suggested an increased susceptibility to ovarian and breast cancers in hereditary mutations in Mre11 complex.

BARD1 Mutations

  • This gene encodes for a peptide that interacts with BRCA1 and forms a heterodiamer that plays a role in homologous recombination mediated repair of double stranded DNA breaks.
  • Mutations in BARD1 have been associated with breast and ovarian cancer.

BRIP1 Mutations

  • BRCA1-interacting protein 1 (BRIP1) encodes for a helicase that interacts with BRCA1 in homologous recombination mediated repair of double stranded DNA breaks.
  • Mutation in BRIP1 gene association with familial ovarian cancer have been demonstrated in some studies. There also been proposed risk for breast cancer but it has yet to be established
Possible Genetic Alteration In Epithelial Ovarian Cancers
Protein Normal Function Function in Malignancy
Human Epidermal growth factor receptor (HER-1)[26][27]
  • Promotes cell proliferation
  • Opposes apoptosis
  • Regulates differentiation
  • Activating mutation
  • Increased cellular proliferation
  • Inhibition of apoptosis
Human Epidermal Growth Factor Receptor 2 (HER-2)[26][27]
  • Promotes cell prolifeartion
  • Inhibition of apoptosis
  • Regulates differentiation
  • Activating mutation
  • Increased cellular proliferation
  • Inhibition of apoptosis
Non-receptor tyrosine kinase Src[28][29] Involved in regulation of:
  • Gene transcription
  • Angiogenesis
  • Cellular adhesion
  • Cellular proliferation
  • Activating mutation
  • Increased angiogenesis
  • Decreased cellular adhesion
  • Increased tumor metastasis
  • Increased cellular proliferation
Colony stimulating factor-1/fms[30][31][32]
  • Increased macrophage survival
  • Increased macrophage proliferation
  • Increased macrophage differentiation
  • Activating mutation
  • Stimulation of tumor cell proliferation
  • Increased angiogenesis
  • Promotes tumor invasion
  • Increased metastasis
  • Decreased anoikis
Insulin-like growth factor/receptor ILGF/ILGFR[33][34][35]
  • Promotes growth
  • Increased survival
  • Activating mutation
  • Increased proliferation
  • Enhanced survival
  • Suppression of cell cycle regulators
k-ras[36][37]
  • Cellular proliferation
  • Cell survival
  • Activating mutation
  • Increased proliferation
  • Enhanced survival
b-raf[38][39]
  • Cellular proliferation
  • Cellular differentiation
  • Activating mutation
  • Increased proliferation
  • Enhanced growth
Transforming growth factor-β[40][41][42]
  • May function as a tumor suppressor and a promoter
  • Promotes growth arrest
  • Maintains cellular homeostasis
  • Increased proliferation
  • Decreased apoptosis
  • Epithelial-to-mesenchymal transition
  • Sustained angiogenesis
  • Evasion of immune surveillance
  • Metastasis
myc[43][44][45]
  • Derives cellular proliferation
  • Increased growth
  • Cell-cycle mediator
  • Inhibits apoptosis
  • Stem-cell renewal
  • Activating mutation
  • Increased proliferation
  • Decreased apoptosis
  • Increased metabolism in tumor cells
Cyclin D/Cdk4/6[46][47][48]
  • Cell-cycle mediator
  • Controls G1 length
  • Activating mutation
  • Decreased G1 length
  • Increased proliferation
  • Increased angiogenesis
Cyclin E/Cdk2[49][50][51]
  • Cellular proliferation
  • Cell-cycle mediator
  • Assembly of the pre-replication complex
  • Promotes G0 to cell cycle entry
  • Promotes G1 to S phase transition
  • Decreased apoptosis
  • Activating mutation
  • Increased cellular proliferation
  • Impaired apoptosis
  • Increased cellular survival
Cyclin B/Cdk1[52][53][54]
  • Cell-cycle mediator
  • Promotes G2 to M phase transition
  • Activating mutation
  • Increased cellular proliferation
  • Promotes malignant transformation
p16[55][56][57]
  • Member of the INK4 family of CDK inhibitors
  • Inhibits Cyclin D/Cdk4/6
  • Decreased G1 to S phase transition
  • Lost or downregulated
  • Decreased G1 length
  • Increased proliferation
  • Increased angiogenesis
p27 (kip-1)[58][59][60]
  • Inhibitor of Cyclin E/Cdk2
  • Mediates cell cycle arrest
  • Decreased G1 to S phase transition
  • May act as oncogen and promote proliferation
  • Lost or dysregulated
  • Increase in cell proliferation
  • Impaired apoptosis
p21 (WAF-1)[61][62][63]
  • Inhibits cyclin-dependant kinases
  • Cell-cycle arrest
  • Decreased proliferation
  • Promotes cellular differentiation
  • May inhibit/promote apoptosis
  • May act as oncogen and promote proliferation
  • Lost or dysregulated
  • Increase in cell proliferation
  • Decreased cellular differentiation
  • Decreased apoptosis
  • Correlates positively
    • Tumor grade
    • Invasiveness
    • Aggressiveness
Nuclear factor-κB[64][65][66]
  • A transcription factor involved in regulation of
    • Immune response to inflammation
    • Expression of cytokines, chemokines, and adhesion molecules
    • Cell cycle
    • Apoptosis
  • May function as a tumor suppressor and a promoter
  • Dysregulated
  • Increased angiogenesis
  • Enhanced tumor growth
  • Induces resistance to chemotherapy by acting as anti-apoptosis
NOEY(ARHI)[67][68][69][70]
  • Inhibits cell growth
  • Induces apoptosis
  • Inhibits tumor cells migration through chemotaxis and haptotaxis
  • Inactivating mutation
  • Enhanced tumor growth
  • Decreased apoptosis
  • Increased chances for metastasis
PIP3/Akt[71][72]
  • Akt is activated by PIP3 and plays a role in:
    • Regulation of cellular growth
    • Cell cycle progression
    • Regulation of glucose metabolism
    • Genome stability
    • Gene transcription
    • Protein synthesis
    • Neovascularization
    • Promotes cell survival by blocking apoptosis
  • Activating mutations
  • Increased cellular proliferation
  • Increased tumor cells survival
  • Increased tumor cells migration
  • Increased tumor cells invasion
  • Chemotherapy resistance
  • Decreased apoptosis
  • May promote angiogenesis
PTEN[73][74][75]
  • Suppresses Akt and thus regulates cell cycle, cellular growth and apoptosis
  • Regulates self-renewal and differentiation of human stem cells
  • Regulates oocyte growth and follicular activation
  • Regulates chemotaxis of neutrophils
  • Inhibit cell invasion and migration
  • Deletion or inactivating mutation
  • Increased cellular proliferation
  • Increased tumor cells survival
  • Increased tumor cells migration
  • Increased tumor cells invasion
  • Decreased apoptosis
p53[76][77][78]
  • A transcription factor that:
    • Regulates cell cycle
    • Promotes DNA damage repair
    • Promotes apoptosis
    • Maintains genomic integrity
  • Loss results in:
    • DNA damage and carcinogenesis
    • Increased tumor cell growth and survival
    • Increased metastasis
    • Decreased apoptosis
    • Resistance to chemotherapy
BRCA1[2][79][80]
  • A tumor suppressor that mediates double stranded DNA repair through
    • Homologous recombination pathway
    • Non-homologous end joining pathway
  • Activates checkpoints in cell cycle
  • Maintains genomic integrity
  • Mutations are responsible for hereditary breast & ovarian tumors
  • Loss results in
    • DNA damage and carcinogenesis
    • Increased tumor cell growth and survival
BRCA2[2][79][80]
  • A tumor suppressor that mediates double stranded DNA repair through
    • Homologous recombination pathway
  • Maintains genomic integrity
  • Protects replication fork and replication fidelity
  • Mutations are responsible for hereditary breast & ovarian tumors
  • Loss results in
    • DNA damage and carcinogenesis
    • increased tumor cell growth and survival
  • Defects in maintenance the length of the nascent strand of DNA
MLH1/MSH2[81][82][83]
  • Tumor suppressors that
  • Mediates DNA damage repair
  • Maintains genomic integrity
  • Possible regulation of cell cycle
  • Loss results in:
    • DNA damage and carcinogenesis
    • Increased survival
    • Resistance to chemotherapy
    • Chromosomal instability
    • Microsatellite instability (MSI)
    • The cytosine phosphate guanine (CpG) island methylator phenotype (CIMP)
Fas ligand[84][85][86]
  • Binds to Fas receptor and induces apoptosis
  • Expressed mainly on T-lymphocytes
  • May induce apoptosis in cancer cells and virus infected cells
  • May also be involved in
    • Liver regeneration following partial hepatectomy
    • Neurite outgrowth
  • Most tumor cells are resistant to Fas-FasL mediated apoptosis
  • Tumor cells express FasL to induce apoptosis in cytotoxic lymphocytes
  • Promotes tumor cells survival
  • Enhances tumor cells invasion
  • Increased tumor cells migration
Human leukocyte antigen-G[87][88][89]
  • Inhibits T-cell function through
    • Inhibiting proliferation
    • Causing cytotoxicity
    • Inducing apoptosis
    • Cytokine production in B lymphocytes
    • Inhibiting differentiation
  • Inhibits proliferation and cytotoxicity of natural killer cells
  • Promotes angiogenesis
  • Inhibits chemotaxis
  • Promotes progression of cancer through evasion of immune response by
    • Inhibiting T-cell functions by inducing apoptosis and decreased proliferation
    • Inhibiting T-cell differentiation through various mechanisms
  • Inhibits proliferation and cytotoxicity of natural killer cells
  • Promotes angiogenesis
  • Inhibits chemotaxis of cytotoxic cells
hTERT[90][91][92]
  • Maintains telomeres length
  • Promotes replication
  • Up-regulated in majority of human cancers
  • Provides limitless replication ability to cancer cells
Vascular endothelial growth factor/Vascular endothelial

growth factor receptor[93][94][95]

  • Stimulates angiogenesis through
    • increased endothelial cell survival
    • Increased endothelial cell proliferation
    • increased endothelial cell migration
  • Increases vascular permeability
  • May regulate fibroblasts in the stroma of tumors
  • May effect tumor stem cells
  • Promotes angiogenesis
  • Promotes tumor cells growth
  • May initiate carcinogenesis
  • Promotes invasion and metastasis of tumor cells
Interleukin-8[96][97][98]
  • Chemokine produced to recruit leukocytes and myeloid-derived suppressor cells
  • Promotes epithelial-to-mesenchymal transition
  • Promotes infection resolution
  • Promotes angiogenesis
  • Promotes epithelial-to-mesenchymal transition in tumor cells
  • Promotes resistance to chemotherapy
  • Tumor progression through immunosuppressive and pro-tumorigenic immune cells
  • Promotes angiogenesis
  • Promotes invasion and metastasis
EphA2[99][100][101]
  • Promotes angiogenesis
  • Plays a key role in development of
    • Lens
    • Inner ear
    • Mammary glands
  • Promotes kidney repair following injury
  • Promotes bone remodeling bone remodeling
  • Over-expressed in ovarian epithelial cancer
  • Promotes tumor initiation
  • Promotes neo-vascularization
  • Promotes tumor invasion
  • Promotes metastasis
Matrix metalloproteinases[102][103][104]
  • Proteases that degrade tissues, matrix and other proteins and play a role in
    • Bone modeling and remodeling
    • Mammary development
    • Blood vessels remodeling
    • A variety of other tissues such as tracheal tube
  • Promotes inflammation through enzymatic activation
  • Over-expressed in ovarian epithelial cancer
  • Promotes tumor invasion through degradation of extra-cellular matrix
  • Promotes metastasis through degradation of extra-cellular matrix
  • May have a role in tumor initiation and angiogenesis
αvβ3[105][106][107]
  • One of the most important mediator of angiogenesis
  • Promotes smooth muscle cells migration and proliferation
  • Promotes angiogenesis
  • Promotes survival
Focal adhesion kinase (FAK)[108][109][110]
  • Promotes endothelial cells migration
  • May play a role in integrin-dependent cell survival signal
  • Inhibits apoptosis
  • Enhances cell motility
  • Promotes angiogenesis
  • Promotes tumor cells survival
  • Inhibits apoptosis
  • Promotes tumor metastasis
E-cadherin[111][112][113]
  • One of the most important promoter of cell-cell adhesion
  • Play critical role in formation and maintenance of epithelia, and tissue formation
  • Loss or mutations results in:
    • Epithelial–mesenchymal transition
    • Decreased cell-cell adhesion
    • Tumor cells invasion
    • Metastasis

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