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[Cowden syndrome. Ä«¿ìµ§ ÁõÈıº, ÄÚµç ÁõÈıº, Äڿ쵧 ÁõÈıº] - ðû

1. Cowden syndromeÀ̶õ?

2. À¯ÀüÀÚ º¯ÀÌ

3. ¾Ç¼ºÁúȯ screening

4. ³»½Ã°æ ¼Ò°ß

5. Vascular abnormality

6. ÄÚµå¿Í »êÁ¤Æ¯·Ê

7. References


1. Cowden syndromeÀ̶õ?

À§³»½Ã°æ ¼Ò°ßÀÔ´Ï´Ù. Áø´ÜÀº ¹«¾ùÀÌ°Ú½À´Ï±î?

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ÈùÆ®ÀÔ´Ï´Ù. À§ÀÇ ¿ëÁ¾ÁõÀε¥ ½Äµµ¿¡´Â glycogen acanthosis°¡ ÇöÀúÇÏ¿´½À´Ï´Ù. 40´ë ÈĹÝÀÓ¿¡µµ ºÒ±¸ÇÏ°í... Áø´ÜÀº ¹«¾ùÀÌ°Ú½À´Ï±î?

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µÎ¹ø° ÈùÆ®ÀÔ´Ï´Ù. ´ëÀå¿¡´Â polyposis°¡ ÀÖ¾ú´Âµ¥ ´ëµÎºÐ inflammatory polyp¾ú°í ÀϺθ¸ adenomatous polypÀ̾ú½À´Ï´Ù.

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¼¼¹ø° ÈùÆ®ÀÔ´Ï´Ù. À¯¹æ ¼ö¼ú°ú, Àڱà ¼ö¼ú°ú, °©»ó¼± ¼ö¼úÀÇ º´·Âµµ ÀÖ¾ú½À´Ï´Ù.

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±×·¸½À´Ï´Ù. Cowden ÁõÈıºÀÔ´Ï´Ù.

Cowden syndrome Ä«¿ìµ§ ÁõÈıºÀº EndoTODAY¿Í Àο¬ÀÌ ±í½À´Ï´Ù. 2010³â EndoTODAY¸¦ mobile versionÀ¸·Î °³ÆíÇÒ ¶§ ù mobile format EndoTODAY Áõ·Ê°¡ Cowden syndromeÀ̾ú½À´Ï´Ù.

Cowden syndromeÀº ȯÀÚ À̸§À» µý Áúº´¸íÀÔ´Ï´Ù. óÀ½ ±â¼úµÈ ȯÀÚ°¡ Cowden ¾¾¿´½À´Ï´Ù (Lloyd KM. Ann Intern Med 1963). Cowden syndromeÀº ÇǺÎ, ±¸°­ Á¡¸·ÀÇ º´º¯À» Ư¡À¸·Î ÇÏ°í ¼ÒÈ­°ü¿¡ polyposis¸¦ ÀÏÀ¸Åµ´Ï´Ù. ¿©·¯ Àå±â¿¡ hamartoma¸¦ µ¿¹ÝÇÕ´Ï´Ù. Ç÷°üÁúȯÀ̳ª ÇǺÎÁúȯÀ» °¡Áø ºÐÀÌ µÚ´Ê°Ô Cowden syndromeÀ¸·Î Áø´ÜµÇ°í ³î¶ó¼­ Å« º´¿øÀ» ã´Â °æ¿ì°¡ ÀÖ½À´Ï´Ù.

Ä«¿ìµ§ ÁõÈıºÀº 10q23¿¡ À§Ä¡ÇÏ´Â Á¾¾ç¾ïÁ¦À¯ÀüÀÚ PTEN µ¹¿¬º¯ÀÌ¿¡ ÀÇÇØ ¹ß»ýÇÏ´Â PTEN °ú¿ÀÁ¾ ÁõÈıº Áß ÇϳªÀÔ´Ï´Ù. ¾à Àý¹ÝÀº ºÎ¸ð·ÎºÎÅÍ »ó¿°»öü ¿ì¼ºÀ¸·Î ¹°·Á¹Þ°í ¾à Àý¹ÝÀº °¡Á··ÂÀÌ ¾ø½À´Ï´Ù. ´Ù¹ß¼º ¾È¸é ÅÐÁ¾(facial trichilemmona), À¯µÎÁ¾¼º ±¸Áø(papillomatous papule), ¸»´Ü °¢È­Áõ(acral keratosis)°ú °°Àº ÇǺÎÁ¡¸·º´¼Ò¸¦ °¡Áö´Â °æ¿ì°¡ ¸¹´Ù. ¾È¸é ÅÐÁ¾Àº ¸ð³¶ÀÇ outer root sheath¿¡ ¹ß»ýÇÏ´Â ¾ç¼º °ú¿ÀÁ¾ º´º¯À¸·Î, õõÈ÷ ÀÚ¶ó°í ÇǺλö°ú ºñ½ÁÇϸç Á÷°æÀº 1-5 mmÀÌ°í ¾ó±¼°ú ¸ñÀÇ Çì¾î¶óÀÎ ±Ùó¿¡¼­ Àß ¹ß°ßµË´Ï´Ù.

À§Àå°ü ¿ëÁ¾Àº ½Äµµ¿¡¼­ ´ëÀå±îÁö ¾îµð¿¡³ª °¡´ÉÇϸç Å©±â´Â 1 mm¿¡¼­ ¼ö cm±îÁö ´Ù¾çÇϳª ´ë°³ Å©Áö ¾Ê°í ÁÖÀ§ Á¡¸·°ú µ¿ÀÏÇÑ »öÁ¶¸¦ º¸ÀÌ¸ç ¹ÐÁýµÇ¾î ³ªÅ¸³ª´Â °ú¿ëÁ¾ÀÔ´Ï´Ù. °¡Á·¼º À¯Àü¼º ¿ëÁ¾Áõ (familial adenomatous polyposis, FAP)¿¡¼­ º¸ÀÌ´Â ºñ±³Àû ±ÕÀÏÇÑ ¼±Á¾¼º ¿ëÁ¾°ú´Â È®¿¬È÷ ±¸ºÐµË´Ï´Ù. ½Äµµ º´¼Ò´Â ±Û¸®ÄÚÁ¨ °¡½Ã¼¼Æ÷ÁõÀÔ´Ï´Ù. ±Û¸®ÄÚÁ¨ °¡½Ã¼¼Æ÷Á¾Àº °í·É¿¡¼­ ÈçÈ÷ ¹ß°ßµÇ´Âµ¥, ºñ±³Àû ÀþÀº ȯÀÚ¿¡¼­ ½ÉÇÑ Å¬¸®ÄÚÁ¨ °¡½Ã¼¼Æ÷Á¾ÀÌ ¹ß°ßµÇ¸é Ä«¿ìµ§ ÁõÈıºÀ» °í·ÁÇØ¾ß ÇÕ´Ï´Ù.

Ä«¿ìµ§ ÁõÈıºÀº ´Ù¹ß¼º ¾Ï ÁõÈıºÀÇ ÇϳªÀ̸ç À¯¹æ¾Ï, °©»ó¼±¾Ï, Àڱ󻸷¾Ï, ´ëÀåÁ÷Àå¾Ï, ½ÅÀå¾Ï ¹× À§¾ÏÀÇ À§ÇèÀÌ ³ô½À´Ï´Ù. ÀϹÝÀûÀÎ °ËÁøº¸´Ù ÈξÀ ªÀº °£°ÝÀ¸·Î ¸¹Àº Àå±â¿¡ ´ëÇÑ °ËÁøÀÌ ÇÊ¿äÇÕ´Ï´Ù.

Cowden syndrome is a hereditary condition which causes multiple types of benign tissue overgrowth (called hamartomas) and a risk of breast, thyroid, and uterine cancers. The most consistent features of CS are small flesh-colored bumps on the skin involving a hair follicle (trichilemmomas) and small wart-like growths (papillomatous papules) on the face, hands and mouth. CS is also often associated with a large head size (macrocephaly) and hamartomatous polyps of the small and large intestine. Thyroid adenomas, goiter, and nodules are also seen at increased frequency. Women are at increased risk for benign breast conditions, such as ductal hyperplasia, papillomatosis, fibrocystic breast disease, or fibroadenomas. Less commonly seen are benign fatty tumors (lipomas), blood vessel growths (hemangiomas), and other changes. (University of Iowa)

Cowden syndrome°ú ºñ½ÁÇÑ ¸î °³ÀÇ Áúº´¸íÀÌ Àִµ¥ ¸ðµÎ PTEN À¯ÀüÀÚ ÀÌ»ó°ú °ü·ÃµÇ¾î À־ ÃÖ±Ù¿¡´Â ÇÑ ÁúȯÀÇ ´Ù¸¥ spectrumÀ¸·Î º¸´Â °æÇâÀÌ ÀÖ½À´Ï´Ù. PTEN harmatoma tumor syndromeÀ¸·Î ºÎ¸¨´Ï´Ù. ±× ÀÓ»óÀû Ư¡Àº ¾Æ·¡¿Í °°½À´Ï´Ù.

¼­¾ç ÀÚ·á¿©¼­ ±×·±Áö À§¾Ï¿¡ ´ëÇÑ ¾ð±ÞÀÌ ¾ø½À´Ï´Ù. ±×·¯³ª Cowden ÁõÈıº¿¡¼­ À§¾Ï ¹ß»ý·üÀÌ ´Ù¼Ò ³ô½À´Ï´Ù.

Non-malignant features of Cowden syndrome

Cowden syndrome¿¡ ´ëÇÑ ÃÖ±Ù ¸®ºä¸¦ ¼Ò°³ÇÕ´Ï´Ù. Á¦¸ñÀÌ Cowden syndrome: Recognizing and managing a not-so-rare hereditary cancer syndromeÀÔ´Ï´Ù. µå¹°±â´Â Çѵ¥ ±×·¸´Ù°í ¾ÆÁÖ µå¹°Áöµµ ¾ÊÀº ÁúȯÀÔ´Ï´Ù.

¾à Àý¹ÝÀº ºÎ¸ð·ÎºÎÅÍ ¹°·Á¹Þ°í ¾à Àý¹ÝÀº sporadicÀÔ´Ï´Ù. Autosomal dominant·Î À¯ÀüµÇ¹Ç·Î ÀÚ³àÀÇ Àý¹Ýµµ °°Àº ÁúȯÀ» °¡Áý´Ï´Ù. µû¶ó¼­ À¯ÀüÇÐÀû °Ë»ç¿Í »ó´ã, ±×¸®°í °¡Á·¿¡ ´ëÇÑ screeningÀÌ ÇÊ¿äÇÕ´Ï´Ù.

¼ÒÈ­±â³»°ú ÀÇ»çÀÎ ÇÊÀÚ´Â Cowden syndromeÀÇ ¾Ï¹ß»ý À§Çè¿¡ °ü½ÉÀ» °¡Áö°í ÀÖÁö¸¸ ¾Ï ÀÌ¿Ü¿¡µµ ¾Æ·¡¿Í °°Àº ½Å°æ, ÇǺΠÁúȯ µîÀÌ Cowden syndromeÀÇ Áß¿ä Ư¡ÀÔ´Ï´Ù.

- Macrocephaly (larger-than-average head size)
- Trichilemmomas (benign skin lesions, skin tags) and papillomatous papules (raised areas on the skin)
- Learning disabilities and/or autism
- Development of lipomas (benign tumors of fatty tissue), intestinal polyps, and uterine fibroids (benign tumors of the uterus)


trichilemmomas

2021³â 10¿ù À̼±¿µ ±³¼ö´Ô ±³À°ÀÚ·á

Cowden ȯÀÚ °ü¸®ÀÇ ÇÙ½ÉÀº ¾Ï°ËÁøÀÔ´Ï´Ù. »ó¼¼ÇÑ ³»¿ëÀº ¾Æ·¡¸¦ Âü°íÇϽñ⠹ٶø´Ï´Ù. À§¾ÏÀÌ ºüÁ³´Âµ¥¿ä, Cowden ÁõÈıº¿¡¼­ À§¾Ïµµ ¾à°£ ¸¹ÀÌ ¹ß»ýÇÑ´Ù°í ¾Ë·ÁÁ® ÀÖ½À´Ï´Ù. À§³»½Ã°æÀ» 1³â¿¡ Çѹø Çϵµ·Ï ±ÇÇÏ°í ÀÖ½À´Ï´Ù.

ÀϺ» Ã¥¿¡ ³ª¿Â »çÁøÀÔ´Ï´Ù.


2. À¯ÀüÀÚ º¯ÀÌ

PTEN is a tumor suppressor gene located on chromosome 10q23.3. It encodes a phosphatase that influences the cell cycle, causing G1 arrest and apoptosis.


[Cowden syndromeÀÌ ÀǽɵǴµ¥ À¯ÀüÀÚ º¯ÀÌ°¡ È®ÀεÇÁö ¾ÊÀ¸¸é?]

PTEN À¯ÀüÀÚ °Ë»ç¸¦ ÇÏ¸é ´ëºÎºÐ ÀÌ»óÀÌ È®Àε˴ϴÙ. °£È¤ PTEN À¯ÀüÀÚ º¯ÀÌ°¡ È®ÀεÇÁö ¾Ê´õ¶óµµ ¾Æ·¡¿Í °°Àº ÀÓ»óÀû Ư¼ºÀÌ ÀÖÀ¸¸é Cowden syndrome¿¡ ÁØÇÏ¿© °ü¸®ÇÏ¸é µË´Ï´Ù.


3. ¾Ç¼ºÁúȯ screening

Cowden syndrome¿¡¼­´Â ´Ù¾çÇÑ ¾Ç¼ºÁúȯÀÌ ¹ß»ýÇÒ ¼ö ÀÖ½À´Ï´Ù.

Cowden syndrome ȯÀÚ¿¡¼­ ¹ß»ýÇÑ ½ÅÀå¾Ï

Cowden syndrome ȯÀÚ °ü¸®ÀÇ ÇÙ½ÉÀº ´Ù¾çÇÑ ¾Ï¿¡ ´ëÇÑ °ËÁø°ú ÀûÀýÇÑ

Link

Cowden syndrome ȯÀÚÀÇ ¾Ç¼ºÁúȯ Á¶±âÁø´ÜÀ» À§ÇÑ °ËÁø ÁöħÀÔ´Ï´Ù.


4. ³»½Ã°æ ¼Ò°ß

[Áõ·Ê 1]

2010³â 9¿ù 9ÀÏ EndoTODAY¸¦ ¸ð¹ÙÀÏ·Î °³ÆíÇÑ ÈÄ Ã¹ ÀÚ·á°¡ Cowden's disease (EndoTODAY 20100909)¿´½À´Ï´Ù. ¾Æ·¡¿¡ ¿Å±é´Ï´Ù.

¿ëÁ¾Áõ(polyposis)´Â ¼±Á¾¼º ¿ëÁ¾Áõ°ú ºñ¼±Á¾¼º ¿ëÁ¾ÁõÀ¸·Î ³ª´©¾îÁý´Ï´Ù. ºñ¼±Á¾¼º ¿ëÁ¾ÁõÀÇ ´ëÇ¥´Â ±× À¯¸íÇÑ Peutz-Jeghers syndromeÀÌÁö¿ä. Cowden¡¯s disease, Bannayan-Ruvalcabe-Riley syndrome, hereditary mixed polyposis syndrome, intestinal ganglioneuromatosis and neurofibromatosis, Devon family syndrome, Basal cell nevus syndromeµîµµ ¸ðµÎ ºñ¼±Á¾¼º ¿ëÁ¾ÁõÀÔ´Ï´Ù.

40´ë ¿©¼ºÀÌ ÃÖ±Ù ¹ß°ßµÈ À§¿Í ÀåÀÇ nonadenomatous polyposis·Î ÀǷڵǾú½À´Ï´Ù. ȯÀÚ´Â °©»ó¼±¾Ï, À¯¹æ¾Ï, ÀڱþÏÀ¸·Î ¼ö¼ú¹ÞÀº °ú°Å·ÂÀÌ ÀÖ¾ú½À´Ï´Ù. ¾ó±¼°ú ¸ñ¿¡ ž ¶§ºÎÅÍ ÁãÁ¥ÀÌ ÀÖ¾ú´Ù°í Çϸç, ¼Õ¹ß¿¡ ¹°Áý¾ç º´º¯ÀÌ ÀÖ¾ú½À´Ï´Ù. ÀÌ ¸ðµç ¼Ò°ßÀº PTEN À¯ÀüÀÚÀÇ µ¹¿¬º¯ÀÌ¿¡ ÀÇÇÑ autosomal dominant ÁúȯÀÎ Cowden's disease¿¡ ÇÕ´çÇÑ ¼Ò°ßÀÔ´Ï´Ù. À§¿¡´Â ¸Å¿ì ¸¹Àº sessile polypÀÌ ÀÖ¾úÀ¸¸ç Á¶Á÷°Ë»ç´Â hyperplastic polypÀ¸·Î º¸°íµÇ¾ú½À´Ï´Ù.

PTEN À¯ÀüÀÚÀÇ µ¹¿¬º¯ÀÌ°¡ ¹ß°ßµÇ¾ú½À´Ï´Ù. PTEN À¯ÀüÀÚ 5¹ø° exon¿¡¼­ 395¹ø° ¿°±â¼­¿­ÀÌ G¿¡¼­ A·Î ġȯµÊ¿¡ µû¶ó 129¹ø° ¾Æ¹Ì³ë»êÀÌ Gly¿¡¼­ ArgÀ¸·Î ¹Ù²î´Â missense variationÀÌ ¹ß°ßµÈ °ÍÀÔ´Ï´Ù.

ÀÌ È¯ÀÚÀÇ ´ëÀå³»½Ã°æ¿¡¼­ ¸Å¿ì ¸¹Àº ¿ëÁ¾ÀÌ ¹ß°ßµÇ¾ú½À´Ï´Ù. Á¶Á÷°Ë»ç´Â inflammatory fibrinoid polypÀ¸·Î º¸°íµÇ¾ú½À´Ï´Ù. À§¿Í ´Þ¸® ´ëÀå ¿ëÁ¾µéÀº Å©±â Â÷ÀÌ°¡ ½ÉÇߴµ¥ ÀÌ Á¡ÀÌ ÀϹÝÀûÀÎ ¼Ò°ßÀÎÁö ¾Æ´Ï¸é ÀÌ È¯ÀÚÀÇ Æ¯º°ÇÑ ¼Ò°ßÀÎÁö Àúµµ Àß ¸ð¸¨´Ï´Ù.


[Áõ·Ê 2]

Gastric hamartomatoous polyps

Colonic inflammatory polyps


[Áõ·Ê 3] À¯ÀüÇÐÀû confirmÀº µÇÁö ¾ÊÀ½.

Gastroduodenal hamartomatous polyposis


Cowden syndromeÀ» ÀǽÉÇÒ ¼ö ÀÖ´Â ÁÁÀº hint Áß Çϳª´Â À¯³­È÷ ½ÉÇÑ ½Äµµ glycogen acanthosisÀÔ´Ï´Ù.

À§Àå°üÀÇ ´Ù¾çÇÑ hamartomatous polyp¿¡ ´ëÇؼ­´Â Gastric Hamartomatous Polyps - Review and Update (Clin Med Insights Gastroenterol 2016)¸¦ Âü°íÇϽñ⠹ٶø´Ï´Ù. ¹®Çå Áß Cowden syndrome ºÎºÐÀ» ¿Å±é´Ï´Ù.

The incidence of CS (Cowden syndrome) in the general population is 1 in 200,000 and more than 90% patients present in the adult life by the late third decade. Mucocutaneous hamartomas (trichilemmomas, acral keratosis, and papillomatous lesions) are pathognomonic features of CS. Macrocephaly and Lhermitte?Duclos disease or dysplastic cerebellar gangliocytoma are two other features considered specific for CS and are included in the major criteria.

These patients have an increased risk of breast, thyroid, and endometrial carcinoma, which are the other major criteria. Patients with CS also have a predisposition to benign hamartomatous outgrowths such as lipomas, arteriovenous malformations, fibrocystic breast disease, benign thyroid nodules, multiple uterine leiomyomas (fibroids) and/or bicornuate uterus, and gastrointestinal polyps. Diffuse esophageal glycogenic acanthosis is present in more than 80% of CS patients and may be diagnostic for CS in the presence of other benign gastrointestinal polyposis.

Gastrointestinal polyps occur in up to 50% of patients with CS with a wide variety of endoscopic and histologic features, including adenomatous, inflammatory, hyperplastic, lymphoid, ganglioneuromatous, and leiomyomatous polyps. The majority of CS patients (>50%) have two or more different polyp histologies. Though most studies describe polyps in CS being colonic, gastric polyps are present in almost all patients with CS and are usually numerous with a variable appearance. Depending on the major histologic component, they can be smooth contoured or have a hyperplastic/papillary configuration endoscopically. The polyps in the stomach are commonly misdiagnosed as hyperplastic hamartomatous polyps. Though dysplasia has not been reported in gastric polyps in CS, patients with CS and gastric cancer have been reported. The risk of colorectal carcinoma in CS is 7%?15%, and 1 in 100 patients with CS may develop gastric malignancy.

Individuals with multiple gastrointestinal hamartomas or ganglioneuromas should be evaluated for PTEN gene mutation. The recommended gastrointestinal surveillance for patients with PTEN gene mutation is colonoscopy and esophagogastroduodenoscopy examination beginning at the age of 15 years and repeated every two years or two to three years, though different suggestions has been suggested.


5. Vascular abnormality

AVMs and haemangiomas are not widely recognised features of Cowden syndrome.

Imaging of the gluteal arteriovenous malformation (AVM) in case 1. All views are in anterior-posterior orientation. (A) Angiogram of the distal aorta and iliac vessels showing the dilated left common iliac and left internal iliac arteries. (B) Computed tomographic angiogram showing a large AVM arising from the left superior gluteal artery and extending through the sciatic notch into the left buttock. (C) A reconstructed rendered surface angiogram showing the AVM arising from the left superior gluteal artery. (J Med Genetics 42(8))

Vascular anomalies in patients with a PTEN mutation are typically multifocal intramuscular combinations of fast-flow channels and ectopic fat. Cerebral DVAs (developmental venous anolamies) are very common. PTEN mutational analysis should be considered for all macrocephalic patients with fast-flow vascular anomalies or multiple intracranial DVAs. (Tan WH. J Med Genet 2007)

(A) Dural arteriovenous (AV) fistula (patient 23); (B, C) gadolinium-enhanced T1-weighted MRI of the brain showing developmental venous anomalies (arrows). (D, E) Aangiography of (D) patient 11 with paraspinal and (E) patient 15 with right lower limb arteriolovenous malformations, showing disproportionate venous ectasia, typical of PTEN lesions. (Tan WH. J Med Genet 2007)

Monitoring for vascular anomalies is not currently part of the ¡°standard of care¡± for these patients.


6. ÄÚµå¿Í »êÁ¤Æ¯·Ê

2016³â 7¿ù 1ÀÏ Èñ±ÍÁúȯ »êÁ¤Æ¯·Ê °í½Ã

Cowden syndromeÀº Q85.84 ÄÚµå·Î »êÁ¤Æ¯·Ê ´ë»óÀÔ´Ï´Ù.


[FAQ]

[2022-7-22. ¾Öµ¶ÀÚ Áú¹®]

Cowden ȯÀÚ¿Í Cronkhite-Canada syndrome ȯÀÚ, juvenile polyposis, FAP µîÀÇ polyposis ȯÀÚµéÀº pathology·Î¸¸À¸·Îµµ Áø´ÜÀÌ °¡´ÉÇÑ °ÍÀÎÁö, ÀÓ»óÁõ»óÀ» Á¾ÇÕÇؼ­ º¸´Â °ÍÀÎÁö Çò°¥¸®´Â °Í °°½À´Ï´Ù. FAP ȯÀÚ´Â 100°³ÀÌ»óÀÇ ¼±Á¾ÀÌ ³ª¿À´Â °ÍÀ¸·Î Áø´ÜÇÏ°í, Cowden ȯÀÚ´Â ½Äµµ achanthosis °¡ ÀÖ°í Á¶Á÷°Ë»ç »ó °ú¿ÀÁ¾ µîÀ¸·Î ³ª¿À°í Cronkhite canada syndrome ȯÀÚ´Â ³¶Æ÷»ó ¼±°üÈ®ÀåÀ¸·Î Áø´ÜÇϴµ¥ juvenile polyposisÇÏ°í´Â ³»½Ã°æÀû ¼Ò°ßÀ» ±¸ºÐÇÏ´Â °ÍÀÌ ¸Â´ÂÁö ±Ã±ÝÇÕ´Ï´Ù.

[2022-7-22. ÀÌÁØÇà ´äº¯]

ÁÁÀº Áú¹®ÀÔ´Ï´Ù. ³»½Ã°æ ¼Ò°ß¿¡ ¾à°£ÀÇ Â÷ÀÌ°¡ ¾ø´Â °ÍÀº ¾Æ´ÏÁö¸¸ Áø´Ü¿¡ »ç¿ëÇÒ Á¤µµ·Î specificÇÑ °ÍÀº ¾Æ´Õ´Ï´Ù. FAP´Â adenomatous polyposisÀ̹ǷΠº´¸®·Î ±¸ºÐµÇ°ÚÀ¸³ª ´Ù¸¥ Á¾·ù´Â Á¶Á÷ÇÐÀû Â÷À̵µ specificÇÏÁö ¾Ê½À´Ï´Ù. ÀÓ»ó»óÀÇ Â÷ÀÌ¿Í À¯ÀüÇÐÀûÀÎ °Ë»ç¸¦ ¸ðµÎ °í·ÁÇÑ´Ù°í º¸´Â °ÍÀÌ ÁÁ°Ú½À´Ï´Ù.


[References]

1) EndoTODAY Cowden º´

2) PTEN À¯ÀüÀÚ Á¤º¸

3) ¿µ¹® ȯÀÚ Á¤º¸
   - MD Anderson Cancer Research Center (PDF)
   - cancer.net
   - University of Iowa

4) ¿ëÁ¾Áõ Æú¸³ÁõÈıº polyposis syndrome - ³»½Ã°æ¼¼¹Ì³ª °­ÀÇ·Ï. ÀÓÁ¾ÇÊ. PDF 0.7M

5) Hamartomatous polyposis syndrome (PDF)

© ÀÏ¿ø³»½Ã°æ±³½Ç ¹Ù¸¥³»½Ã°æ¿¬±¸¼Ò ÀÌÁØÇà. EndoTODAY Endoscopy Learning Center. Lee Jun Haeng