SARC SARC Participant Login
 
 
Collaborating for a Cure.
 








 

 

 

Sarcoma Genetic Markers: Fusion Proteins and Translocations

Recurrent Genetic Abnormalities in Sarcoma

A chromosome is a single long strand of DNA that is wound up and bunched together into a compact structure. (Human chromosomes are depicted in figure to the left.)  A gene is a segment of DNA on a chromosome and is the basic unit of heredity, directing the development and maintenance of cells and the organism.

When a human cell is preparing to divide, it copies each of its 23 pairs of chromosomes so that each new cell can receive a complete set.  Occasionally, a strand of DNA will break during this process.  The cell usually repairs these fractures correctly.  If it cannot be fixed, the cell will induce programmed cell death, or apoptosis. 

However, on occasion a cell will incorrectly join two or more different chromosomes, yielding what is called a translocation.  If the cell subsequently escapes its own destruction, the new cells can inherit an incorrect number of copies of that piece of chromosome.  Furthermore, if the DNA is snapped and incorrectly repaired in a region that specifies a gene, that valuable piece of the genetic code may be damaged, leaving the cell with only one remaining copy on the unbroken partner in the chromosome pair.  Another possibility is that the improperly repaired DNA will encode a "fusion protein," made from the sequences of two different genes spliced together.  Many fusion proteins are harmless and merely ineffective, but some can have detrimental effects.  If the original gene – the one damaged – carried out a vital function in the cell, such as regulating cell division, the fusion protein can cause big problems.

These breaking-and-joining events do not happen randomly, and certain translocations can lead to specific kinds of cancer.  For instance, when an extra copy of the long arm of chromosome 12 is inherited, this may lead to liposarcoma.  With two normal copies of chromosome 12 plus the extra fragment, cells manufacture too much of the protein encoded by one of the resident genes: the cyclin-dependent kinase 4 gene, known commonly as CDK4.  The CDK4 protein is a kinase, meaning it is an enzyme that adds phosphate groups onto other proteins to activate or inactivate them.  CDK4 acts on retinoblastoma tumor suppressor, or RB, which helps control cell division.  When there is too much CDK4 (as happens when it inherits excess copies of the gene), this causes RB to have an excessive number of phosphate groups, thereby heightening the rate of cell-division, a trademark characteristic of cancer.

There are several other characteristic translocations and resultant fusion proteins that have been discovered that may lead to developing certain subtypes of sarcoma.  Several are listed in the table below. 

They are listed in a specific format that is indicated below:

abn abbrev (first chrom; second chrom) (arm band location/number; arm band location/number)

abn abbrev: The aberration abbreviation, AKA the chromosomal abnormality type.  This could be a chromosomal translocation (t), deletion (del), duplication (dup), etc.

first chrom: The first chromosome involved in the abnormality

Second chrom: The second chromosome involved

Arm band location/number: This is a description of the location on a chromosome arm, in order from the centromere out to the end of the chromosome. The letter q indicates the abnormality involves the long arm of the chromosome.  The letter p indicates the short arm.  These numbers are a standard determined by the International System for human Cytogenetic nomenclature (ISCN), revised in 2005.

Sarcoma Molecular Markers Obtained from Genetic Testing

Tumor

Chromosomal Abnormality

Gene(s) Involved

Malignant Round Cell tumors

Ewings sarcoma/Peripheral neuroectodermal tumor

 

Desmoplastic small round cell tumor

 

Embryonal rhabdomyosarcoma

 

Alveolar Rhabdomyosarcoma

 

t(11;22)(q24;q12)

t(21;22)(q22;q12)

 

t(11;22)(p13;q12)

 

Complex alterations

 

t(2;13)(q35;q14)

t(1 ;13)(p36 ;14)

 

EWS-FLI1

EWS-ERG

 

EWS-WT1

 

Unknown

 

PAX3-FKHR

PAX7-FKHR

Lipomatous Tumors

Myxoid/round cell liposarcoma

 

Atypical lipomatous tumor/well differentiated liposarcoma (ALT/WDLPS)

 

 

Dedifferentiated liposarcoma

 

Pleomorphic liposarcoma

 

t(12;16)(q13;p11)

 

supernumerary ring chromosomes; giant marker chromosomes

 

 

Same as for ALT/WDLPS

 

Complex alterations

 

TLS-CHOP

 

Amplification of region 12q14-15, including MDM2, CDK4, HMGA2, SAS, GL1

 

Same as for ALT/WDLPS

 

Unknown

Spindle Cell Tumors

Desmoid fibromatosis

 

 

Synovial Sarcoma

 

 

Malignant peripheral nerve sheath tumor

 

Leiomyosarcoma

 

Congenital/infantile – fibrosarcoma

 

Inflammatory myofibroblastic tumor

 

Dermatofibrosarcoma protuberans

 

 

 

Angiomatoid fibrous histiocytoma

 

Low grade fibromyxoid sarcoma

 

Gastrointestinal Stromal tumor

 

Trisomy 8 or 20; loss of 5q

 

t(X;18)(p11;q11)

t(X;18)(p11;q11)

 

Complex alterations

 

 

Complex alterations

 

t(12;15)(p13;q25)

 

Rearrangements of 2p23

 

t(17;22)(q22;p13) and derivative ring chromosomes

 

t(12;16)(q13;p11)

 

t(7;16)(q34;p11)

 

Activating mutations

 

CTNNB1 or APC mutations

 

SYT-SSX1

SYT-SSX2

 

Unknown

 

 

Unknown

 

ETV6-NTRK3

 

ALK

 

COL1A1-PDGFB

 

 

 

TLS-ATF1

 

TLS-BBF2H7

 

C-KIT or PDGFRA

Miscellaneous tumors

Clear cell sarcoma

 

Extraskeletal myxoid chondrosarcoma

 

Alveolar soft part sarcoma

 

Extrarenal rhabdoid tumor

 

 

Epithelioid sarcoma (proximal type)

 

 

Tenosynovial giant cell tumor/pigmented villonodular synovitis (TGCT/PVNS)

t(12;22)(q13;q12)

 

Rearrangements of 9q22

 

der(17)(X;17)(p11;q25)

 

Bi-allelic inactivation of 22q11.2

 

Bi-allelic inactivation of 22q11.2

 

t(1;2)(p13;q35)

 

EWS-ATF1

 

CHN

 

ASPL-TFE3

 

INI1

 

 

INI1

 

 

CSF1

Der - Derivative chromosome (used when only one chromosome from a translocation is present, or when one chromosome has two or more structural abnormalities)

t – translocation

 
Sitemap | Terms of Use | Contact SARC | Contact Webmaster SARC | 24 Frank Lloyd Wright Drive, Lobby A, Suite 3100 | Ann Arbor, MI 48106 | phone 734.930.7600 | fax 734.930.7557