Etiology
The etiology for most patients with soft-tissue sarcoma (STS) is unknown, but there is evidence to suggest an association between some inherited germline mutations, and environmental factors which may increase the risk for the development of STS.
Germline mutations
Neurofibromatosis type 1 (NF1) von Recklinghausen disease
NF1 is an autosomal dominant condition caused by mutations NF1-gene, which codes for a protein called neurofibromin.[17] Patients with NF1 syndrome have an 8% to 13% lifetime risk of developing malignant peripheral nerve sheath tumor, an aggressive, genetically complex STS that comprises 2% of all sarcomas.[18][19][20]
Li-Fraumeni syndrome
A rare autosomal dominant disorder caused by mutations in the TP53 gene (17p 13.1) which codes for p53 (tumor suppressor gene) has been associated with an increased risk of cancer, including sarcoma, of approximately 50% by age 40 and 90% by age 60 in mutation carriers.[21][22]
Familial retinoblastoma
An increased risk of sarcomas, both bone and soft tissue, has been demonstrated in patients who have had a familial retinoblastoma, caused by inherited mutations in the RB1 gene.[23]
Familial adenomatous polyposis (FAP)
FAP is an autosomal dominant syndrome caused by germline mutation of adenomatous polyposis coli (APC). A 15% absolute lifetime risk of developing desmoid tumors in patient FAP has been demonstrated.[24] Evidence suggests that the incidence of FAP among patients with desmoid tumors is 7.5%, with 85% of these FAP associated desmoid tumors diagnosed in the setting of known FAP.[25]
Environmental factors
Radiation
Therapeutic radiation is an important environmental factor that increases the risk of sarcoma, it is commonly associated with angiosarcoma, undifferentiated pleomorphic sarcoma, and leiomyosarcoma.[26][27]
Human herpesvirus-8 (HHV-8) infection
Human herpesvirus 8 (HHV8), also known as Kaposi sarcoma-associated herpesvirus (KSHV), is one of the few pathogens recognized as direct carcinogen, being involved in the pathogenesis of Kaposi sarcoma, primary effusion lymphoma and multicentric Castleman disease.[28][29][30]
Congenital disorders
Beckwith-Wiedemann syndrome is a mostly sporadic disorder due to faulty gene imprinting, resulting in overgrowth and developmental anomalies. There is a 7.5% to 10% incidence of cancer, including rhabdomyosarcoma, myxoma, fibromas, and hamartomas.[31]
Chronic Lymphedema
There is a connection between long-standing chronic lymphedema and angiosarcoma known as Stewart-Treves syndrome, evidence suggests it occurs in 0.5% of patients who have undergone radical mastectomy with axillary node dissection, followed by adjuvant radiation therapy.[32][33][34]
Carcinogens
Occupational exposure to industrial materials including vinyl chloride monomer, iatrogenic exposure to colloidal thorium dioxide (thorotrast) for radiologic exams in the past, chronic arsenic ingestion, and androgen have been associated with an increased risk of sarcoma.[35][36]
Pathophysiology
The development of a sarcoma results from a complex biological process. Their development combines the emergence of a first genetic alteration that activates an oncogene, or oncogenic hit, which gives a cell a growth advantage and promotes cancer. The first oncogenic hit is followed by oncogenic and epigenetic events in combination with a permissive microenvironment composed by cell types from mesodermal tissue, immune infiltrate, vascular and extracellular matrix components.[37]
Sarcoma cells interact with their close environment through direct contact, enhanced cytokine/growth factors/miRNA signaling under a soluble form, or encapsulated in extracellular vesicles. Sarcoma cells are characterized by a phenotypic and genetic heterogeneity coming from the successive oncogenic/epigenetic events occurring during tumor development and by cancer cells acquiring the ability to self-renew, differentiate and proliferate, which becomes progressively quiescent.[37]
Metastases occur as sarcomas are prone to induce distant metastatic foci spread by circulating tumor cells.[37]
Classification
World Health Organization classification of tumors of soft tissue and bone[10]
Tumors are classified by differentiation and biological behavior. The major groups under this classification are:
Adipocytic tumors
Fibroblastic/myofibroblastic tumors
So-called fibrohistiocytic tumors
Smooth muscle tumors
Pericytic (perivascular) tumors
Skeletal muscle tumors
Vascular tumors
Chondro-osseous tumors
Gastrointestinal stromal tumors
Nerve sheath tumors
Tumors of uncertain differentiation
Undifferentiated/unclassified sarcomas.
Biological potential is divided into:
Benign: rarely recur locally, and if so, are nondestructive
Intermediate (locally aggressive): often recur locally, with infiltrative and locally destructive growth; lesions do not have any evident potential to metastasize
Intermediate (rarely metastasizing): are locally aggressive, but can sometimes produce distant metastases
Malignant: significant risk of distant metastases, as well as local destruction and recurrence; known as soft-tissue sarcomas.
Malignant and intermediate subtypes of soft-tissue sarcoma from this classification are as follows:
Adipocytic tumors
Malignant
Dedifferentiated liposarcoma
Myxoid liposarcoma
Pleomorphic liposarcoma
Liposarcoma, not otherwise specified.
Intermediate (locally aggressive)
Atypical lipomatous tumor/well-differentiated liposarcoma.
Fibroblastic/myofibroblastic tumors
Malignant
Adult fibrosarcoma
Myxofibrosarcoma
Low-grade fibromyxoid sarcoma
Sclerosing epithelioid fibrosarcoma
Giant cell fibroblastoma
Dermatofibrosarcoma protuberans.
Intermediate (rarely metastasizing)
Extrapleural solitary fibrous tumor
Inflammatory myofibroblastic tumor
Low-grade myofibroblastic sarcoma
Myxoinflammatory fibroblastic sarcoma
Infantile fibrosarcoma.
Intermediate (locally aggressive)
Superficial fibromatoses (palmar/plantar)
Desmoid-type fibromatoses
Lipofibromatosis.
So-called fibrohistiocytic tumors
Malignant
Pleomorphic malignant fibrohistiocytic (MFH)/undifferentiated pleomorphic sarcoma
Giant cell MFH/undifferentiated pleomorphic sarcoma with giant cells
Inflammatory MFH/undifferentiated pleomorphic sarcoma with prominent inflammation.
Intermediate (rarely metastasizing)
Plexiform fibrohistiocytic tumor
Giant cell tumor of soft tissues.
Smooth muscle tumors
Leiomyoma of deep soft tissue
Leiomyosarcoma.
Pericytic (perivascular) tumors
Glomus tumors
Angioleiomyoma
Myopericytoma, including myofibroma.
Skeletal muscle tumors
Malignant
Embryonal rhabdomyosarcoma (including botryoid, anaplastic)
Alveolar rhabdomyosarcoma (including solid, anaplastic)
Pleomorphic rhabdomyosarcoma
Spindle cell/sclerosing rhabdomyosarcoma.
Vascular tumors
Malignant
Epithelioid hemangioendothelioma
Angiosarcoma of soft tissue.
Intermediate (rarely metastasizing)
Retiform hemangioendothelioma
Papillary intralymphatic angioendothelioma
Composite hemangioendothelioma
Kaposi sarcoma.
Intermediate (locally aggressive)
Kaposiform hemangioendothelioma.
Chondro-osseous tumors
Soft-tissue chondroma
Extraskeletal osteosarcoma.
Gastrointestinal stromal tumors
Nerve sheath tumors
Tumors of uncertain differentiation
Malignant
Synovial sarcoma
Epithelioid sarcoma
Alveolar soft part sarcoma
Clear cell sarcoma of soft tissue
Extraskeletal myxoid chondrosarcoma
Primitive neuroectodermal tumor (PNET)/extraskeletal Ewing tumor: peripheral primitive neuroectodermal tumor (pPNET), extraskeletal Ewing tumor
Desmoplastic small round cell tumor
Extra-renal rhabdoid tumor
Malignant mesenchymoma
Neoplasms with perivascular epithelioid cell differentiation (PEComa)/clear cell myomelanocytic tumor
Intimal sarcoma.
Intermediate (rarely metastasizing)
Angiomatoid fibrous histiocytoma
Ossifying fibromyxoid tumor (including atypical/malignant)
Mixed tumor/myoepithelioma/parachordoma.
Undifferentiated/unclassified sarcomas
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