Editing Chromosomal translocation

{{Short description|Phenomenon that results in unusual rearrangement of chromosomes}}
{{more medical citations needed|date=December 2011}}
{{Use mdy dates|date=March 2016}}
[[File:Translocation-4-20.png|thumb|Chromosomal reciprocal translocation of the 4th and 20th [[chromosome]].]]
In [[genetics]], '''chromosome translocation''' is a phenomenon that results in unusual rearrangement of chromosomes. This includes "balanced" and "unbalanced" translocation, with three main types: "reciprocal", "nonreciprocal" and "Robertsonian" translocation. Reciprocal translocation is a [[chromosome abnormality]] caused by exchange of parts between non-homologous [[chromosomes]]. Two detached fragments of two different chromosomes are switched. Robertsonian translocation occurs when two non-homologous chromosomes get attached, meaning that given two healthy pairs of chromosomes, one of each pair "sticks" and blends together homogeneously. Each type of chromosomal translocation can result in disorders for growth, function and the development of an individuals body, often resulting from a change in their genome.<ref name=eurogentest>{{Cite web|url=http://www.eurogentest.org/index.php?id=612|title=EuroGentest: Chromosome Translocations|website=www.eurogentest.org|access-date=2019-03-29|archive-date=January 24, 2018|archive-url=https://web.archive.org/web/20180124111046/http://www.eurogentest.org/index.php?id=612|url-status=dead}}</ref>

A [[gene fusion]] may be created when the translocation joins two otherwise-separated genes. It is detected on [[cytogenetics]] or a [[karyotype]] of affected [[cell (biology)|cells]].  Translocations can be balanced (in an even exchange of material with no genetic information extra or missing, and ideally full functionality) or unbalanced (in which the exchange of [[chromosome]] material is unequal resulting in extra or missing [[gene]]s).<ref name=eurogentest/><ref>{{cite web |title=Can changes in the structure of chromosomes affect health and development? |url=https://ghr.nlm.nih.gov/primer/mutationsanddisorders/structuralchanges |website=Genetics Home Reference |publisher=National Library of Medicine |access-date=15 July 2020 |language=en}}</ref> Ultimately, these changes in chromosome structure can be due to deletions, duplications and inversions, and can result in 3 main kinds of structural changes.

==History==
Chromosomal translocations – in which a segment of one chromosome breaks off and attaches to another – were first observed in the early 20th century. In 1916, American zoologist William R. B. Robertson documented a chromosomal fusion in grasshoppers (now known as a [[Robertsonian translocation]]).<ref name=":19">{{Cite journal |last1=HROMAS |first1=ROBERT |last2=WILLIAMSON |first2=ELIZABETH |last3=LEE |first3=SUK-HEE |last4=NICKOLOFF |first4=JAC |date=2016 |title=Preventing the Chromosomal Translocations That Cause Cancer |journal=Transactions of the American Clinical and Climatological Association |language=en |volume=127 |pages=176–195 |pmc=5216476 |pmid=28066052}}</ref> In 1938, Karl Sax demonstrated that X-ray irradiation could induce chromosomal translocations, observing radiation-induced fusions between different chromosomes in plant cells.<ref name=":19" /> During the 1940s, Barbara McClintock’s maize cytogenetics experiments revealed the breakage–fusion–bridge cycle of chromosomes, further illuminating mechanisms of chromosomal rearrangement.<ref name=":5">{{Cite journal |last=Oviedo de Valeria |first=Jenny |date=1994-08-02 |title=Problemas multiplicativos tip transformacion lineal: tareas de compra y venta |url=https://doi.org/10.24844/em0602.06 |journal=Educación matemática |volume=6 |issue=2 |pages=73–86 |doi=10.24844/em0602.06 |issn=2448-8089}}</ref> A major breakthrough came in 1960 with the discovery of the [[Philadelphia chromosome]] in [[chronic myelogenous leukemia]] – the first consistent chromosomal abnormality linked to a human cancer.{{citation needed|date=March 2025}} In 1973, Janet Rowley identified the Philadelphia chromosome as a translocation between chromosomes 9 and 22, definitively linking a specific chromosomal translocation to leukemia <ref>{{Cite journal |last=Rowley |first=Janet D. |date=June 1973 |title=A New Consistent Chromosomal Abnormality in Chronic Myelogenous Leukaemia identified by Quinacrine Fluorescence and Giemsa Staining |url=https://www.nature.com/articles/243290a0 |journal=Nature |language=en |volume=243 |issue=5405 |pages=290–293 |bibcode=1973Natur.243..290R |doi=10.1038/243290a0 |issn=1476-4687|url-access=subscription }}</ref>

In subsequent decades, technological advances greatly enhanced the detection and understanding of translocations. The introduction of chromosome banding techniques in the 1970s (e.g. [[Q-banding]] and [[G banding|G-banding]]) allowed more precise identification of individual chromosomes and their abnormalities in karyotypes.<ref name=":6">{{Cite web |last=Case |first=Sean |date=2020-07-27 |title=History and Evolution of Cytogenetics |url=https://www.thermofisher.com/blog/behindthebench/history-and-evolution-of-cytogenetics/#:~:text=Starting%20in%20the%201970s,%20fluorescent,These%20staining |access-date=2025-03-13 |website=Behind the Bench |language=en-US}}</ref> The development of fluorescence in situ hybridization ([[Fluorescence in situ hybridization|FISH]]) in the early 1980s enabled researchers to label specific DNA sequences with fluorescent probes on chromosomes, dramatically improving the mapping of translocation breakpoints.<ref name=":6" /> In the 21st century, high-throughput DNA sequencing (such as whole-genome sequencing) has made it possible to detect translocations at single-nucleotide resolution, leading to the discovery of numerous previously undetected translocations across different cancers and genetic disorders.<ref name=":5" />

==Balanced reciprocal translocations==
Reciprocal translocations involve an ''exchange'' of material between non-homologous chromosomes.<ref name=":7">{{Citation |last1=Therman |first1=Eeva |title=Reciprocal Translocations |date=1993 |work=Human Chromosomes: Structure, Behavior, and Effects |pages=273–287 |editor-last=Therman |editor-first=Eeva |url=https://link.springer.com/chapter/10.1007/978-1-4684-0529-3_26 |access-date=2025-04-02 |place=New York, NY |publisher=Springer US |language=en |doi=10.1007/978-1-4684-0529-3_26 |isbn=978-1-4684-0529-3 |last2=Susman |first2=Millard |editor2-last=Susman |editor2-first=Millard|url-access=subscription }}</ref> Such translocations are usually harmless, as they do not result in a gain or loss of genetic material, as is the case with nonreciprocal translocations. This type of translocation is often caused by erroneous repair of double stranded breaks or non-homologous crossing over in meiosis.<ref name=":7" />

A common balanced reciprocal translocation is the exchange of material between chromosome 11 and 22. Individuals with this chromosomal abnormality do not experience any phenotypic effects but are subject to issues with fertility since carriers of balanced reciprocal translocations may create [[gamete]]s with ''unbalanced'' reciprocal or nonreciprocal chromosome translocations.<ref name=":8">{{Citation |last1=Wilch |first1=Ellen S. |title=Historical and Clinical Perspectives on Chromosomal Translocations |date=2018 |work=Chromosome Translocation |pages=1–14 |editor-last=Zhang |editor-first=Yu |url=https://link.springer.com/chapter/10.1007/978-981-13-0593-1_1 |access-date=2025-04-02 |place=Singapore |publisher=Springer |language=en |doi=10.1007/978-981-13-0593-1_1 |isbn=978-981-13-0593-1 |last2=Morton |first2=Cynthia C.|volume=1044 |pmid=29956287 |url-access=subscription }}</ref> The combination of the carrier’s gamete with the wild type gamete from the other parent may result in duplication or deletion of genetic material based on segregation of chromosomes during meiosis.<ref name=":8" /> This can lead to infertility, [[miscarriage]]s or [[children]] with abnormalities. [[Genetic counseling|Genetic counselling]] and [[genetic testing]] are often offered to families that may carry a translocation. A common example of a birth defect that may result from the carrier of the translocation mentioned above is Emanuel Syndrome.<ref name=":9">{{Cite web |last=PMC |first=Europe |title=Europe PMC |url=https://europepmc.org/article/NBK/nbk1263 |access-date=2025-04-02 |website=europepmc.org |language=en}}</ref>

{{Heading|Unbalanced reciprocal translocations}}

Unbalanced reciprocal translocations are similar to balanced reciprocal translocations in that they involve the ''exchange'' of genetic information between two non-homologous chromosomes.<ref name=":10">{{cite journal |last1=Parslow |first1=Malcolm |last2=Chambers |first2=Diana |last3=Aftimos |first3=Salim |title=An inherited reciprocal translocation—balanced or unbalanced? |journal=Pathology |date=1981 |volume=13 |issue=1 |pages=174 |doi=10.1016/S0031-3025(16)38470-7 }}</ref> However, with unbalanced reciprocal translocations, the process results in the duplication or deletion of some genetic material as well. Since there is a genetic imbalance, individuals with an unbalanced reciprocal translocation will often exhibit [[phenotype]] reflective of the abnormal gene expression.<ref name=":10" />

Most unbalanced reciprocal translocations are a result of inheritance from a parent with a balanced translocation.<ref name=":11">{{cite journal |last1=Chen |first1=Chih-Ping |last2=Wu |first2=Pei-Chen |last3=Lin |first3=Chen-Ju |last4=Chern |first4=Schu-Rern |last5=Tsai |first5=Fuu-Jen |last6=Lee |first6=Chen-Chi |last7=Town |first7=Dai-Dyi |last8=Chen |first8=Wen-Lin |last9=Chen |first9=Li-Feng |last10=Lee |first10=Meng-Shan |last11=Pan |first11=Chen-Wen |last12=Wang |first12=Wayseen |title=Unbalanced reciprocal translocations at amniocentesis |journal=Taiwanese Journal of Obstetrics and Gynecology |date=March 2011 |volume=50 |issue=1 |pages=48–57 |doi=10.1016/j.tjog.2011.02.001 |pmid=21482375 |doi-access=free }}</ref> As mentioned previously, parents with balanced translocations are likely to give birth to children with unbalanced translocations. Although less common, unbalanced translocations may form due to errors during [[gametogenesis]] or errors in repair of double stranded DNA breaks.<ref name=":11" />

==Nonreciprocal translocation==

Nonreciprocal translocation is a chromosomal abnormality that involves the one-way transfer of [[genes]] from one [[chromosome]] to another [[Non-homologous recombination|non-homologous]] chromosome. This transfer will always be unbalanced resulting in genetic imbalance. This excess or deletion of genetic material compared to a normal genome is likely to result in disease.

Nonreciprocal translocations can occur as a result of three main processes. Errors during [[DNA replication]], unequal [[Chromosomal crossover|crossing over]] in meiosis or mitosis and/or exogenous factors causing double stranded DNA damage.<ref name=":12">{{Cite journal |last1=Ali |first1=Hanif |last2=Daser |first2=Angelika |last3=Dear |first3=Paul |last4=Wood |first4=Henry |last5=Rabbitts |first5=Pamela |last6=Rabbitts |first6=Terence |date=2013 |title=Nonreciprocal chromosomal translocations in renal cancer involve multiple DSBs and NHEJ associated with breakpoint inversion but not necessarily with transcription |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/gcc.22038 |journal=Genes, Chromosomes and Cancer |language=en |volume=52 |issue=4 |pages=402–409 |doi=10.1002/gcc.22038 |pmid=23341332 |issn=1098-2264|url-access=subscription }}</ref> When a chromosome experiences a double strand break at one or more locations it may rejoin to a non-homologous chromosome.<ref name=":12" /> In the case of nonreciprocal translocations, the acceptor chromosome gains material but the donor chromosome does not accept material in exchange. This unequal transfer causes loss of genetic material which may have varying degrees of impact.

A number of factors affect the impact of the translocation. The segment of the chromosome affected by the double strand break may be in a coding or noncoding region.<ref name=":13">{{Cite journal |last1=Nikitin |first1=Dmitri |last2=Tosato |first2=Valentina |last3=Zavec |first3=Apolonija Bedina |last4=Bruschi |first4=Carlo V. |date=2008-07-15 |title=Cellular and molecular effects of nonreciprocal chromosome translocations in Saccharomyces cerevisiae |journal=Proceedings of the National Academy of Sciences |volume=105 |issue=28 |pages=9703–9708 |doi=10.1073/pnas.0800464105 |doi-access=free |pmc=2474487 |pmid=18599460|bibcode=2008PNAS..105.9703N }}</ref> Therefore, the rearrangement may result in a number of affects to the gene. Essential genes may be silenced or [[oncogene]]s may be activated.<ref name=":13" /> The chromosome on which the translocation occurs may also affect the result due to certain chromosomes containing more [[essential gene]]s. Which cell type the translocation occurs in may also have an affect. [[Somatic cell]]s are more likely to result in cancer, where [[germ line cell]]s are more likely to result in birth defects including miscarriages and still births.<ref>{{cite journal |last1=Nambiar |first1=Mridula |last2=Kari |first2=Vijayalakshmi |last3=Raghavan |first3=Sathees C. |title=Chromosomal translocations in cancer |journal=Biochimica et Biophysica Acta (BBA) - Reviews on Cancer |date=December 2008 |volume=1786 |issue=2 |pages=139–152 |doi=10.1016/j.bbcan.2008.07.005 |pmid=18718509 }}</ref>

One specific example of an unbalanced nonreciprocal translocation is [[Emanuel syndrome|Emanuel Syndrome]]. At the chromosomal level, a fragment from chromosome 11 is non-reciprocally translocated to chromosome 22 creating genetic imbalances.<ref name=":9" /> Phenotypically, Emanuel Syndrome presents as neurological and physical developmental disorders, [[microcephaly]], and [[congenital defects]].<ref name=":9" />

==Robertsonian translocations==
{{main|Robertsonian translocation}}
[[Robertsonian translocation]] is a type of translocation caused by breaks at or near the centromeres of two [[centromere#Acrocentric|acrocentric]] chromosomes. The reciprocal exchange of parts gives rise to one large [[centromere#Metacentric|metacentric]] chromosome and one extremely small chromosome that may be lost from the organism with little effect because it contains few genes. The resulting [[karyotype]] in humans leaves only 45 chromosomes, since two chromosomes have fused together.<ref>{{cite book|last=Hartwell|first=Leland H.|title=Genetics: From Genes to Genomes|year=2011|publisher=McGraw-Hill|location=New York|isbn=978-0-07-352526-6|page=443}}</ref>   This has no direct effect on the phenotype, since the only genes on the short arms of acrocentrics are common to all of them and are present in variable copy number (nucleolar organiser genes).

Robertsonian translocations have been seen involving all combinations of acrocentric chromosomes. The most common translocation in humans involves chromosomes [[chromosome 13 (human)|13]] and [[chromosome 14 (human)|14]] and is seen in about 0.97 / 1000 newborns.<ref>{{cite journal | author = E. Anton |author2=J. Blanco |author3=J. Egozcue |author4=F. Vidal  | date = April 29, 2004 | title = Sperm FISH studies in seven male carriers of Robertsonian translocation t(13;14)(q10;q10) | journal = Human Reproduction | volume = 19 | issue = 6 | pages = 1345–1351 | issn = 1460-2350 | pmid = 15117905 | doi = 10.1093/humrep/deh232| doi-access = free }}</ref> Carriers of Robertsonian translocations are not associated with any phenotypic abnormalities, but there is a risk of unbalanced gametes that lead to miscarriages or abnormal offspring.  For example, carriers of Robertsonian translocations involving [[chromosome 21 (human)|chromosome 21]] have a higher risk of having a child with [[Down syndrome]]. This is known as a 'translocation Downs'. This is due to a mis-segregation ([[nondisjunction]]) during gametogenesis. The mother has a higher (10%) risk of transmission than the father (1%). Robertsonian translocations involving chromosome 14 also carry a slight risk of [[uniparental disomy]] 14 due to [[trisomy rescue]].

==Chromosomal Structural Changes==
Changes in chromosome structure can be due to deletions, duplications and inversions, ultimately resulting in 3 main kinds of structural changes.

[[Isochromosome]]s result when a chromosome has two identical arms, such as two P or two Q arms, instead of the expected Q and P pairing. These isochromosomal structural changes can result in a loss of information, as well as a change in expression within the body due to the duplication of one set of chromosomal arms.<ref name=":14">{{Cite web |last=Mehta |first=Parang |title=What Are Translocations? |url=https://www.webmd.com/children/what-are-translocations |access-date=2025-04-02 |website=WebMD |language=en}}</ref>

[[Dicentric chromosome]]s are chromosomes with two centromeres, resulting in an instability within the chromosome and a loss of genetic information due to the fusion of two chromosome pieces with a centromere.<ref name=":14" /> This results in a singular chromosome having two centromeres, due to the fusion of two chromosomal pieces with one centromere each, therefore resulting in the fusion of two centromeres.

Ring chromosomes are chromosomes that form when the ends of the previous chromosomes break off to form a circular structure.<ref>{{cite journal |last1=Yip |first1=Moh-Ying |title=Autosomal ring chromosomes in human genetic disorders |journal=Translational Pediatrics |date=April 2015 |volume=4 |issue=2 |pages=164–174 |doi=10.3978/j.issn.2224-4336.2015.03.04 |pmid=26835370 |pmc=4729093 }}</ref> This results in a loss of genetic material as well as the potential loss of the chromosomal centromere.<ref name=":14" />

==DNA double-strand breaks with translocations==

The initiating event in the formation of a translocation is generally a [[DNA damage (naturally occurring)|double-strand break in chromosomal DNA]].<ref name="Agarwal2006">{{cite journal |last1=Agarwal |first1=S. |last2=Tafel |first2=A. A. |last3=Kanaar |first3=R. |date=2006 |title=DNA double-strand break repair and chromosome translocations |journal=DNA Repair |volume=5 |issue=9–10 |pages=1075–1081 |doi=10.1016/j.dnarep.2006.05.029 |pmid=16798112}}</ref>  Double stranded breaks in chromosomal DNA can occur for many reasons, however a major role in generating these translocations is the [[non-homologous end joining]] (NHEJ) pathway.<ref name="Agarwal2006" /><ref>{{cite book |doi=10.1007/978-3-319-20291-4_1 |chapter=DNA Repair and Chromosomal Translocations |title=Chromosomal Instability in Cancer Cells |series=Recent Results in Cancer Research |date=2015 |last1=Bohlander |first1=Stefan K. |last2=Kakadia |first2=Purvi M. |volume=200 |pages=1–37 |isbn=978-3-319-20290-7 }}</ref>  When this pathway functions appropriately, it restores a DNA double-strand break by reconnecting the originally broken ends using their sticky or blunt ends that have been generated by the enzyme and protein machinery. However, when the NHEJ pathway acts inappropriately, it may join ends incorrectly, therefore resulting in genomic rearrangements including translocations. These incorrect combinations are the result of sequences in close proximity that have similar homology, but not perfect homology, yet it is recognized by the repair machinery as perfect. This then leads the machinery to begin repairing using NHEJ with the wrong sequences, resulting in deletions and insertions of specific nucleotides, or the joining of incorrect end sequences.<ref>{{cite journal |last1=Steyer |first1=Benjamin |last2=Cory |first2=Evan |last3=Saha |first3=Krishanu |title=Developing precision medicine using scarless genome editing of human pluripotent stem cells |journal=Drug Discovery Today: Technologies |date=August 2018 |volume=28 |pages=3–12 |doi=10.1016/j.ddtec.2018.02.001 |pmid=30205878 |pmc=6136251 |quote=Non-homologous end joining (NHEJ)—an error prone DNA repair process where double strand breaks are directly ligated, commonly resulting in insertion or deletion mutations. }}</ref> Ultimately, these issues arise due to a misread of the homologous sequences by the protein or enzyme machinery, and leads to the mis-incorporation of incorrect sequences into the genome. when the genomes of slightly homologous sequences are in too close of proximity, resulting in the machinery becoming confused or mistaking the wrong sequence for the correct one.<ref>{{cite journal |last1=Rocha |first1=P. P. |last2=Chaumeil |first2=J. |last3=Skok |first3=J. A. |date=2013 |title=Molecular biology. Finding the right partner in a 3D genome |journal=Science |volume=342 |issue=6164 |pages=1333–1334 |doi=10.1126/science.1246106 |pmc=3961821 |pmid=24337287}}</ref>

Another influence in generating DNA double stranded break translocations is through the creation of AID translocations. These sequences are the result of a deamination procedure of a cytosine nucleotide into a uracil nucleotide. This change ultimately results in a mismatch between the complementary sequence and its target sequence, therefore resulting in a translocation. When further processed by specific endonucleases, this uracil leads to a mutation or a double stranded break.<ref>{{Cite journal |last1=Nambiar |first1=Mridula |last2=Raghavan |first2=Sathees C. |date=August 2011 |title=How does DNA break during chromosomal translocations? |journal=Nucleic Acids Research |volume=39 |issue=14 |pages=5813–5825 |doi=10.1093/nar/gkr223 |issn=1362-4962 |pmc=3152359 |pmid=21498543}}</ref> Once again, these double stranded break and the mismatch that occurred lead to a translocation of the genomic sequence, which in turn have effect on the chromosome the DNA is present on.

Finally, new information is surfacing regarding the influence of exogenous rare-cutting endonucleases on DNA double stranded breaks and their resulting chromosomal translocations.<ref>{{cite journal |last1=Jasin |first1=Maria |title=Genetic manipulation of genomes with rare-cutting endonucleases |journal=Trends in Genetics |date=June 1996 |volume=12 |issue=6 |pages=224–228 |doi=10.1016/0168-9525(96)10019-6 |pmid=8928227 |doi-access=free }}</ref><ref name=":17">{{cite journal |last1=Povirk |first1=Lawrence F. |title=Biochemical mechanisms of chromosomal translocations resulting from DNA double-strand breaks |journal=DNA Repair |date=September 2006 |volume=5 |issue=9–10 |pages=1199–1212 |doi=10.1016/j.dnarep.2006.05.016 |pmid=16822725 }}</ref> Specifically, during DNA double strand break repair, reflections of misjoining of exchanged sequence ends have be noted, primarily due to the mishomology present by the NHEJ pathway. However, at these specific break points, additional nucleic acid and DNA sequence loss has been found, therefore leading to the conclusion that additional exogenous rare-cutting endonucleases are present at various locations on these strands. Each deletion results in a varying size, location or cut version, ultimately suggesting DNA degradation by endonucleases prior to NHEJ joining.<ref name=":17" /> Additional influences on DNA degradation similar to that of exogenous rare-cutting endonucleases has also been noted as a result of cytotoxic chemotherapy,<ref>{{Cite web |title=Chemotherapy - What it is, types, treatment and side effects |url=https://www.macmillan.org.uk/cancer-information-and-support/treatment/types-of-treatment/chemotherapy#:~:text=we%20can%20help-,What%20is%20chemotherapy?,are%20carried%20in%20the%20blood. |access-date=2025-04-11 |website=www.macmillan.org.uk |language=en}}</ref> [[ionizing radiation]], although further research is needed in order to provide more conclusive and viable answers.<ref name=":18">{{Cite journal |last1=Qiu |first1=Zhijun |last2=Zhang |first2=Zhenhua |last3=Roschke |first3=Anna |last4=Varga |first4=Tamas |last5=Aplan |first5=Peter D. |date=2017-02-22 |title=Generation of Gross Chromosomal Rearrangements by a Single Engineered DNA Double Strand Break |journal=Scientific Reports |language=en |volume=7 |issue=1 |pages=43156 |bibcode=2017NatSR...743156Q |doi=10.1038/srep43156 |pmid=28225067 |pmc=5320478 |issn=2045-2322|hdl=2437/288170 |hdl-access=free }}</ref>

Overall, through various mechanisms,  DNA double-strand breaks and sources of DNA double-strand break repair are able to generate both reciprocal and non reciprocal chromosomal translocations.<ref name=":17"/> Such DNA breaks and repair mechanisms are also able to generate gross chromosomal mutations, inclusive of not only translocations, but also inversions, amplifications and simple deletions, all resulting in null or dangerous transformations.<ref name=":18" />

== Role in Disease ==
Chromosomal translocations can cause a diverse array of diseases, mutations or other heritable changes within an individuals genomes. Often, these mutations are caused by the loss of genetic information resulting from a structural change in the chromosome. There are three main forms of structural changes, and each of these has a role within the creation of disease. Whether it be from the structural changes themselves, or directly from the loss of genetic information, many varying diseases or mutations can be acquired due to chromosomal translocations.

A prevalent and dangerous disease resulting from chromosomal translocations is Cancer.<ref>{{Cite web |title=Cancer - Symptoms and causes |url=https://www.mayoclinic.org/diseases-conditions/cancer/symptoms-causes/syc-20370588#:~:text=Cancer%20refers%20to%20any%20one,of%20death%20in%20the%20world |access-date=2025-04-11 |website=Mayo Clinic |language=en}}</ref> There are several forms of cancer that are caused by acquired translocations, many of them falling within the classifications of leukemia,<ref>{{Cite web |title=Leukemia—Patient Version - NCI |url=https://www.cancer.gov/types/leukemia#:~:text=Leukemia%20is%20a%20broad%20term,in%20children%20younger%20than%2015 |access-date=2025-04-11 |website=www.cancer.gov |language=en}}</ref> acute myelogenous leukemia,<ref>{{Cite web |date=2025-04-04 |title=Acute Myeloid Leukemia Treatment - NCI |url=https://www.cancer.gov/types/leukemia/patient/adult-aml-treatment-pdq#:~:text=and%20treatment%20options.-,Adult%20acute%20myeloid%20leukemia%20(AML)%20is%20a%20type%20of%20cancer,if%20it%20is%20not%20treated. |access-date=2025-04-11 |website=www.cancer.gov |language=en}}</ref> and chronic myelogenous leukemia,<ref>{{Cite web |title=Chronic myelogenous leukemia - Symptoms and causes |url=https://www.mayoclinic.org/diseases-conditions/chronic-myelogenous-leukemia/symptoms-causes/syc-20352417 |access-date=2025-04-11 |website=Mayo Clinic |language=en}}</ref> with additional translation classifications being detected within solid malignancies such as Ewing's sarcoma.<ref>{{Cite web |title=Ewing sarcoma - Symptoms and causes |url=https://www.mayoclinic.org/diseases-conditions/ewing-sarcoma/symptoms-causes/syc-20351071#:~:text=Ewing%20sarcoma%20is%20a%20type,can%20happen%20in%20any%20bone. |access-date=2025-04-11 |website=Mayo Clinic |language=en}}</ref> Regardless of the cancer classification, the most common process for generation of these cancers is through the disruption or misregulation of normal gene function. This results in the molecular rearrangement of the genes necessary for proper gene regulation, therefore resulting in cancer formation.<ref name=":15">{{Cite web |title=Human Chromosome Translocations and Cancer {{!}} Learn Science at Scitable |url=https://www.nature.com/scitable/topicpage/human-chromosome-translocations-and-cancer-23487/ |access-date=2025-04-02 |website=www.nature.com |language=en}}</ref> An alternative way that such cancers can be formed is through the fusion of coding sequences. This fusion results from the translation forcing the generation of a ring or iso chromosome, or from DNA end joining due to a close proximity between homologues genes, therefore creating a potent, fused oncogene.<ref>{{cite journal |last1=Streb |first1=Patrick |last2=Kowarz |first2=Eric |last3=Benz |first3=Tamara |last4=Reis |first4=Jennifer |last5=Marschalek |first5=Rolf |title=How chromosomal translocations arise to cause cancer: Gene proximity, trans-splicing, and DNA end joining |journal=iScience |date=June 2023 |volume=26 |issue=6 |pages=106900 |doi=10.1016/j.isci.2023.106900 |pmid=37378346 |pmc=10291325 |bibcode=2023iSci...26j6900S }}</ref><ref>{{Cite journal |last=Aplan |first=Peter D. |date=January 2006 |title=Causes of oncogenic chromosomal translocation |journal=Trends in Genetics |volume=22 |issue=1 |pages=46–55 |doi=10.1016/j.tig.2005.10.002 |issn=0168-9525 |pmc=1762911 |pmid=16257470}}</ref>

Infertility is also a prevalent and common form of disease that is generated by chromosomal translocations, and often can be asymptomatic or symptomatic within fetuses.<ref>{{Cite web |title=Infertility |url=https://www.who.int/news-room/fact-sheets/detail/infertility#:~:text=Infertility%20is%20a%20disease%20of,male,%20female%20or%20unexplained%20factors. |access-date=2025-04-11 |website=www.who.int |language=en}}</ref> Commonly influenced by one of the parents being a carrier for a balanced translocation yet being asymptomatic, the offspring often acquire additional mutations prior to birth resulting in the effect and symptomatic response due to the presence of the translocation within their genome. Ultimately, this symptomatic response is discovered when homology between two individuals genomes results in the loss of genetic information from the asymptomatic chromosomal translocation becoming problematic.<ref name=":15" /><ref>{{Cite journal |last1=Zhang |first1=Hong-Guo |last2=Wang |first2=Rui-Xue |last3=Pan |first3=Yuan |last4=Zhang |first4=Han |last5=Li |first5=Lei-Lei |last6=Zhu |first6=Hai-Bo |last7=Liu |first7=Rui-Zhi |date=2018-01-25 |title=A report of nine cases and review of the literature of infertile men carrying balanced translocations involving chromosome 5 |journal=Molecular Cytogenetics |volume=11 |issue=1 |pages=10 |doi=10.1186/s13039-018-0360-x |doi-access=free |pmid=29416565 |issn=1755-8166|pmc=5785882 }}</ref>

In addition, the inheritance of Down syndrome<ref>{{Cite web |last=CDC |date=2024-12-26 |title=Down Syndrome |url=https://www.cdc.gov/birth-defects/about/down-syndrome.html#:~:text=Down%20syndrome%20is%20a%20condition,their%20body%20and%20brain%20develop |access-date=2025-04-11 |website=Birth Defects |language=en-us}}</ref> can be caused by chromosomal translocations. In a minority (approximately 3 - 4%) of Down syndrome syndrome cases, the cause for this mutation is that of a Robertsonian translocation of chromosomes. This results from the Robertsonian translocation of the chromosome 21 long arm, onto the long arm of chromosome 14.<ref name=":16">{{Cite web |last=Philadelphia |first=The Children's Hospital of |title=Translocation Down Syndrome {{!}} Children's Hospital of Philadelphia |url=https://www.chop.edu/conditions-diseases/translocation-down-syndrome |access-date=2025-04-02 |website=www.chop.edu |language=en}}</ref> These translocations can also occur onto other chromsomes, such as chromosome 13, 15, or 22 resulting in these chromosomes also being referred to as Robertsonian chromosomes. Regardless of where, the result is a loss of information on chromosome 21 genes, and an addition of genetic information on the altering chromosome.<ref name=":16" />

Finally, chromosomal translocations between the sex chromosomes can also result in a number of genetic conditions, such as [[XX male syndrome]],<ref>{{cite book |last1=Gilbert |first1=Scott F. |title=Developmental Biology. 6th edition |date=2000 |publisher=Sinauer Associates |chapter-url=https://www.ncbi.nlm.nih.gov/books/NBK9967/ |chapter=Chromosomal Sex Determination in Mammals }}</ref> which is caused by a translocation of the SRY gene from the Y to the X chromosome.<ref>{{Cite web |title=SRY gene |url=https://medlineplus.gov/download/genetics/gene/sry.pdf |website=medlineplus.gov}}</ref> Alternatively, additional genetic diseases can also be a result of chromosomal translocations, such as Emmanuel syndrome,<ref>{{cite web | url=https://medlineplus.gov/genetics/condition/emanuel-syndrome/ | title=Emanuel syndrome: MedlinePlus Genetics }}</ref> Klinfelter syndrome<ref>{{cite journal |last1=Gaviria |first1=Anibal |last2=Cadena-Ullauri |first2=Santiago |last3=Cevallos |first3=Francisco |last4=Guevara-Ramirez |first4=Patricia |last5=Ruiz-Pozo |first5=Viviana |last6=Tamayo-Trujillo |first6=Rafael |last7=Paz-Cruz |first7=Elius |last8=Zambrano |first8=Ana Karina |title=Clinical, cytogenetic, and genomic analyses of an Ecuadorian subject with Klinefelter syndrome, recessive hemophilia A, and 1;19 chromosomal translocation: a case report |journal=Molecular Cytogenetics |date=5 September 2022 |volume=15 |issue=1 |pages=40 |doi=10.1186/s13039-022-00618-w |doi-access=free |pmid=36064723 |pmc=9446752 }}</ref> and Turner syndrome.<ref>{{cite web | url=https://www.mayoclinic.org/diseases-conditions/turner-syndrome/symptoms-causes/syc-20360782 | title=A genetic disorder that affects females-Turner syndrome - Symptoms & causes | website=[[Mayo Clinic]] }}</ref>

==By chromosome==
[[File:Chromosomal translocations.svg|thumb|350px|right|Overview of some chromosomal translocations involved in different cancers, as well as implicated in some other conditions, e.g. schizophrenia,<ref name="semple" /> with chromosomes arranged in standard [[karyogram]] order.
Abbreviations:
<br>ALL – [[Acute lymphoblastic leukemia]]
<br>AML – [[Acute myeloid leukemia]]
<br>CML – [[Chronic myelogenous leukemia]]
<br>DFSP – [[Dermatofibrosarcoma protuberans]]]]
[[File:Human karyotype with bands and sub-bands.png|thumb|300px|Human [[karyotype]] with annotated bands and sub-bands as used for the nomenclature of chromosomal abnormalities. It shows dark and white regions as seen on [[G banding]]. Each row is vertically aligned at [[centromere]] level. It shows 22 [[Homologous chromosome|homologous]] [[autosomal]] chromosome pairs as well as both the female (XX) and male (XY) versions of the two [[sex chromosome]]s. {{further|Karyotype}}]]

===Denotation===
The International System for Human Cytogenetic Nomenclature (ISCN) is used to denote a translocation between [[chromosome]]s.<ref>Schaffer, Lisa. (2005) ''International System for Human Cytogenetic Nomenclature'' S. Karger AG {{ISBN|978-3-8055-8019-9}}</ref>  The designation "t(A;B)(p1;q2)" is used to denote a translocation between [[chromosome]] A and chromosome B. The information in the second set of parentheses, when given, gives the precise location within the chromosome for chromosomes A and B respectively—with ''p'' indicating the short arm of the chromosome, ''q'' indicating the long arm, and the numbers after p or q refers to regions, bands and sub-bands seen when staining the chromosome with a [[staining dye]].<ref>{{cite web|title=Characteristics of chromosome groups: Karyotyping|url=http://www.rerf.jp/dept/genetics/giemsa_4_e.html|website=rerf.jp|publisher=Radiation Effects Research Foundation|access-date=June 30, 2014}}</ref> See also the definition of a [[locus (genetics)|genetic locus]].

The translocation is the mechanism that can cause a gene to move from one linkage group to another.

===Examples of translocations on human chromosomes===
{{For|an explanation of the symbols and abbreviations used in these examples|Cytogenetic notation}}

{| class="wikitable"
! rowspan="2" | Translocation !! rowspan="2" | Associated diseases !! colspan="2" | Fused genes/proteins
|-
! First !! Second
|-
| t(8;14)(q24;q32) || [[Burkitt's lymphoma]] 
– occurs in ~70% of cases, places '''MYC''' under IGH enhancer control <ref>{{Cite journal |last=Zheng |first=Jie |date=2013-11-01 |title=Oncogenic chromosomal translocations and human cancer (Review) |url=https://www.spandidos-publications.com/10.3892/or.2013.2677#:~:text=The%20reason%20why%2070,stimulated,%20the%20MYC%20gene%20is |journal=Oncology Reports |volume=30 |issue=5 |pages=2011–2019 |doi=10.3892/or.2013.2677 |pmid=23970180 |issn=1021-335X}}</ref> 
| [[c-myc]] on chromosome 8,<br> gives the [[fusion protein]] lymphocyte-proliferative ability || [[IGH@]] (immunoglobulin heavy locus) on chromosome 14,<br> induces massive transcription of fusion protein
|-
| t(11;14)(q13;q32) || [[Mantle cell lymphoma]]<ref name="jy" /> – present in most cases <ref>{{Cite journal |last=Zheng |first=Jie |date=2013-11-01 |title=Oncogenic chromosomal translocations and human cancer (Review) |url=https://www.spandidos-publications.com/10.3892/or.2013.2677#:~:text=be%20used%20to%20distinguish%20follicular,transcriptional%20repressor%20that%20inhibits%20the |journal=Oncology Reports |volume=30 |issue=5 |pages=2011–2019 |doi=10.3892/or.2013.2677 |pmid=23970180 |issn=1021-335X}}</ref>
| [[cyclin D1]]<ref name="jy">{{cite journal |vauthors=Li JY, Gaillard F, Moreau A |title=Detection of translocation t(11;14)(q13;q32) in mantle cell lymphoma by fluorescence in situ hybridization |journal=Am. J. Pathol. |volume=154 |issue=5 |pages=1449–52 |date=May 1999 |pmid=10329598 |pmc=1866594 |doi= 10.1016/S0002-9440(10)65399-0|display-authors=etal}}</ref> on chromosome 11,<br> gives fusion protein cell-proliferative ability || [[IGH@]]<ref name="jy" /> (immunoglobulin heavy locus) on chromosome 14,<br> induces massive transcription of fusion protein
|-
| t(14;18)(q32;q21) || [[Follicular lymphoma]] (~90% of cases)<ref name="Tietz2011" /> || [[IGH@]]<ref name="jy" /> (immunoglobulin heavy locus) on chromosome 14,<br> induces massive transcription of fusion protein || [[Bcl-2]] on chromosome 18,<br> gives fusion protein anti-apoptotic abilities
|-
| t(10;(various))(q11;(various)) || [[Papillary thyroid cancer]]<ref name="Kumar20" /> || [[RET proto-oncogene]]<ref name="Kumar20" /> on chromosome 10 || PTC (''Papillary Thyroid Cancer'') – Placeholder for any of several other genes/proteins<ref name="Kumar20" />
|-
| t(2;3)(q13;p25) || [[Follicular thyroid cancer]]<ref name="Kumar20">{{cite book |last4=Mitchell|first4=Richard Sheppard |last1=Kumar|first1=Vinay |last2=Abbas|first2=Abul K. |last3=Fausto|first3=Nelson |title=Robbins Basic Pathology|publisher=Saunders |location=Philadelphia |isbn=978-1-4160-2973-1 |year=2007|edition=8th|chapter=Chapter 20: The Endocrine System }}</ref> || PAX8 – [[paired box gene 8]]<ref name="Kumar20" /> on chromosome 2 || PPARγ1<ref name="Kumar20" /> ([[peroxisome proliferator-activated receptor γ]] 1) on chromosome 3
|-
| t(8;21)(q22;q22)<ref name="Tietz2011" /> || [[Acute myeloblastic leukemia with maturation]] || [[RUNX1T1|ETO]] on chromosome 8 || [[RUNX1|AML1]] on chromosome 21<br>found in ~7% of new cases of AML, carries a favorable prognosis and predicts good response to [[cytosine arabinoside]] therapy<ref name="Tietz2011" />
|-
| t(9;22)(q34;q11) [[Philadelphia chromosome]]|| [[Chronic myelogenous leukemia]] (CML), [[acute lymphoblastic leukemia]] (ALL) || [[Abl gene|''Abl1'' gene]] on chromosome 9<ref name="pmid12755554" /> || ''[[BCR gene|BCR]]'' ("breakpoint cluster region" on [[chromosome 22]]<ref name="pmid12755554">{{cite journal |vauthors=Kurzrock R, Kantarjian HM, Druker BJ, Talpaz M |title=Philadelphia chromosome-positive leukemias: from basic mechanisms to molecular therapeutics |journal=Ann. Intern. Med. |volume=138 |issue=10 |pages=819–30 |date=May 2003 |pmid=12755554 |doi= 10.7326/0003-4819-138-10-200305200-00010|s2cid=25865321 }}</ref>
|-
| t(15;17)(q22;q21)<ref name="Tietz2011">{{cite book|last1=Burtis|first1=Carl A. |last2=Ashwood|first2=Edward R. |last3=Bruns|first3=David E. |title=Tietz Textbook of Clinical Chemistry and Molecular Diagnostics|chapter-url=https://books.google.com/books?id=BBLRUI4aHhkC|access-date=November 5, 2012|date=December 16, 2011|publisher=Elsevier Health Sciences|isbn=978-1-4557-5942-2|pages=1371–1396|chapter=44. Hematopoeitic malignancies}}</ref> || [[Acute promyelocytic leukemia]] || [[PML protein]] on chromosome 15 || [[Retinoic acid receptor alpha|RAR-α]] on chromosome 17<br>persistent laboratory detection of the PML-RARA transcript is strong predictor of relapse<ref name="Tietz2011" />
|-
| t(12;15)(p13;q25) || Acute myeloid leukemia, congenital fibrosarcoma, secretory breast carcinoma, mammary analogue secretory carcinoma of salivary glands, cellular variant of mesoblastic nephroma || [[ETV6|TEL]] on chromosome 12 || [[TrkC receptor]] on chromosome 15
|-
| t(9;12)(p24;p13) || [[chronic myelogenous leukemia|CML]], [[acute lymphoblastic leukemia|ALL]] || [[Janus kinase 2|JAK]] on chromosome 9 || [[ETV6|TEL]] on chromosome 12
|-
| t(12;16)(q13;p11) || [[Myxoid liposarcoma]] || [[DDIT3]] (formerly CHOP) on chromosome 12 || [[FUS (gene)|FUS]] gene on chromosome 16
|-
| t(12;21)(p12;q22) || [[Acute lymphoblastic leukemia|ALL]] || TEL on chromosome 12 || [[RUNX1|AML1]] on chromosome 21
|-
| t(11;18)(q21;q21) || [[MALT lymphoma]]<ref name="Robbins626">{{cite book |last4=Mitchell|first4=Richard Sheppard |last1=Kumar|first1=Vinay |last2=Abbas|first2=Abul K. |last3=Fausto|first3=Nelson |title=Robbins Basic Pathology|publisher=Saunders |location=Philadelphia |isbn=978-1-4160-2973-1 |year=2007|page=626 |edition=8th}}</ref> || [[Baculoviral IAP repeat-containing protein 3|BIRC3]] (API-2) || [[Paracaspase|MLT]]<ref name="Robbins626" />
|-
| t(1;11)(q42.1;q14.3) || [[Schizophrenia]]<ref name="semple">{{cite journal |vauthors=Semple CA, Devon RS, Le Hellard S, Porteous DJ |title=Identification of genes from a schizophrenia-linked translocation breakpoint region |journal=Genomics |volume=73 |issue=1 |pages=123–6 |date=April 2001 |pmid=11352574 |doi=10.1006/geno.2001.6516 }}</ref> (familial translocation disrupting '''DISC1''')<ref name=":0">{{Cite journal |last1=Eykelenboom |first1=Jennifer E |last2=Briggs |first2=Gareth J |last3=Bradshaw |first3=Nicholas J |last4=Soares |first4=Dinesh C |last5=Ogawa |first5=Fumiaki |last6=Christie |first6=Sheila |last7=Malavasi |first7=Elise LV |last8=Makedonopoulou |first8=Paraskevi |last9=Mackie |first9=Shaun |last10=Malloy |first10=Mary P |last11=Wear |first11=Martin A |last12=Blackburn |first12=Elizabeth A |last13=Bramham |first13=Janice |last14=McIntosh |first14=Andrew M |last15=Blackwood |first15=Douglas H |date=2012-04-30 |title=A t(1;11) translocation linked to schizophrenia and affective disorders gives rise to aberrant chimeric DISC1 transcripts that encode structurally altered, deleterious mitochondrial proteins |journal=Human Molecular Genetics |language=en |volume=21 |issue=15 |pages=3374–3386 |doi=10.1093/hmg/dds169 |pmid=22547224 |pmc=3392113 }}</ref>||  [[DISC1]] (1q42)<ref name=":0" />||DISC1FP1 (11q14)<ref name=":0" />
|-
| t(2;5)(p23;q35) || [[Anaplastic large cell lymphoma]] || [[Anaplastic lymphoma kinase|ALK]] || [[NPM1]]
|-
| t(11;22)(q24;q11.2-12) || [[Ewing's sarcoma]] || [[FLI1]] || [[Ewing sarcoma breakpoint region 1|EWS]]
|-
| t(17;22) || [[Dermatofibrosarcoma protuberans|DFSP]] || COL1A1/[[COL1A1|Collagen I]] on chromosome 17 || [[PDGFB|Platelet derived growth factor B]] on chromosome 22
|-
| t(1;12)(q21;p13) || [[Acute myelogenous leukemia]] (rare subtype)<ref name=":1">{{Cite web |title=t(1;12)(q21;p13) ETV6/ARNT |url=https://atlasgeneticsoncology.org/haematological/1171/t(1;12)(q21;p13)#:~:text=leukemia%20treated%20with%20imatinib%20600,S%C3%A1nchez%20J%20et%20al |access-date=2025-03-12 |website=atlasgeneticsoncology.org}}</ref>||  ETV6 (TEL, 12p13)<ref name=":1" />||ARNT (1q21)<ref name=":1" />
|-
| t(X;18)(p11.2;q11.2) || [[Synovial sarcoma]] - 90% of cases<ref name=":2">{{cite journal |last1=Przybyl |first1=Joanna |last2=Sciot |first2=Raf |last3=Rutkowski |first3=Piotr |last4=Siedlecki |first4=Janusz A. |last5=Vanspauwen |first5=Vanessa |last6=Samson |first6=Ignace |last7=Debiec-Rychter |first7=Maria |title=Recurrent and novel SS18-SSX fusion transcripts in synovial sarcoma: description of three new cases |journal=Tumor Biology |date=December 2012 |volume=33 |issue=6 |pages=2245–2253 |doi=10.1007/s13277-012-0486-0 |pmc=3501176 |pmid=22976541 }}</ref>||  SS18 (18q11)<ref name=":2" />||[[SSX1]]/[[SSX2]] (Xp11)<ref name=":2" />
|-
| t(1;19)(q10;p10) || [[Oligodendroglioma]] and [[oligoastrocytoma]] || colspan="2" |  Associated with the 1p/19q co-deletion in oligodendroglioma and oligoastrocytoma, rather than a specific gene fusion<ref>{{Cite journal |last1=Eckel-Passow |first1=Jeanette E. |last2=Lachance |first2=Daniel H. |last3=Molinaro |first3=Annette M. |last4=Walsh |first4=Kyle M. |last5=Decker |first5=Paul A. |last6=Sicotte |first6=Hugues |last7=Pekmezci |first7=Melike |last8=Rice |first8=Terri |last9=Kosel |first9=Matt L. |last10=Smirnov |first10=Ivan V. |last11=Sarkar |first11=Gobinda |last12=Caron |first12=Alissa A. |last13=Kollmeyer |first13=Thomas M. |last14=Praska |first14=Corinne E. |last15=Chada |first15=Anisha R. |date=2015-06-25 |title=Glioma Groups Based on 1p/19q, IDH, and TERT Promoter Mutations in Tumors |journal=The New England Journal of Medicine |volume=372 |issue=26 |pages=2499–2508 |doi=10.1056/NEJMoa1407279 |issn=1533-4406 |pmc=4489704 |pmid=26061753}}</ref><ref>{{cite journal |last1=Cairncross |first1=Gregory |last2=Jenkins |first2=Robert |title=Gliomas With 1p/19q Codeletion:a.k.a. Oligodendroglioma |journal=The Cancer Journal |date=November 2008 |volume=14 |issue=6 |pages=352–357 |doi=10.1097/PPO.0b013e31818d8178 |pmid=19060598 }}</ref>
|-
| t(17;19)(q22;p13) || [[Acute lymphoblastic leukemia|Acute Lymphoblastic Leukemia]] very rare subtype, <1% of Acute Lymphoblastic Leukemia. (associated with poor prognosis)<ref name=":3">{{Cite journal |last1=Wu |first1=Shuiyan |last2=Lu |first2=Jun |last3=Su |first3=Dongni |last4=Yang |first4=Fan |last5=Zhang |first5=Yongping |last6=Hu |first6=Shaoyan |date=March 2021 |title=The advantage of chimeric antigen receptor T cell therapy in pediatric acute lymphoblastic leukemia with E2A-HLF fusion gene positivity: a case series |journal=Translational Pediatrics |language=en |volume=10 |issue=3 |pages=686–691 |doi=10.21037/tp-20-323 |doi-access=free |pmid=33880339 |pmc=8041607 |issn=2224-4344}}</ref>||  [[TCF3]] (E2A, 19p13)<ref name=":3" />||[[HLF (gene)|HLF]] (17q22)<ref name=":3" />
|-
| t(7,16) (q32-34;p11) or t(11,16) (p11;p11) || [[Low-grade fibromyxoid sarcoma]] – most cases <ref name=":4">{{cite journal |last1=Mohamed |first1=Mustafa |last2=Fisher |first2=Cyril |last3=Thway |first3=Khin |title=Low-grade fibromyxoid sarcoma: Clinical, morphologic and genetic features |journal=Annals of Diagnostic Pathology |date=June 2017 |volume=28 |pages=60–67 |doi=10.1016/j.anndiagpath.2017.04.001 |pmid=28648941 }}</ref>|| [[FUS (gene)|FUS]] (16p11)<ref name=":4" />|| [[CREB3L1]] (11p11)<ref name=":4" />
|}

==See also==
* [[Accipitridae]]
* [[Aneuploidy]]
* [[Chromosome abnormalities]]
* [[DbCRID]]
* [[Fusion gene]]
* [[Pseudodiploid]]
* ''[[Takifugu rubripes]]''

== References ==
{{Reflist}}

== External links ==
* {{Commons category-inline|Chromosomal translocations}}

{{chromo}}
{{Chromosomal abnormalities}}
{{Mutation}}
{{Authority control}}

{{DEFAULTSORT:Chromosomal Translocation}}
[[Category:Chromosomal abnormalities]]
[[Category:Cytogenetics]]
[[Category:Modification of genetic information]]