Stages and Grades of Ductal Carcinoma in Situ. Carcinoma in situ шейки матки


nsitu Meme Kanserinde Tedavi

NSTU MEME KANSERNDE TEDAV

n situ kanser duktal epitelden gelien intraduktal in situ karsinom (DCIS) veya lobl epitelinden gelien lobler in situ karsinom (LCIS) olarak snflandrlr.1 Mammografik taramalarn giderek artan oranda kullanm, noninvaziv kanserlerin daha sk tanmlanmalarn salamtr, bu tan u anda tm meme kanserlerinin % 15-20'sini oluturmaktadr. DCIS genellikle mikrokalsifikasyonlar veya yumuak doku dzensizlii olarak belirlenir. Birka histolojik alt grubu vardr: Mikropapiller, papiller, solid, kribriform, ve komedokarsinom. Baz bulgular komedokarsinomun daha agresif olduunu ve mikroinvazyon olaslnn yksekliini gstermektedir.2 LCIS genellikle baka bir nedenle yaplan biopside rastlantsal olarak saptanr. Premalign bir lezyondan ok, geliecek bir invazif hastaln belirtisi olarak deerlendirilir. DCIS'yi atipik hiperplaziden ayrdetmek g olabilecei ve DCIS'nin baz tipleri LCIS ile karabilecei iin, biopsi materyelinin ikinci bir incelemesi yararl olabilir.

ntraduktal karsinoma

DCIS'nin geleneksel tedavisi mastektomi olmutur. Bu tedavi %1-2 orannda lokal rekrrens veya uzak metastazla sonulanr. Konservatif cerrahi ve radyoterapi deneyimi, makul bir alternatif olabileceini gstermitir. % 9-21 orannda meme kanseri rekrrensi grlr ki, bunun da yars invaziv karsinom eklindedir. Rekrrenste mastektomi yaplmas akllca olur ve sakalm, primer mastektomi kadar mkemmeldir.3 Mastektomi ile konservatif cerrahi art radyoterapiyi kyaslayan randomize almalar yaplmamtr ancak NSABBP alma B-17'de lokalize DCIS nedeniyle temiz snrlarla eksizyonel biopsi yaplm 790 hasta, ek olarak radyoterapi (50 Gy) veya tedavisiz olarak gruplandrlmtr.4 Her iki kolda da hastalarn %80'i mammografi ile saptanmtr ve % 70'inde lezyonlar kktr ( 1 cm.). Radyoterapi alm grupta 5 yllk hastalksz yaam, o taraf memede geliecek kanser orannn dmesine bal olarak daha yksek bulunmutur. Beinci ylda tedavisiz grupta rekrrens DCIS grlme kmlatif oran % 10.4 iken radyoterapili grupta % 7.5'a (p=0.05), daha da nemlisi invaziv kanser geliimi % 10.5'den % 2.9'a dmtr(p< 0.001). Bu almada imdiye kadar meme kanserinden sadece 3 lm (%0.4) bildirilmitir ki, bu oran mastektomi serilerinde bildirilenden hi de farkl deildir. NSABBP aratrmaclar lokalize DCIS tedavisinde lokal eksizyon ve meme irradyasyonunun, mastektomiye kabul edilebilir bir alternatif olduu sonucuna varmlardr.

Rekrrens asndan yksek riskli hastalarn saptanabilmesi iin B-17 almasndaki 790 hastann patolojik materyelleri tekrar irdelenmitir.5 Bu almann sonucu, cerrahi snrlarn temiz olmamas ile orta veya belirgin komedonekrozun varlnn ayn taraf memede rekrrens asndan etkili bamsz prediktrler olduu gzlenmitir. Ancak bu zelliklerdeki olgularda dahi rekrrens oran, mastektomiyi tercih etmeyi dayatacak kadar yksek bulunmamtr.

Bu sonulara ek olarak, baz retrospektif non-randomize aratrmalarda, dikkatle seilmi olgularda, sadece lokal eksizyon sonras, ayn memede dk rekrrens oranlar gsterilmitir. rradyasyonun eklenmesi, en dk riskli gruplarda dahi, rekrrens ve invaziv kanser geliimi olasln azaltmaktadr. Bu sonu, sadece eksizyonu tercih edenlerin karar verirken gz nnde tutmalar gereken bir faktrdr. Son zamanlarda Patologlar arasnda, dk riskli DCIS olgularnn tanmlanmas konusunda tartmalar vardr. Planlanp retrospektif olarak test edilen patolojik evreleme sistemleri konusunda hala tam bir fikir birlii oluturulamamtr.6-9 Sadece cerrahi veya cerrahi+radyoterapi uygulandktan sonra median 79 ay takip edilmi 333 hastann retrospektif analizi iin kullanlan Van Nuys Prognostik Endeksinin (VNPI) tedavide yol gsterici olabilmesi iin bamsz ve prospektif deerlendirmesinin yaplmas gereklidir.10

Mammografide saptanan non-palpabl lezyon ve mikrokalsifikasyon nedeniyle meme koruyucu tedavi planlanan hastalara, ine lokalizasyon biopsisi uygulanr. Koruyucu meme cerrahisi sonras, lezyonlarn tam eksize edildiini kontrol etmek ve patolojik rneklemeye yol gstermek iin spesmen radyografisi ekilmelidir. Patolog eksize edilmi segmentin makroskopik detayl bir tanmn yapmal ve asl kesitlerde snrlarn belirlenebilmesi iin kenarlarnda boyama yapmaldr. Lezyon ile kalsifikasyonlar arasndaki iliki ve tmrn boyanm rezeksiyon snrlar ile mesafesi net olarak tanmlanmaldr. Operasyon sonras, pheli mikrokalsifikasyonlarn hepsinin karldndan emin olmak iin mammografi tekrarlanmaldr. ekilen mammografide, kalm mikrokalsifikasyonlar varsa, radyoterapi ncesi reeksizyon uygulanmaldr. Cerrahi snrn tmrle tutulu olmas durumundaki tedavi seenei halen tartmaldr. Sklkla, ilk eksizyon pozitif snr tanmlyorsa, eksizyon tekrarlanr. Reeksizyon materyelinde hastaln uzanm deerlendirilip, mastektomi veya radyoterapi konusunda bir seim yaplr. Pozitif lenf bezi nadir olduu iin, ayn seansta dk seviyeli bir aksiller disseksiyon art deildir.11 Lenf bezi tutulumu gsterilen hastalar, Evre II gibi tedavi edilmelidirler.

Lokal eksizyon sonras devam eden cerrahi snr mikroskopik tutulumu veya DCIS tans ile birlikte yaygn pheli mikrokalsifikasyonlarda tedavi genellikle mastektomidir.

Optimal tedavi yant ve tatmin edici kozmetik sonular iin cerrahi ve radyoterapi teknikleri ok nem tar. Dikkatli planlama ve teknik ile radyasyonun; soldaki lezyonlarda myokardial zarar, radyasyon pnmonisi, kol demi, brakial pleksopati, sekonder maligniteler gibi yan etkileri en aza indirilebilir. Tedavi sahasnda sarkom ve sekonder lenfomalar ok nadirdir. 45 yan altndaki radyoterapi alm kadnlarda dier memede kanser riskinde art tanmlayan bir rapor mevcuttur. Bu riski mmkn olduunca dk tutmak iin, dier memenin en az radyasyon dozu alaca teknikler uygulanmaldr.12, 13

Standart Tedavi 14-19

Konservatif cerrahi(yeterli eksizyon) + Memeye 50Gy Radyoterapi

Ayn memedeki olas asenkron hastal saptamak iin dzenli mammografi ve fizik muayene uygulanmaldr.20

n situ lobuler karsinom

LCIS ok tartmal bir terimdir; bazlar bu lezyonu ''lobuler neoplazi'' olarak tanmlamay tercih ederler. Bu lezyon genellikle memede yaygn ve sklkla bilateraldir. Premalign bir lezyondan ok invaziv bir hastaln gelieceinin gstergesi olarak deerlendirilir. LCIS'li bir hastada 25 yl iinde nvasif kanser (lobuler veya daha sk olmak zere invaziv duktal kanser) geliim olasl % 25'tir. Geliebilecek kanser riski, memedeki LCIS odaklarnn yaygnl ile balantl deildir. LCIS'li hastalarn tedavisi konusu olduka tartmaldr; biyopsi sonras herhangi bir tedavi planlamadan fizik muayene ve mammografi ile dikkatli takipten, profilaktik bilateral mastektomiye dek deiik neriler mevcuttur. n situ bir lezyon iin aksiller disseksiyon gerekli deildir. Birok hekim hastann metastatik kanser geliim olasl konusunda aydnlatldktan sonra fizik muayene ve mammografi ile takip edilmesini yelemektedirler.21, 22 nvaziv kanser geliimini engellemek iin Tamoxifen kullanmnn sonularn deerlendirmek iin yaplacak ok merkezli almalarda LCIS nedeniyle lokal eksizyon yaplm hastalar tercih edilmelidir.23 LCIS veya DCIS nedeniyle mastektomi yaplm hastalarda mastektominin yaratt anatomik bozukluu gidermek iin rekonstrktif cerrahi uygulanmaktadr. Bu operasyon mastektomi ile birlikte olabilecei gibi belli bir sre sonra da gndeme gelebilir.24-27 Meme hatlar silikon veya serum fizyolojikle doldurulan submuskuler bir implantla veya rektus kas veya baka bir flep kullanlarak oluturulabilir. Her iki yntem de tatminkar kosmetik sonu salar. mplant konmas greceli olarak daha kolay bir ilemdir. nce pektoral kasn arkasna serum fizyolojikle doldurulan doku geniletici (expander) yerletirilir. Verilen miktar haftalar veya aylar boyunca yeterli hacme ulalncaya kadar yava yava artrlr. Bundan sonra doku geniletici karlp kalc implant yerletirilir. Daha iyi bir kozmetik sonu salayan rektus kas flebi daha komplike ve kan nakli gereksinimi dourabilen uzun bir ameliyatla gerekletirilebilir. Silikon implantlarn kanser veya otoimmun hastalklar gelitirdiine dair bir bulgu yoktur. Silikon implantlarda geliebilecek problemler olarak sertleme ve arya neden olan implant etrafndaki kapsln kontraksiyonu, implantn yrtlmas ile silikon jelinin akmas ve enfeksiyon saylabilir.28-30 Nadir de olsa, her iki yntem de kanser rekrrensinin erken tannmasn gletirebilir. Meme rekonstruksiyonu sonras adjuvan olarak veya lokal rekrrens durumunda, gs duvar ve blgesel lenfatiklere radyoterapi uygulanabilir. Bu durum tedaviyi olumsuz etkilemez ancak kozmetik sonu olumsuz etkilenebilir, kapsl fibrozisi, ar ve implantn karlma olaslklarn artrr.29 Meme bytmek iin kullanlan silikon implantlar, meme dokusunu rtp basklamak suretiyle meme kanserinin erken tansn gletirebilirler.

Standart Tedavi 31-34

Biyopsi sonras baka bir tedavi planlamadan yllk mammografi ve periyodik kontrollerle uzun sreli takip.

Kaynaklar:

  1. Ariel IM, Cleary JB, Eds.: Breast Cancer - Diagnosis and Treatment. New York: McGraw-Hill, 1987.

  2. Patchefsky AS, Schwartz GF, Finkelstein SD, et al.: Heterogeneity of intraductal carcinoma of the breast. Cancer 63(4): 731-741, 1989.

  3. Solin LJ, Fourquet A, McCormick B, et al.: Salvage treatment for local recurrence following breast-conserving surgery and definitive irradiation for ductal carcinoma in situ (intraductal carcinoma) of the breast. International Journal of Radiation Oncology, Biology, Physics 30(1): 3-9, 1994.

  4. Fisher B, Costantino J, Redmond C, et al.: Lumpectomy compared with lumpectomy and radiation therapy for the treatment of intraductal breast cancer. New England Journal of Medicine 328(22): 1581-1586, 1993.

  5. Fisher ER, Costantino J, Fisher B, et al.: Pathologic findings from the National Surgical Adjuvant Breast Project (NSABP) protocol B-17. Cancer 75(6): 1310-1319, 1995.

  6. Page DL, Lagios MD: Pathologic analysis of the National Surgical Adjuvant Breast Project (NSABP) B-17 trial: unanswered questions remaining unanswered considering current concepts of ductal carcinoma in situ. Cancer 75(6): 1219-1222, 1995.

  7. Fisher ER, Costantino J, Fisher B, et al.: Response - blunting the counterpoint. Cancer 75(6): 1223-1227, 1995.

  8. Holland R, Peterse JL, Millis RR, et al.: Ductal carcinoma in situ: a proposal for a new classification. Seminars in Diagnostic Pathology 11(3): 167-180, 1994.

  9. Silverstein MJ, Poller DN, Waisman JR, et al.: Prognostic classification of breast ductal carcinoma-in-situ. Lancet 345(8958): 1154-1157, 1995.

  10. Silverstein MJ, Lagios MD, Craig PH, et al.: A prognostic index for ductal carcinoma in situ of the breast. Cancer 77(11): 2267-2274, 1996.

  11. Silverstein MJ, Gierson ED, Colburn WJ, et al.: Axillary lymphadenectomy for intraductal carcinoma of the breast. Surgery, Gynecology and Obstetrics 172(3): 211-214, 1991.

  12. Boice JD, Harvey EB, Blettner M, et al.: Cancer in the contralateral breast after radiotherapy for breast cancer. New England Journal of Medicine 326(12): 781-785, 1992.

  13. Fraass BA, Roberson PL, Lichter AS: Dose to the contralateral breast due to primary breast irradiation. International Journal of Radiation Oncology, Biology, Physics 11(3): 485-497, 1985.

  14. Stotter AT, McNeese M, Oswald MJ, et al.: The role of limited surgery with irradiation in primary treatment of ductal in situ breast cancer. International Journal of Radiation Oncology, Biology, Physics 18(2): 283-287, 1990.

  15. Bornstein BA, Recht A, Connolly JL, et al.: Results of treating ductal carcinoma in situ of the breast with conservative surgery and radiation therapy. Cancer 67(7): 7-13, 1991.

  16. McCormick B, Rosen PP, Kinne D, et al.: Duct carcinoma in situ of the breast: an analysis of local control after conservation surgery and radiotherapy. International Journal of Radiation Oncology, Biology, Physics 21(2): 289-292, 1991.

  17. Silverstein MJ, Waisman JR, Gierson ED, et al.: Radiation therapy for intraductal carcinoma. Is it an equal alternative? Archives of Surgery 126(4): 424-428, 1991.

  18. Schnitt SJ, Silen W, Sadowsky NL, et al.: Ductal carcinoma in situ (intraductal carcinoma) of the breast. New England Journal of Medicine 318(14): 898-903, 1988.

  19. Solin LJ, Fowble BL, Yeh I, et al.: Microinvasive ductal carcinoma of the breast treated with breast-conserving surgery and definitive irradiation. International Journal of Radiation Oncology, Biology, Physics 23(5): 961-968, 1992.

  20. Orel SG, Troupin RH, Patterson EA, et al.: Breast cancer recurrence after lumpectomy and irradiation: role of mammography in detection. Radiology 183(1): 201-206, 1992.

  21. Frykberg ER, Santiago F, Betsill WL, et al.: Lobular carcinoma in situ of the breast. Surgery, Gynecology and Obstetrics 164(3): 285-301, 1987.

  22. Ciatto S, Cataliotti L, Cardona G, et al.: Risk of infiltrating breast cancer subsequent to lobular carcinoma in situ. Tumori 78(4): 244-246, 1992.

  23. Wolmark N, National Surgical Adjuvant Breast and Bowel Project: Randomized, Placebo-Controlled Clinical Trial to Determine the Worth of Tamoxifen for Preventing Breast Cancer (Summary Last Modified 02/97), NSABP-P-1, clinical trial, active, 04/16/92.

  24. Feller WF, Holt R, Spear S, et al.: Modified radical mastectomy with immediate breast reconstruction. American Surgeon 52(3): 129-133, 1986.

  25. Cunningham BL: Breast reconstruction following mastectomy. In: Najarian JS, Delaney JP, Eds.: Advances in Breast and Endocrine Surgery. Chicago: Year Book Medical Publishers, 1986, pp 213-226.

  26. Scanlon EF.: The role of reconstruction in breast cancer. Cancer 68(Suppl 5): 1144-1147, 1991.

  27. Hang-Fu L, Snyderman RK.: State-of-the-art breast reconstruction. Cancer 68(Suppl 5): 1148-1156, 1991.

  28. Council on Scientific Affairs, American Medical Association: Silicone gel breast implants. Journal of the American Medical Association 270(21): 2602-2606, 1993.

  29. Kuske RR, Schuster R, Klein E, et al.: Radiotherapy and breast reconstruction: clinical results and dosimetry. International Journal of Radiation Oncology, Biology, Physics 21(2): 339-346, 1991.

  30. Bridges AJ, Vasey FB: Silicone breast implants: history, safety, and potential complications. Archives of Internal Medicine 153(23): 2638-2644, 1993.

  31. Walt AJ, Simon M, Swanson GM: The continuing dilemma of lobular carcinoma in situ. Archives of Surgery 127(8): 904-909, 1992.

  32. Rosen PP: Lobular Carcinoma In Situ and Intraductal Carcinoma of the Breast. In: McDivitt RW, Okerman MA, Ozzello L, et al., Eds.: The Breast Book. Baltimore: Williams and Wilkens, 1984, pp 59-105.

  33. Osborne MP, Hoda SA: Current management of lobular carcinoma in situ of the breast. Oncology (Huntington NY) 8(2): 45-49, 1994.

  34. Jager JJ, Langendijk JA, Dohmen JP, et al.: Mammography in the follow-up after breast-conserving treatment in cancer of the breast: suitability for mammographic interpretation, validity and interobserver variation. British Journal of Radiology 68(811): 754-760, 1995.

Ana Sayfaya Dn Dr.Kaan OYSUL tarafndan hazrlanmaktadr

radonk.tripod.com

Urothelial carcinoma in situ - Libre Pathology

Urothelial carcinoma in situSynonyms LM LM DDx IHC Site Signs Prevalence Endoscopy Clin. DDx
Diagnosis in short
Urothelial carcinoma in situ. H&E stain.
urothelial cell carcinoma in situ, high-grade dysplasia
nuclear changes (enlargement of nuclei (often 4-5x the size of stromal lymphocytes), nuclear pleomorphism - marked variation in size of nuclei), +/-disordered arrangement/crowding of cells, +/-mitoses, +/-enlarged nucleoli
urothelial carcinoma, urothelial dysplasia, urothelial atypia of unknown significance
CK20 +ve (full thickness), Ki-67 high, p53 +ve, CD44 -ve, CK7 +ve
urothelium - urinary bladder, ureter, renal pelvis, prostatic urethra
+/-hematuria
relatively uncommon
erythema or edema, may be unremarkable
invasive (flat) urothelial carcinoma, inflammation (cystitis)

Urothelial carcinoma in situ, also known as high-grade (urothelial) dysplasia, a non-invasive urothelial neoplasm without papillae.

It is also known as carcinoma in situ (abbreviated CIS) and urothelial cell carcinoma in situ (abbreviated UCC in situ). Urothelial carcinoma in situ may be abbreviated UCIS.

General

  • Lack papillae.
  • Uncommon in relation to other urothelial lesions.
    • Less common than invasive flat urothelial carcinoma ~3-4x more common than UCIS.[1]

Classification of flat urothelial lesions

The World Health Organization classification is:[2]

  • Reactive urothelial atypia.
  • Flat urothelial hyperplasia.
  • Urothelial atypia of unknown significance.
  • Urothelial dysplasia (low-grade dysplasia).
  • Urothelial carcinoma in situ (high-grade dysplasia).
  • Invasive urothelial carcinoma.

Gross

  • Flat lesion - erythema or edema, may be unremarkable.[3]

Microscopic

Features:

  • Nuclear changes key feature.
    • Enlargement of nuclei (often 4-5x the size of stromal lymphocytes) -- diagnostic.[4]
      • Normal urothelium approx. 2x the size of stromal lymphocytes.
    • Nuclear pleomorphism - marked variation in size of nuclei.
  • +/-Disordered arrangement/crowding of cells.
    • In normal urothelium the cell line-up on the basement membrane.
  • Umbrella cells often absent.
  • +/-Mitoses present.
  • +/-Enlarged nucleoli.

Note:

  • The urothelium may be "depleted", i.e. exist only of rare large cells on the basement membrane.
    • This is known as clinging urothelial carcinoma in situ.[5]

DDx:

Images

  • UCIS - intermed. mag. (WC)

  • UCIS - very high mag. (WC)

  • UCIS - intermed. mag. (WC)

  • UCIS - CK20 - intermed. mag. (WC)

  • UCIS - p63 - intermed. mag. (WC)

  • UCIS - Ki-67 - high mag. (WC)

www

IHC

ISUP consensus panel:[6]

  • CK20 +ve in deep cells.
    • Normal urothelium -- only the umbrella cells.
  • p53 +ve.
  • CD44 -ve.
    • Positive in indeterminant and negative.

Another panel

Another panel for benign urothelium versus CIS:[7]

  • CK20 +ve in deep cells (23/26 cases).
    • Normal urothelium -- only the umbrella cells.
  • Ki-67 ~50% of cells - deep and superficial.
    • Normal ~10% of cells, confined to basal aspect.
  • CD44 -ve.[8]
    • Positive in indeterminant and negative.
Others
  • AMACR +ve (80% and 50% of untreated and treated CIS respectively[8]).

Images

  • UCIS - CK20 - intermed. mag.

  • UCIS - CK20 - very high mag.

  • Benign urothelium - CK20 - high mag.

  • UCIS - Ki-67 - intermed. mag.

  • UCIS - Ki-67 - very high mag.

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URINARY BLADDER LESION ("TUMOUR"), TRANSURETHRAL RESECTION URINARY BLADDER TUMOUR (TURBT): - UROTHELIAL CARCINOMA IN SITU. - BENIGN MUSCULARIS PROPRIA PRESENT. URINARY BLADDER, RANDOM BIOPSIES: - UROTHELIAL CARCINOMA IN SITU, SEE COMMENT. -- NO EVIDENCE OF LAMINA PROPRIA INVASION. - CHRONIC INFLAMMATION, MILD. - BENIGN MUSCULARIS PROPRIA PRESENT. COMMENT: A CK20 immunostain marks the full thickness of the urothelium in atypical areas. A p53 immunostain moderately marks up to 20% of atypical cells focally. A Ki-67 immunostain marks 20-50% of the cells in the atypical areas.

Micro

The sections show multiple fragments of urothelium with nuclear hyperchromasia, nuclear crowding, mild-to-moderate nuclear enlargement, several atypical mitoses, and lack of maturation to the surface. There is no evidence of invasion. Benign muscularis propria is present.

See also

References

  1. ↑ Nielsen, ME.; Smith, AB.; Meyer, AM.; Kuo, TM.; Tyree, S.; Kim, WY.; Milowsky, MI.; Pruthi, RS. et al. (Jan 2014). "Trends in stage-specific incidence rates for urothelial carcinoma of the bladder in the United States: 1988 to 2006.". Cancer 120 (1): 86-95. doi:10.1002/cncr.28397. PMID 24122346.
  2. ↑ Hodges, KB.; Lopez-Beltran, A.; Davidson, DD.; Montironi, R.; Cheng, L. (Feb 2010). "Urothelial dysplasia and other flat lesions of the urinary bladder: clinicopathologic and molecular features.". Hum Pathol 41 (2): 155-62. doi:10.1016/j.humpath.2009.07.002. PMID 19762067.
  3. ↑ Nese, N.; Gupta, R.; Bui, MH.; Amin, MB. (Jan 2009). "Carcinoma in situ of the urinary bladder: review of clinicopathologic characteristics with an emphasis on aspects related to molecular diagnostic techniques and prognosis.". J Natl Compr Canc Netw 7 (1): 48-57. PMID 19176205.
  4. ↑ Zhou, Ming; Magi-Galluzzi, Cristina (2006). Genitourinary Pathology: A Volume in Foundations in Diagnostic Pathology Series (1st ed.). Churchill Livingstone. pp. 161. ISBN 978-0443066771.
  5. ↑ Amin, Mahul B. (2010). Diagnostic Pathology: Genitourinary (1st ed.). Amirsys. pp. 2-55. ISBN 978-1931884280.
  6. ↑ Amin MB, Epstein JI, Ulbright TM, et al. (August 2014). "Best practices recommendations in the application of immunohistochemistry in urologic pathology: report from the international society of urological pathology consensus conference". Am. J. Surg. Pathol. 38 (8): 1017–22. doi:10.1097/PAS.0000000000000254. PMID 25025364.
  7. ↑ Yin, H.; He, Q.; Li, T.; Leong, AS. (Sep 2006). "Cytokeratin 20 and Ki-67 to distinguish carcinoma in situ from flat non-neoplastic urothelium.". Appl Immunohistochem Mol Morphol 14 (3): 260-5. PMID 16932015.
  8. ↑ 8.08.1 Aron, M.; Luthringer, DJ.; McKenney, JK.; Hansel, DE.; Westfall, DE.; Parakh, R.; Mohanty, SK.; Balzer, B. et al. (Dec 2013). "Utility of a triple antibody cocktail intraurothelial neoplasm-3 (IUN-3-CK20/CD44s/p53) and α-methylacyl-CoA racemase (AMACR) in the distinction of urothelial carcinoma in situ (CIS) and reactive urothelial atypia.". Am J Surg Pathol 37 (12): 1815-23. doi:10.1097/PAS.0000000000000114. PMID 24225842.

librepathology.org

Adenocarcinoma in situ, minimally invasive adenocarcinoma and invasive adenocarcinoma of lung | Radiology Reference Article

Adenocarcinoma in situ, minimally invasive adenocarcinoma and invasive adenocarcinoma of the lung are relatively new classification entities which replace the now-defunct term bronchoalveolar carcinoma (BAC).

In 2011 the International Association for the Study of Lung Cancer (IASLC) and several other societies jointly revised the classification for adenocarcinoma of lung 13. The new classification strategy is based on a multidisciplinary approach to the diagnosis of lung adenocarcinoma. The terms bronchoalveolar carcinoma and mucinous and non-mucinous bronchoalveolar carcinoma have been rendered obsolete.

Before a general discussion of the topic, it is worth highlighting some of the updated terminology and concepts, as for many who were taught the term bronchoalveolar carcinoma, some adjustment will be necessary 5:

  • adenocarcinoma in situ of lung (AIS) (≤3 cm) has a number of subtypes
    • the most common subtype is non-mucinous and rarely mucinous or mixed subtypes
    • histological pattern: no growth pattern other than lepidic and no feature of necrosis or invasion
  • minimally invasive adenocarcinoma of lung (MIA) ≤3 cm
    • describes small solitary adenocarcinomas with either pure lepidic growth or predominant lepidic growth with ≤5 mm of stromal invasion

The two invasive adenocarcinomas previously termed non-mucinous and mucinous bronchoalveolar carcinoma have been renamed:

AIS and MIA are an uncommon type of bronchial carcinoma which occurs most frequently among non-smokers, women and Asians. It is a subtype of adenocarcinoma, but has a significantly different presentation, treatment and prognosis. Adenocarcinoma in situ and minimally invasive adenocarcinoma represent between 2-14% of all primary pulmonary malignancies 11. There is no significant gender predilection, unlike other lung cancer types which are more prevalent in men.

Risk factors

A focus of pulmonary fibrosis, e.g. tuberculosis scar, infarct, scleroderma.

Presentation is often insidious, and a large proportion (50%) of patients may be asymptomatic at the time of detection 1.  Alternatively, as these tumours can produce large quantities of mucus, patients may present with bronchorrhea.

Persistent consolidation for weeks despite appropriate antimicrobial therapy should raise the suspicion of a neoplastic process. CT or guided biopsy may be planned in such cases.

Adenocarcinoma in situ: ≤3 cm, demonstrates a lepidic growth pattern, spreading along the walls of the lung without destroying the underlying architecture. In addition, they are characterised by the absence of stromal, vascular or pleural invasion.

Minimally invasive adenocarcinoma: ≤3 cm, describes small solitary adenocarcinomas with either pure lepidic growth or predominant lepidic growth with ≤5 mm of stromal invasion.

Three pathological subtypes are recognised 3:

  • non-mucinous
  • mucinous: goblet cell (mucus secreting), often multi-centric
  • mixed

There are three recognised radiographic patterns 1

  • single mass or nodular form (commonest): ~45 %
  • consolidative form: ~30 %
  • multinodular form: ~25 %
Plain radiograph

May show segmental or lobar consolidation with chronic unilateral airspace opacification and air bronchograms. Can also present as a pulmonary nodule, mass or a cluster of diffuse nodules 1,2. The nodular form (commonest) can be indistinguishable from another adenocarcinoma subtype or inflammatory granuloma on plain film 1.

CT

The appearance of bronchoalveolar carcinoma on CT depends on its pattern of growth; hence, it may appear as:

  • a peripheral nodule
    • commonest appearance
    • typically solitary and well circumscribed 5
    • the nodule may be surrounded by a halo of ground-glass opacity, the so-called fried egg sign
    • cavitation
      • pseudocavitation (presence of bubble-like lucencies) is recognised 1,5
      • overt cavitary changes rarely occur (~7%)
      • cavitating pulmonary metastases may occur (Cheerios sign 9)
  • a focal area of ground glass (early sign)
    • heterogeneous attenuation
  • a region of ground glass, with or without consolidation
  • hilar and mediastinal adenopathy and pleural effusion are uncommon
Nuclear medicine

18F-FDG-PET is often negative 6,7.

Treatment and prognosis

Surgical resection is required with a lobectomy or pneumonectomy.

Overall, tumours that demonstrate only lepidic growth tend to be indolent, with a high 5-year survival. However, solid, invasive components are frequently present and despite radical treatment, recurrence rates are high. Mucinous subtypes have worse prognosis 4, probably due to aerogenous spread that forms infiltrating, multifocal, or satellite tumours 11.

History and etymology

The entity formerly known as bronchoalveolar carcinoma was first described by Malassez in 1876, as a bilateral, multinodular form of malignant lung tumour 11-12.

General imaging differential considerations are broad, so it is useful to consider differentials for specific patterns, which include:

radiopaedia.org

Cervical Carcinoma In Situ: Causes, Symptoms & Diagnosis

What Is Cervical Carcinoma in Situ?

Carcinoma in situ (CIS) is a general term for an early stage cancer. Cervical carcinoma in situ is also referred to as stage 0 cervical cancer. It’s noninvasive, which means the cancerous cells are confined to the surface of your cervix and haven’t penetrated more deeply into the tissues.

The cervix is the narrow, lower part of the uterus. It’s the passageway from the uterus to the vaginal canal. Cervical cancer begins on the surface of the cervix and tends to grow slowly. It’s caused by several different strains of the human papillomavirus virus (HPV), which are spread by sexual contact.

According to the Centers for Disease Control and Prevention (CDC), over 12,000 women in the United States were diagnosed with cervical cancer in 2012. Most of these women were younger than 55. Cervical cancer is rare in women under 20 years old. It used to be the leading cause of cancer among women, but cases of it have decreased over the last 40 years.

What Are the Symptoms of Cervical CIS?

Cervical cancer typically doesn’t cause symptoms until its later stages, so you may not have any symptoms with cervical CIS. That’s why having regular Pap smears are important for catching any abnormal cell changes early.

What Causes Cervical CIS?

HPV is the main risk factor for developing cervical CIS. There are hundreds of strains of HPV, which are divided up into either low risk or high risk. There are 10 high-risk strains that are associated with abnormal cell changes in the cervix that can lead to cancer, but two of the strains (HPV 16 and HPV 18) are responsible for 70 percent of cases of cervical cancer.

Other risk factors may also play a role in the development of cervical CIS including:

  • having multiple sexual partners
  • smoking cigarettes
  • having a weakened immune system
  • having sexual intercourse at an early age
  • having a diet low in fruits and vegetables
  • using birth control pills for an extended period
  • being infected with chlamydia

How Is Cervical CIS Diagnosed?

A Pap smear can collect abnormal cells that are then identified in a lab. An HPV test may be performed on the sample to check for the virus and to see whether high-risk or low-risk strains are present.

A colposcopy is an in-office procedure that allows your doctor to view your cervix with a special magnifying tool called a colposcope. Your doctor will apply a solution to the surface of your cervix to show any abnormal cells. They can then take a small piece of tissue called a biopsy. They’ll send this to a lab for a more definitive diagnosis.

If the biopsy shows CIS, your doctor might want to remove a larger piece of your cervix. If they remove the area with abnormal cells, they’ll also remove a surrounding margin of healthy tissue.

Treatment for Cervical CIS

The treatment for cervical CIS is similar to that for cervical dysplasia. Although it’s called carcinoma in situ, it’s often treated like a precancerous growth because it’s not invasive.

Possible treatments include the following:

  • A hysterectomy is an option for women who don’t want to preserve their fertility.
  • Cryosurgery, or freezing the abnormal cells, can be done in your doctor’s office.
  • Laser surgery or loop electrosurgical excision procedure are surgical options that are done on an outpatient basis. They involve removing the abnormal tissue with lasers or an electrically charged wire loop.
  • Conization, another outpatient procedure, is used less often. It involves removing a larger, cone-sized piece of the cervix to ensure removal of the entire abnormal area.

Talk with your doctor about your treatment options to find the best one for you. Your treatment will depend on your age, desire to preserve your fertility, general health, and other risk factors.

Follow-Up Care for Cervical CIS

After you have treatment for cervical CIS, your doctor will want to see you for follow-up visits and Pap smears every three to six months. Cervical cancer can come back, but regular Pap smears and checkups will allow your doctor to catch and treat abnormal cells early.

Your doctor will also address any concerns you may have about your cervical health.

Having cervical CIS can be emotionally trying, especially if you’re concerned about your fertility. Talk with your doctor about any support groups or finding a counselor if you need extra support.

www.healthline.com

Lung Cancer In-Situ

UNDERSTANDING YOUR PATHOLOGY REPORT: FAQ SHEET

When your lung was biopsied, the samples taken were studied under the microscope by a specialized doctor with many years of training called a pathologist. The pathology report is used by your treating doctor to help make decisions about managing your care. This FAQ sheet is designed to help you understand the medical language used in the pathology report.

1. What is “in-situ carcinoma”?

In-situ carcinoma is a pre-cancer. The normal lung is made of air passages (bronchi) that end in a group of blind-ending sacs (acini) where your blood gets oxygenated. Carcinomas originate in the bronchi or acini and when they are confined to the inner lining of these structures, they are considered “in-situ carcinoma.” Once in-situ carcinoma growth has broken out of the inner lining of the ducts or lobules it is no longer “in-situ” and is referred to as “invasive” or “infiltrating” carcinoma, which means that the cells now have the potential to spread (metastasize) to other parts of your body.

2. What does it mean if my pre-cancer is called “squamous cell carcinoma in-situ” or “atypical adenomatous hyperplasia”?

These are the pre-cancers that precede invasive squamous cell carcinoma and adenocarcinoma, respectively. If they are present in a biopsy, it may mean that there is invasive carcinoma elsewhere in the lung that was not sampled on biopsy. If an excisional biopsy or lobe resection (lobectomy) shows only squamous cell carcinoma in situ or atypical adenomatous hyperplasia, the prognosis is excellent, although there may be other noncontiguous areas (skip areas) of the precancer.

3. What is “squamous metaplasia”?

When the air passages are irritated, their lining cells change their shape so that they are stacked on top of each other, a reaction called “squamous metaplasia”. When the irritation disappears, as for example when you stop smoking or pneumonia clears, the lining cells return to their normal appearance. Squamous metaplasia is not considered a pre-cancer, but if the irritation persists it can progress to “squamous dysplasia”. (See FAQ 4)

4. What is “squamous dysplasia”?

Dysplasia is an early form of precancer. It is often separated, by increasing abnormality, into “mild dysplasia”, “moderate dysplasia”, or “severe dysplasia”. The more severe the dysplasia the more it is similar to “squamous cell carcinoma in-situ”. If it is seen on biopsy, it may mean that there is in-situ or invasive carcinoma, not sampled by the biopsy, elsewhere in the lung.

5. What if my report on carcinoma in-situ or atypical adenomatous hyperplasia mentions “margins” or “ink”?

When an excisional biopsy is performed, the pathologist coats the outer aspect, or margin, of the specimen with ink, sometimes different colored ink. If precancer extends to the ink, it may mean that it has not been completely removed, depending on what additional specimens the surgeon may have removed. Typically additional treatment (surgery or radiation) is used to get rid of the residual precancer. Management of precancerous lesions at a margin is best discussed with your treating physician.

6. What does it mean if my report also says any of the following terms: “scarring”, “emphysema”, “emphysematous changes”, or “inflammation”?

All of these terms are non-cancerous changes that the pathologist sees under the microscope. They are usually of no great importance when seen on a biopsy which also contains cancer.

7. What if my report mentions any of the following: “granulomas”, “methenamine silver (GMS)”, “acid fast bacilli (AFB), or Periodic Acid Schiff (PAS).

Granulomas are structures seen under the microscope that are often, although not necessarily, an indication of certain types of infection. Sometimes, infectious organisms can be detected with special stains (i.e. GMS, stains for AFB, and PAS) that the pathologist can apply to the microscopic slides. While most granulomas are infectious, other causes will be considered by your physician, including sarcoidosis, allergic reactions, and “dust” induced lung disease (pneumoconiosis).

www.adasp.org

Ductal carcinoma in situ | Radiology Reference Article

Ductal carcinoma in situ (DCIS) refers to a breast carcinoma limited to the ducts with no extension beyond the basement membrane, as a result of which the disease has not infiltrated the parenchyma of the breast and the lymphatics and cannot therefore metastasise.

The detection of DCIS has increased markedly in recent years secondary to the widespread use of screening mammography, and it now accounts for 25-40% of mammographically detected breast cancers 1,3. It also accounts for approximately 15-20% of all detected breast cancers

Risk factors for DCIS are similar to those for invasive carcinoma and include:

  • increasing age
  • family history of breast cancer
  • nulliparity
  • age of 30 years or older at the birth of the first child

Although most patients are asymptomatic, some present with nipple-related disease (nipple discharge or Paget disease of the breast) or have palpable abnormalities.

DCIS is the non-obligate precursor of infiltrating ductal carcinoma (IDC). In the context of "over diagnosis" the low grade DCIS cases found on screening mammography are likely to cause to the number of cases where the diagnosis of breast malignancy has been made but could conceivably not have been fatal to the patient. Remember that to try and guess the grade of DCIS on the mammogram images is not plausible or reproducible. Low grade DCIS is not a dangerous disease and there is actually some thought on following the disease with MRI after a histological diagnosis has been made.

DCIS is not a single entity, but rather a spectrum of disease 3. In essence, it refers to breast epithelial cells that have become "cancerous" but still reside in their normal place in the ducts and lobules 10.

Markers

In some situations immunohistochemical staining for E-cadherin may help to differentiate from lobular carcinoma in situ.

Sub types

 The traditional classification broadly divided DICS lesions into two types mainly based on central necrosis, grade, and cell type: 

  • comedo - large cell: more aggressive form; also referred to as comedocarcinoma
  • non-comedo - small cell: less aggressive; can be further divided into
    • cribriform
    • micropapillary
    • papillary
    • solid

New pathologic classification of DCIS is based on nuclear atypia and degree of necrosis.

Associations
  • up to 11% of predetermined DCIS on imaging may have an invasive component at the time a biopsy is done 2
  • 20-25% of DCIS revealed on core biopsy may have invasive ductal carcinoma following surgical excision
Mammography

There are varied mammographic manifestations of DCIS, with casting-type calcifications being the most common (present in 50-75% of cases 3). Other manifestations include a soft-tissue opacity either with or without associated calcifications.

Although DCIS calcifications may assume varied appearances, linear calcifications are more likely to be associated with comedo-type DCIS, while granular calcifications are more often correlated with non-comedo DCIS.

Occasionally DCIS appears as a simple mass or asymmetry without calcification (~8% of cases) 12. 

There may be a significant discrepancy between the distribution of the disease as seen on the mammogram and the distribution of the disease on the pathology specimen of the breast as examined by the pathologist. In general, the calcification underestimates the distribution of DCIS in the breast, i.e. not all the DCIS calcifies.

Breast ultrasound

One of the benefits of identifying a corresponding sonographic abnormality in women with mammographically detected DCIS is to use ultrasound to guide interventional (e.g. biopsy/hookwire) procedures. A microlobulated mild hypoechoic mass with ductal extension and normal acoustic transmission is considered the most common feature in sonographically detected DCIS.

With good quality ultrasound and enough effort, it is possible in everyday practice to identify the DCIS process as it grows in the ductal system of the breast. It is quite possible to identify those minute wild and crazy calcifications of DCIS in the ducts itself and ultrasound guided biopsy of DCIS is now an everyday procedure.

Breast MRI

DCISs can present as "no mass enhancement",  "clustered ring enhancement", or a " mass or focus" on a contrast MRI. When enhanced, DCIS does not show a specific pattern and instead may be seen as a segmental or regional enhancement, branching and linear or mass enhancement with or without an irregular shape.

Treatment and prognosis

Treatment options for DCIS include mastectomy, lumpectomy with breast irradiation, or, for patients with small lesions (<1-2 cm) of low-grade DCIS, lumpectomy alone.

This disease is likely the precursor of IDC at a stage of the disease when the therapy is potentially curable. The advantage of diagnosis DCIS is that the chances of encountering metastatic disease are in theory zero when compared with IDC. With the introduction of screening mammography, the decreased mortality of breast carcinoma is in some part due to the identification of DCIS and effective therapy. In large screening programmes DCIS make up to 30% of malignancies diagnosed.

History and etymology

With the widespread use of screening mammography this disease is now commonly found before infiltrating ductal carcinoma (IDC)  develops 15. 

The historical background and current perspectives of DCIS need to acknowledge the role Roland Holland played in the process in the Netherlands 14.

radiopaedia.org

Stages and Grades of Ductal Carcinoma in Situ

Breast cancer is graded on a scale of 0 to 4. The earliest stage of breast cancer is stage 0, which is where all DCIS is staged. When referring to the stage of a DCIS, it is actually the distance of which the cancerous cells have spread beyond the location of the original tumor. It is always considered a stage 0; however, it is possible for it to be any size, as well as located within the breast in any number of areas. When you and your Doctor know the grade and type of DCIS that you have, it is easier to decide on the best treatment for you.

When you have a biopsy performed, a pathologist will review the tissue samples retrieved under microscope in order to determine if there any abnormal cells present. If the pathologist identifies any abnormal cells, they will send a report of the variation between the abnormal cells in the healthy, normal breast cells that surround it. The image shown illustrates the possible range of findings, progressing from a normal cell to a fully invasive ductal cancer. 

There are six categories in which to classify the condition of a breast cell. The first is normal cells. The second is ductal hyperplasia, which means there is an overgrowth of the cells within the tissue. The third is atypical hyperplasia, which means too many cells are accumulating and beginning to develop an abnormal appearance. The fourth is ductal carcinoma in situ, which indicates too many cells are present and include the features of cancer; however, they remain within the confines of the milk duct. The fifth as DCIS-MI (ductal carcinoma in situ with micro-invasion) which means that some of the cancer cells have begun to break through the wall of the milk duct, and this is treated more seriously than traditional DCIS, as it is considered a more serious form. The final category is invasive ductal cancer, in which the cancerous cells have broken past the milk duct. Once the cells reach this category, they are no longer ductal carcinoma in situ, but instead are an invasive ductal carcinoma, which is the most common type of invasive breast cancer.

Now that you understand how DCIS is staged, it is time to explain grading. Grading is done on a graduated scale from grade I to grade III. Grade I is considered low grade. Grade II is considered moderate. Grade III is considered high. The grade level explains how similar or different the abnormal cells are from a normal cell and the rate at which they grow. A lower grade is more similar to normal cells and grows more slowly, whereas the higher grade is more abnormal and grows faster. Since two factors are considered, it is possible for a difficulty presents itself in clearly distinguishing between two grades. When this happens, it is graded as “borderline.”

Grade I and grade II are slower growing, and are often described as “non-comedo.” This term means that the tumor does not contain many dead cells, which indicates a slow-growing cancer because there is sufficient nourishment for all the cells to feed off. The faster a tumor grows, the more quickly the cells within it begin to die out at a faster rate. Grade I looking very similar to normal or atypical ductal hyperplasia cells, and grade II cells look less like them. The higher the grade, the greater the chance of recurrence and/or the development of the new cancer. The speed at which a new cancer develops is also affected by the grade of DCIS. There are three patterns of low- to moderate-grade DCIS; papillary, cribriform, and solid. Papillary cells are most similar to normal cells, with large gaps between the abnormal cells and the healthy cells. Cribriform DCIS has smaller gaps between the two types of cells and resembles the hole pattern in Swiss cheese. In a solid DCIS, the affected breast duct is completely filled with cancer cells.

High-grade pattern DCIS, or grade III, the cells are fast-growing and vary significantly from normal, healthy breast cells. Individuals with grade III DCIS have the highest risk of invasive cancer, either at the same time DCIS is diagnosed, or at some time in the future. The speed of which cancer is likely to come back is also greater, with the risk of recurrence within five years being greater than after five years. This grade of DCIS is called “comedo” or “comedo necrosis” because the cells have a large amount of dead or in aquatic cancer cells, which often build up within the tumor. Quick growing cancer cells require a lot of nourishment, and the cells that do not receive enough nourishment will die off, which leaves areas of necrosis.

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