مواد ڏانھن هلو

ڪارڪينوما

کليل ڄاڻ چيڪلي، وڪيپيڊيا مان
Not to be confused with carcinoid, which is sometimes a type of carcinoma but is more often benign.
اسڪوامس سيل ڪارڪينوما، برونچس تي مشتمل، لمف نوڊ ميٽاساسس سان
ڪارڪينوما
Carcinoma
هڪ ڦڦڙن جي سرطان، اسمال سيل ڪارڪينوما، ڪارڪينوما جو هڪ قسم، جو مائيڪروگراف. ڪلسٽر ٿيل سرطان وارا جهڙو گهرڙا جيڪا خاص ڪري نيوڪليئس (جامني رنگ ۾) تي مشتمل هوندا آهن، جنهن جي گرد باريڪ سائٽوپلازم جي پرت هوندي آهي. ارد گرد جا ڌٻي وارا، قرصي سيل رت جا سيل آهن.
مھارت آنڪولاجي

ڪارڪينوما (Carcinoma) هڪ خرابي آهي جيڪا ايپي ٿيليل جيو گهرڙن (عام طور تي چمڙي جي) مان پيدا ٿئي ٿي.[1] خاص طور تي، هڪ ڪارڪينوما هڪ سرطان آهي جيڪو هڪ ٽشو ۾ شروع ٿئي ٿو جيڪو جسم جي اندرين يا ٻاهرئين سطحن کي لڪائيندو آهي ۽ اهو جيو گهرڙن مان پيدا ٿيندڙ انڊوڊرمل، ميسوڊرمل،[2] يا اڪٽوڊرمل جراثيم جي پرت جي ايمبريوجنسيس جي دوران، پيدا ٿئي ٿو.[3]

ڪارڪينوما تڏهن ٿيندو آهي جڏهن ڪنهن جيو گهرڙي جي ڊي اين اي کي خراب يا تبديل ڪيو ويندو آهي ۽ اها بي ضابطه طور تي وڌندو آهي ۽ خراب ٿي ويندو آهي. اها يوناني ٻولي جي لفظ، ڪارڪينوما (καρκίνωμα، معني:زخم، السر، سرطان) مان آهي. خود ڪارڪينوما لاطيني ٻولي جي لفظ، "ڪارڪينوس" (karkinos؛ معنيٰ:ڪيڪڙو) مان نڪتل آهي.

قسمون

[سنواريو]
زبان جو ڪينسر
  • واٽ يا زبان: اڪثر واٽ/زبان جا ڪينسر اسڪواومس سيل ڪارڪينوما آهن
  • ڦڦڙ: ڪارڪينوما سڀني ڦڦڙن جي ڪينسر جي 98 سيڪڙو کان وڌيڪ تي مشتمل آهي.
  • ڇاتی: لڳ ڀڳ سڀ ڇاتی جا ڪينسر ڊڪٽل ڪارڪينوما (ductal carcinoma) آهن.
  • پروسٽيٽ: پروسٽيٽ ​​جي ڪارڪينوما جو سڀ کان عام روپ ائڊينوڪارڪينوما (adenocarcinoma) آهي.
  • ڪولون ۽ ريڪٽم: ڪولون ۽ ريڪٽم جون لڳ ڀڳ سڀئي خرابيون يا ته ايڊينوڪارڪينوما يا اسڪوامس سيل ڪارڪينوما آهن.
  • لبلبو: پينڪريٽڪ ڪارڪينوما لڳ ڀڳ هميشه ايڊينوڪارڪينوما قسم جو هوندو آهي ۽ انتهائي جان ليوا هوندو آهي.
  • بيضه داني: دير سان ڳولڻ سبب سڀ کان وڌيڪ خطرناڪ شڪلن مان هڪ آهي.

ڪجھ ڪارڪينوما جا نالا انھن جي اصليت واري جيو گهرڙي جي لاءِ رکيا ويا آھن، مثال طور، ڪليجي لاء، ھيپاٽو سيلولر ڪارڪينوما ۽ بکين لاء رينل سيل ڪارڪينوما.

درجه بندي

[سنواريو]

As of 2004, no simple and comprehensive classification system has been devised and accepted within the scientific community.[4] Traditionally, however, malignancies have generally been classified into various types using a combination of criteria, including:[5]

The cell type from which they start; specifically:

Other criteria that play a role include:

  • The degree to which the malignant cells resemble their normal, untransformed counterparts
  • The appearance of the local tissue and stromal architecture
  • The anatomical location from which tumors arise
  • Genetic, epigenetic, and molecular features

Histological types

[سنواريو]
Adenocarcinoma with typical features, although they vary substantially from case to case.
Squamous cell carcinoma with typical features.
Histopathology of small-cell carcinoma, with typical findings.[6]
Adenocarcinoma (adeno = gland)
Refers to a carcinoma featuring microscopic glandular-related tissue cytology, tissue architecture, and/or gland-related molecular products, e.g., mucin.
Squamous cell carcinoma
Refers to a carcinoma with observable features and characteristics indicative of squamous differentiation (intercellular bridges, keratinization, squamous pearls).
Adenosquamous carcinoma
Refers to a mixed tumor containing both adenocarcinoma and squamous cell carcinoma, wherein each of these cell types comprise at least 10% of the tumor volume.
Anaplastic carcinoma
Refers to a heterogeneous group of high-grade carcinomas that feature cells lacking distinct histological or cytological evidence of any of the more specifically differentiated neoplasms. These tumors are referred to as anaplastic or undifferentiated carcinomas.
Large cell carcinoma
Composed of large, monotonous rounded or overtly polygonal-shaped cells with abundant cytoplasm.
Small cell carcinoma
Cells are usually round and are less than approximately three times the diameter of a resting lymphocyte and with little evident cytoplasm. Occasionally, small cell malignancies may themselves have significant components of slightly polygonal and/or spindle-shaped cells.[7]

There are a large number of rare subtypes of anaplastic, undifferentiated carcinoma. Some of the more well known include the lesions containing pseudo-sarcomatous components: spindle cell carcinoma (containing elongated cells resembling connective tissue cancers), giant cell carcinoma (containing huge, bizarre, multinucleated cells), and sarcomatoid carcinoma (mixtures of spindle and giant cell carcinoma). Pleomorphic carcinoma contains spindle cell and/or giant cell components, plus at least a 10% component of cells characteristic of more highly differentiated types (i.e. adenocarcinoma and/or squamous cell carcinoma). Very rarely, tumors may contain individual components resembling both carcinoma and true sarcoma, including carcinosarcoma and pulmonary blastoma.[7] A history of cigarette smoking is the most common cause of large cell carcinoma.

  • Adenosquamous carcinoma, with glandular features at left and squamous features at right.
    Adenosquamous carcinoma, with glandular features at left and squamous features at right.
  • Anaplastic tumor cells.
    Anaplastic tumor cells.
  • Large cell carcinoma.
    Large cell carcinoma.
  • Carcinosarcoma, having mixed carcinomatous and sarcomatous elements
    Carcinosarcoma, having mixed carcinomatous and sarcomatous elements

Carcinoma of unknown primary site

[سنواريو]

The term carcinoma has also come to encompass malignant tumors composed of transformed cells whose origin or developmental lineage is unknown (see cancer of unknown primary origin; CUP), but that possess certain specific molecular, cellular, and histological characteristics typical of epithelial cells. This may include the production of one or more forms of cytokeratin or other intermediate filaments, intercellular bridge structures, keratin pearls, and/or tissue architectural motifs such as stratification or pseudo-stratification.[4][5]

ICD-10 code

[سنواريو]

Carcinoma In situ

[سنواريو]

The term carcinoma in situ (or CIS) is a term for cells that are significantly abnormal but not cancer.[8] They are thus not typically carcinomas.[9]

پيٿاجينئسس

[سنواريو]

Cancer occurs when a single progenitor cell accumulates mutations and other changes in the DNA, histones, and other biochemical compounds that make up the cell's genome. The cell genome controls the structure of the cell's biochemical components, the biochemical reactions that occur within the cell, and the biological interactions of that cell with other cells. Certain combinations of mutations in the given progenitor cell ultimately result in that cell (also called a cancer stem cell) displaying a number of abnormal, malignant cellular properties that, when taken together, are considered characteristic of cancer, including:

  • the ability to continue to divide perpetually, producing an exponentially (or near-exponentially) increasing number of new malignant cancerous "daughter cells" (uncontrolled mitosis);
  • the ability to penetrate normal body surfaces and barriers, and to bore into or through nearby body structures and tissues (local invasiveness);
  • the ability to spread to other sites within the body (metastasize) by penetrating or entering into the lymphatic vessels (regional metastasis) and/or the blood vessels (distant metastasis).[10]

If this process of continuous growth, local invasion, and regional and distant metastasis is not halted via a combination of stimulation of immunological defenses and medical treatment interventions, the result is that the host has a continuously increasing burden of tumor cells throughout the body. Eventually, the tumor burden increasingly interferes with normal biochemical functions carried out by the host's organs, and death ultimately ensues.

Carcinoma is but one form of cancer—one composed of cells that have developed the cytological appearance, histological architecture, or molecular characteristics of epithelial cells.[4][5] A progenitor carcinoma stem cell can be formed from any of a number of oncogenic combinations of mutations in a totipotent cell,[11] a multipotent cell,[11] or a mature differentiated cell.[12]

Metastatic carcinoma

[سنواريو]
پڻ ڏسو: Metastasis

Metastatic carcinoma is cancer that is able to grow at sites distant from the primary site of origin; thus, dissemination to the skin may occur with any malignant neoplasm, and these infiltrates may result from direct invasion of the skin from underlying tumors, may extend by lymphatic or hematogenous spread, or may be introduced by therapeutic procedures.[13]:628-9

Mutation

[سنواريو]

Whole genome sequencing has established the mutation frequency for whole human genomes. The mutation frequency in the whole genome between generations for humans (parent to child) is about 70 new mutations per generation.[14]

Carcinomas, however, have much higher mutation frequencies. The particular frequency depends on tissue type, whether a mis-match DNA repair deficiency is present, and exposure to DNA damaging agents such as components of tobacco smoke. Tuna and Amos have summarized the mutation frequencies per megabase (Mb) in some carcinomas,[15] as shown in the table (along with the indicated frequencies of mutations per genome).

Mutation frequencies
Cell type Mutation frequency
Per megabase Per diploid genome
Germline 0.023 70
Prostate cancer 0.9 5,400
Colorectal carcinoma ~5 ~30,000
Microsatellite stable (MSS) colon cancer 2.8 16,800
Microsatellite instable (MSI) colon cancer (mismatch repair deficient) 47 282,000
Hepatocellular carcinoma 4.2 25,200
Breast cancer 1.18–1.66 7,080–9,960
Lung cancer 17.7 106,200
Small cell lung cancer 7.4 44,400
Non-small cell lung cancer (smokers) 10.5 63,000
Non-small cell lung cancer (never-smokers) 0.6 3,600
Lung adenocarcinoma (smokers) 9.8 58,500
Lung adenocarcinoma (never-smokers) 1.7 10,200

Cause of mutations

[سنواريو]
وڌيڪ ڏسو: DNA damage (naturally occurring)

The likely major underlying cause of mutations in carcinomas is DNA damage.[حوالو گهربل] For example, in the case of lung cancer, DNA damage is caused by agents in exogenous genotoxic tobacco smoke (e.g. acrolein, formaldehyde, acrylonitrile, 1,3-butadiene, acetaldehyde, ethylene oxide and isoprene).[16] Endogenous (metabolically caused) DNA damage is also very frequent, occurring on average more than 60,000 times a day in the genomes of human cells.[حوالو گهربل] Externally and endogenously caused damages may be converted into mutations by inaccurate translesion synthesis or inaccurate DNA repair (e.g. by non-homologous end joining).

High frequency
[سنواريو]

The high frequency of mutations in the total genome within carcinomas suggests that, often, an early carcinogenic alteration may be a deficiency in DNA repair. For instance, mutation rates substantially increase (sometimes by 100-fold) in cells defective in DNA mismatch repair.[17]

A deficiency in DNA repair, itself, can allow DNA damages to accumulate, and error-prone translesion synthesis past some of those damages may give rise to mutations. In addition, faulty repair of these accumulated DNA damages may give rise to epigenetic alterations or epimutations. While a mutation or epimutation in a DNA repair gene, itself, would not confer a selective advantage, such a repair defect may be carried along as a passenger in a cell when the cell acquires an additional mutation/epimutation that does provide a proliferative advantage. Such cells, with both proliferative advantages and one or more DNA repair defects (causing a very high mutation rate), likely give rise to the high frequency of total genome mutations seen in carcinomas.

DNA repair

[سنواريو]

In somatic cells, deficiencies in DNA repair sometimes arise by mutations in DNA repair genes, but much more often are due to epigenetic reductions in expression of DNA repair genes. Thus, in a sequence of 113 colorectal carcinomas, only four had somatic missense mutations in the DNA repair gene MGMT, while the majority of these cancers had reduced MGMT protein expression due to methylation of the MGMT promoter region.[18]

تشخيص

[سنواريو]

Carcinomas can be definitively diagnosed through biopsy, including fine-needle aspiration (FNA), core biopsy, or subtotal removal of single node,.[19] Microscopic examination by a pathologist is then necessary to identify molecular, cellular, or tissue architectural characteristics of epithelial cells.

Types

[سنواريو]
  • Oral: Most oral cancers are squamous-cell carcinoma
  • Lung: Carcinoma comprises >98% of all lung cancers.
  • Breast: Nearly all breast cancers are ductal carcinoma.
  • Prostate: The most common form of carcinoma of the prostate is adenocarcinoma.
  • Colon and rectum: Nearly all malignancies of the colon and rectum are either adenocarcinoma or squamous cell carcinoma.
  • Pancreas: Pancreatic carcinoma is almost always of the adenocarcinoma type and is highly lethal.
  • Ovaries: One of the most deadly forms due to late detection.[20]

Some carcinomas are named for their or the putative cell of origin, (e.g.hepatocellular carcinoma, renal cell carcinoma).

Staging

[سنواريو]

Staging of carcinoma refers to the process of combining physical/clinical examination, pathological review of cells and tissues, surgical techniques, laboratory tests, and imaging studies in a logical fashion to obtain information about the size of the neoplasm and the extent of its invasion and metastasis. Carcinoma stage is the variable that has been most consistently and tightly linked to the prognosis of the malignancy.

Carcinomas are usually staged with Roman numerals. In most classifications, Stage I and Stage II carcinomas are confirmed when the tumor has been found to be small and/or to have spread to local structures only. Stage III carcinomas typically have been found to have spread to regional lymph nodes, tissues, and/or organ structures, while Stage IV tumors have already metastasized through the blood to distant sites, tissues, or organs.

In some types of carcinomas, Stage 0 carcinoma has been used to describe carcinoma in situ, and occult carcinomas detectable only via examination of sputum for malignant cells (in lung carcinomas).

In more recent staging systems, substages (a, b, c) are becoming more commonly used to better define groups of patients with similar prognosis or treatment options.

The criteria for staging can differ dramatically based upon the organ system in which the tumor arises. For example, the colon[21] and bladder cancer[22] staging system relies on depth of invasion, staging of breast carcinoma is more dependent on the size of the tumor, and in renal carcinoma, staging is based on both the size of the tumor and the depth of the tumor invasion into the renal sinus. Carcinoma of the lung has a more complicated staging system, taking into account a number of size and anatomic variables.[23]

The UICC/AJCC TNM systems are most often used.[وضاحت گهربل][24] For some common tumors, however, classical staging methods (such as the Dukes classification for colon cancer) are still used.

Grading

[سنواريو]

Grading of carcinomas refers to the employment of criteria intended to semi-quantify the degree of cellular and tissue maturity seen in the transformed cells relative to the appearance of the normal parent epithelial tissue from which the carcinoma derives.

Grading of carcinoma is most often done after a treating physician and/or surgeon obtains a sample of suspected tumor tissue using surgical resection, needle or surgical biopsy, direct washing or brushing of tumor tissue, sputum cytopathology, etc. A pathologist then examines the tumor and its stroma, perhaps utilizing staining, immunohistochemistry, flow cytometry, or other methods. Finally, the pathologist classifies the tumor semi-quantitatively into one of three or four grades, including:

  • Grade 1, or well differentiated: there is a close, or very close, resemblance to the normal parent tissue, and the tumor cells are easily identified and classified as a particular malignant histological entity;
  • Grade 2, or moderately differentiated: there is considerable resemblance to the parent cells and tissues, but abnormalities can commonly be seen and the more complex features are not particularly well-formed;
  • Grade 3, or poorly differentiated: there is very little resemblance between the malignant tissue and the normal parent tissue, abnormalities are evident, and the more complex architectural features are usually rudimentary or primitive;
  • Grade 4, or undifferentiated carcinoma: these carcinomas bear no significant resemblance to the corresponding parent cells and tissues, with no visible formation of glands, ducts, bridges, stratified layers, keratin pearls, or other notable characteristics consistent with a more highly differentiated neoplasm.

Although there is definite and convincing statistical correlation between carcinoma grade and tumor prognosis for some tumor types and sites of origin, the strength of this association can be highly variable. It may be stated generally, however, that the higher the grade of the lesion, the worse is its prognosis.[25][26]

ايپيڊميولوجي

[سنواريو]

جڏهن ته ڪينسر عام طور تي وڏي عمر جي بيماري سمجهي ويندي آهي، ٻارن کي پڻ سرطان ٿي سگهي ٿو. بالغن جي ابتڙ، ڪارڪينوما ٻارن ۾ غير معمولي طور تي ناياب آهن. ڪارڪينوما جي تشخيص جو هڪ سيڪڙو کان گهٽ ٻارن ۾ آهي.

عورتن ۾ بيضه داني جي ڪارڪينوما لاءِ ٻه وڏا خطري وارا عنصر، عمر ۽ خانداني تاريخ آهن.

گيلري

[سنواريو]
فائل:Big liver carcinoma.jpg
کليجي جو ڪينسر
فائل:Renal cell Carcinoma.jpg
بکين جو ڪينسر

پڻ ڏسو

[سنواريو]

ٻاهريان ڳنڍڻا

[سنواريو]
Search Wikimedia Commons وڪيميڊيا العام ۾ ڪارڪينوما سان لاڳاپيل ابلاغي مواد ڏسو.
Search Wiktionary ڪارڪينوما جي لغوي معنائن جي لاءِ وڪي لغت ۾ ڏسو

حوالا

[سنواريو]
  1. ↑ Progress in pathology. London: Greenwich Medical Media. 2001. p. 52. ISBN 9781841100500. https://books.google.com/books?id=xiHcyr-BHeQC&pg=PT61. 
  2. ↑ The biology of cancer (Second ed.). New York. 24 May 2013. ISBN 9780815345282. OCLC 841051175. 
  3. ↑ "Definition of Carcinoma". وقت 10 October 2012 تي اصل کان آرڪائيو ٿيل. حاصل ڪيل 27 January 2014. 
  4. ↑ 4.0 4.1 4.2 "Tumor classification: molecular analysis meets Aristotle". BMC Cancer 4 (1): 10. March 2004. doi:10.1186/1471-2407-4-10. PMID 15113444. 
  5. ↑ 5.0 5.1 5.2 "Tumor taxonomy for the developmental lineage classification of neoplasms". BMC Cancer 4 (1): 88. November 2004. doi:10.1186/1471-2407-4-88. PMID 15571625. 
  6. ↑ Image by Mikael Häggström, MD. Source for findings: Caroline I.M. Underwood, M.D., Carolyn Glass, M.D., Ph.D. "Lung - Small cell carcinoma". Pathology Outlines.  Last author update: 20 September 2022
  7. ↑ 7.0 7.1 Pathology and Genetics of Tumours of the Lung, Pleura, Thymus and Heart. World Health Organization Classification of Tumours. Lyon: IARC Press. 2004. ISBN 978-92-832-2418-1. http://www.iarc.fr/en/publications/pdfs-online/pat-gen/bb10/bb10-cover.pdf. Retrieved 27 January 2014. 
  8. ↑ Oncology: An Evidence-Based Approach. Springer. 2007. p. 162. ISBN 9780387310565. https://books.google.com/books?id=vxh6u1-ETk0C&pg=PA162. 
  9. ↑ "Gonadal tumours and DSD". Best Practice & Research. Clinical Endocrinology & Metabolism 24 (2): 291–310. April 2010. doi:10.1016/j.beem.2009.10.002. PMID 20541153. 
  10. ↑ Carcinoma. Academic Press Dictionary of Science and Technology. 
  11. ↑ 11.0 11.1 "Links between DNA Replication, Stem Cells and Cancer". Genes 8 (2): 45. January 2017. doi:10.3390/genes8020045. PMID 28125050. 
  12. ↑ "Estimating the number of genetic mutations (hits) required for carcinogenesis based on the distribution of somatic mutations". PLOS Computational Biology 15 (3): e1006881. March 2019. doi:10.1371/journal.pcbi.1006881. PMID 30845172. Bibcode: 2019PLSCB..15E6881A. 
  13. ↑ James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology. (10th ed.). Saunders. ISBN 0-7216-2921-0.
  14. ↑ "Analysis of genetic inheritance in a family quartet by whole-genome sequencing". Science 328 (5978): 636–639. April 2010. doi:10.1126/science.1186802. PMID 20220176. Bibcode: 2010Sci...328..636R. 
  15. ↑ "Genomic sequencing in cancer". Cancer Letters 340 (2): 161–170. November 2013. doi:10.1016/j.canlet.2012.11.004. PMID 23178448. 
  16. ↑ "A novel application of the Margin of Exposure approach: segregation of tobacco smoke toxicants". Food and Chemical Toxicology 49 (11): 2921–2933. November 2011. doi:10.1016/j.fct.2011.07.019. PMID 21802474. 
  17. ↑ "Differing patterns of genetic instability in mice deficient in the mismatch repair genes Pms2, Mlh1, Msh2, Msh3 and Msh6". Carcinogenesis 27 (12): 2402–2408. December 2006. doi:10.1093/carcin/bgl079. PMID 16728433. 
  18. ↑ "O(6)-methylguanine methyltransferase in colorectal cancers: detection of mutations, loss of expression, and weak association with G:C>A:T transitions". Gut 54 (6): 797–802. June 2005. doi:10.1136/gut.2004.059535. PMID 15888787. 
  19. ↑ "Principles of Surgical Oncology". Cancer Management: A Multidisciplinary Approach (11th ed.). 2008. http://www.cancernetwork.com/cancer-management-11/chapter01/article/10165/1399286. Retrieved 8 June 2009. 
  20. ↑ "Ovarian carcinoma associated with endometriosis". European Journal of Obstetrics, Gynecology, and Reproductive Biology 170 (1): 211–213. September 2013. doi:10.1016/j.ejogrb.2013.06.001. PMID 23849309. 
  21. ↑ "TNM staging system of colorectal carcinoma: a critical appraisal of challenging issues". Archives of Pathology & Laboratory Medicine 134 (6): 837–852. June 2010. doi:10.5858/134.6.837. PMID 20524862. 
  22. ↑ "Update on clinical and radiological staging and surveillance of bladder cancer". The Canadian Journal of Urology 13 (Suppl 1): 71–76. February 2006. PMID 16526987. 
  23. ↑ "How well does the new lung cancer staging system predict for local/regional recurrence after surgery?: A comparison of the TNM 6 and 7 systems". Journal of Thoracic Oncology 6 (4): 757–761. April 2011. doi:10.1097/JTO.0b013e31821038c0. PMID 21325975. 
  24. ↑ "What is Cancer Staging?". وقت 25 October 2007 تي اصل کان آرڪائيو ٿيل. حاصل ڪيل 27 January 2014.  Unknown parameter |url-status= ignored (مدد)
  25. ↑ "Histologic grade is an independent prognostic factor for survival in non-small cell lung cancer: an analysis of 5018 hospital- and 712 population-based cases". The Journal of Thoracic and Cardiovascular Surgery 131 (5): 1014–1020. May 2006. doi:10.1016/j.jtcvs.2005.12.057. PMID 16678584. 
  26. ↑ "Poorly differentiated cancer from an unknown primary site". حاصل ڪيل 6 June 2022. 
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