Cancer cell

{{Short description|Tumor cell}}

{{About|cancer cells|the scientific journal|Cancer Cell (journal)}}

Cancer cells are cells that divide continually, forming solid tumors or flooding the blood or lymph with abnormal cells.{{Cite journal |last=Chakradhar |first=Shraddha |date=2019-01-15 |title=Arrested cells may awaken yet |url=https://www.nature.com/articles/d41591-019-00004-x |journal=Nature Medicine |language=en |doi=10.1038/d41591-019-00004-x|url-access=subscription }} Cell division is a normal process used by the body for growth and repair. A parent cell divides to form two daughter cells, and these daughter cells are used to build new tissue or to replace cells that have died because of aging or damage.{{Cite journal |last1=Ong |first1=Joseph Y. |last2=Torres |first2=Jorge Z. |date=July 2019 |title=Dissecting the mechanisms of cell division |journal=Journal of Biological Chemistry |language=en |volume=294 |issue=30 |pages=11382–11390 |doi=10.1074/jbc.AW119.008149|doi-access=free |pmc=6663871 }} Healthy cells stop dividing when there is no longer a need for more daughter cells, but cancer cells continue to produce copies. They are also able to spread from one part of the body to another in a process known as metastasis.{{cite web|title=National Cancer Institute: is this cancer?|url=http://www.cancer.gov/about-cancer/understanding/what-is-cancer|access-date=1 August 2016|date=2007-09-17}}

File:Breast cancer cells.jpg cells]]

Classification

There are different categories of cancer cell, defined according to the cell type from which they originate.{{cite web|title=Histological types of cancer - CRS - Cancer Research Society|url=http://www.crs-src.ca/page.aspx?pid=1765|website=www.crs-src.ca|access-date=2016-08-02|archive-url=https://web.archive.org/web/20170827123133/https://www.crs-src.ca/page.aspx?pid=1765|archive-date=2017-08-27|url-status=dead}}

  • Carcinoma, the majority of cancer cells are epithelial in origin, beginning in a tissue that lines the inner or outer surfaces of the body.{{Cite web |title=Cancer Classification {{!}} SEER Training |url=https://training.seer.cancer.gov/disease/categories/classification.html |access-date=2025-02-24 |website=training.seer.cancer.gov}}
  • Leukaemia, originate in the tissues responsible for producing new blood cells, most commonly in the bone marrow.{{Citation |last1=Chennamadhavuni |first1=Adithya |title=Leukemia |date=2025 |work=StatPearls |url=https://www.ncbi.nlm.nih.gov/books/NBK560490/ |access-date=2025-02-24 |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=32809325 |last2=Lyengar |first2=Varun |last3=Mukkamalla |first3=Shiva Kumar R. |last4=Shimanovsky |first4=Alex}}{{Cite web |title=Leukemia - Symptoms and causes |url=https://www.mayoclinic.org/diseases-conditions/leukemia/symptoms-causes/syc-20374373 |access-date=2025-02-24 |website=Mayo Clinic |language=en}}
  • Lymphoma and myeloma, derived from cells of the immune system.{{Cite journal |last1=Díaz-Tejedor |first1=Andrea |last2=Lorenzo-Mohamed |first2=Mauro |last3=Puig |first3=Noemí |last4=García-Sanz |first4=Ramón |last5=Mateos |first5=María-Victoria |last6=Garayoa |first6=Mercedes |last7=Paíno |first7=Teresa |date=2021-03-17 |title=Immune System Alterations in Multiple Myeloma: Molecular Mechanisms and Therapeutic Strategies to Reverse Immunosuppression |journal=Cancers |language=en |volume=13 |issue=6 |pages=1353 |doi=10.3390/cancers13061353 |doi-access=free |pmid=33802806 |pmc=8002455 |issn=2072-6694}}
  • Sarcoma, originating in connective tissue, including fat, muscle, and bone.{{Citation |last1=Popovich |first1=John R. |title=Sarcoma |date=2025 |work=StatPearls |url=https://www.ncbi.nlm.nih.gov/books/NBK519533/ |access-date=2025-02-24 |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=30137818 |last2=Kashyap |first2=Sarang |last3=Gasalberti |first3=David P. |last4=Cassaro |first4=Sebastiano}}
  • Central nervous system, derived from cells of the brain and spinal cord.{{Cite web |date=2017-11-10 |title=Central Nervous System: brain and spinal cord |url=https://qbi.uq.edu.au/brain/brain-anatomy/central-nervous-system-brain-and-spinal-cord |access-date=2025-02-24 |website=qbi.uq.edu.au |language=en}}
  • Mesothelioma, originating in the mesothelium; the lining of body cavities.{{Cite journal |last1=Hiriart |first1=Emilye |last2=Deepe |first2=Raymond |last3=Wessels |first3=Andy |date=2019-04-08 |title=Mesothelium and Malignant Mesothelioma |journal=Journal of Developmental Biology |language=en |volume=7 |issue=2 |pages=7 |doi=10.3390/jdb7020007 |doi-access=free |pmid=30965570 |pmc=6630312 |issn=2221-3759}}

File: Apocrine carcinoma - high mag.jpg|Carcinoma

File:Acute lymphoblastic leukaemia smear.jpg|Leukaemia

File:Burkitt lymphoma, touch prep, Wright stain.jpg|Lymphoma

File:Multiple myeloma (1) MG stain.jpg|Myeloma

File:Ewing sarcoma cells.png|Sarcoma

File:Well-differentiated papillary mesothelioma - alt 2 -- intermed. mag.jpg|Mesothelioma

Histology

File:Normal and cancer cells structure.jpg features of normal cells and cancer cells]]

Cancer cells have distinguishing histological features visible under the microscope.{{Citation |last1=Baba |first1=Alecsandru Ioan |title=TUMOR CELL MORPHOLOGY |date=2007 |work=Comparative Oncology |url=https://www.ncbi.nlm.nih.gov/books/NBK9553/ |access-date=2025-02-24 |publisher=The Publishing House of the Romanian Academy |language=en |last2=Câtoi |first2=Cornel}}{{Cite journal |last1=Kumar |first1=Rajesh |last2=Srivastava |first2=Rajeev |last3=Srivastava |first3=Subodh |date=2015-08-23 |title=Detection and Classification of Cancer from Microscopic Biopsy Images Using Clinically Significant and Biologically Interpretable Features |journal=Journal of Medical Engineering |language=en |volume=2015 |pages=1–14 |doi=10.1155/2015/457906 |doi-access=free |issn=2314-5129}} The nucleus is often large and irregular, and the cytoplasm may also display abnormalities.{{cite book| vauthors = Baba AT, Câtoi C | chapter = Comparative Oncology |title= Tumor Cell Morphology |publisher=The Publishing House of the Romanian Academy |url=https://www.ncbi.nlm.nih.gov/books/NBK9553/ |language=en |year=2007 }}

= Nucleus =

The shape, size, protein composition, and texture of the nucleus are often altered in malignant cells. The nucleus may acquire grooves, folds or indentations, chromatin may aggregate or disperse, and the nucleolus can become enlarged. In normal cells, the nucleus is often round or solid in shape, but in cancer cells the outline is often irregular. Different combinations of abnormalities are characteristic of different cancer types, to the extent that nuclear appearance can be used as a marker in cancer diagnostics and staging.{{cite journal | vauthors = Zink D, Fischer AH, Nickerson JA | title = Nuclear structure in cancer cells | journal = Nature Reviews. Cancer | volume = 4 | issue = 9 | pages = 677–687 | date = September 2004 | pmid = 15343274 | doi = 10.1038/nrc1430 | s2cid = 29052588 }}

Causes

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|File:Life of a Cancer Cell.png

|alt1=Cell Life Cycle for Cancer

|Life cycle of a cancer cell}}

{{main|Carcinogenesis}}Cancer cells are created when the genes responsible for regulating cell division are damaged.{{Cite web |title=Cell Division, Cancer {{!}} Learn Science at Scitable |url=https://www.nature.com/scitable/topicpage/cell-division-and-cancer-14046590/ |access-date=2025-02-24 |website=www.nature.com |language=en}} Carcinogenesis is caused by mutation and epimutation of the genetic material of normal cells, which upsets the normal balance between proliferation and cell death. This results in uncontrolled cell division in the body. The uncontrolled and often rapid proliferation of cells can lead to benign or malignant tumours (cancer). Benign tumors do not spread to other parts of the body or invade other tissues. Malignant tumors can invade other organs, spread to distant locations (metastasis) and become life-threatening.{{Citation |last1=Martin |first1=Tracey A. |title=Cancer Invasion and Metastasis: Molecular and Cellular Perspective |date=2013 |work=Madame Curie Bioscience Database [Internet] |url=https://www.ncbi.nlm.nih.gov/books/NBK164700/ |access-date=2025-02-24 |publisher=Landes Bioscience |language=en |last2=Ye |first2=Lin |last3=Sanders |first3=Andrew J. |last4=Lane |first4=Jane |last5=Jiang |first5=Wen G.}}{{Cite web |date=2015-05-12 |title=Metastatic Cancer: When Cancer Spreads - NCI |url=https://www.cancer.gov/types/metastatic-cancer |access-date=2025-02-24 |website=www.cancer.gov |language=en}}

More than one mutation is necessary for carcinogenesis. In fact, a series of several mutations to certain classes of genes is usually required before a normal cell will transform into a cancer cell.{{cite journal | vauthors = Fearon ER, Vogelstein B | title = A genetic model for colorectal tumorigenesis | journal = Cell | volume = 61 | issue = 5 | pages = 759–767 | date = June 1990 | pmid = 2188735 | doi = 10.1016/0092-8674(90)90186-I | s2cid = 22975880 | doi-access = free }}

Damage to DNA can be caused by exposure to radiation, chemicals, and other environmental sources, but mutations also accumulate naturally over time through uncorrected errors in DNA transcription, making age another risk factor.{{Cite journal |last1=Ribeiro |first1=Jessica Honorato |last2=Altinisik |first2=Nazlican |last3=Rajan |first3=Nicholas |last4=Verslegers |first4=Mieke |last5=Baatout |first5=Sarah |last6=Gopalakrishnan |first6=Jay |last7=Quintens |first7=Roel |date=2023-10-10 |title=DNA damage and repair: underlying mechanisms leading to microcephaly |journal=Frontiers in Cell and Developmental Biology |volume=11 |doi=10.3389/fcell.2023.1268565 |doi-access=free |issn=2296-634X|hdl=1854/LU-01HCQGJ4BBKZRSHZ3JRPFBQPDG |hdl-access=free }} Oncoviruses can cause certain types of cancer, and genetics are also known to play a role.{{Cite web |date=2017-08-30 |title=About Cancer |url=https://www.cancerresearchuk.org/about-cancer |access-date=2025-02-24 |website=Cancer Research UK |language=en-gb}}

Stem cell research suggests that excess SP2 protein may turn stem cells into cancer cells.{{Cite web |title=Too much SP2 protein turns stem cells into 'evil twin' cancer cells |url=https://www.sciencedaily.com/releases/2010/10/101027151209.htm |access-date=2025-02-24 |website=ScienceDaily |language=en}} However, a lack of particular co-stimulated molecules that aid in the way antigens react with lymphocytes can impair the natural killer cells' function, ultimately leading to cancer.{{cite news|title=The Innate Immune System: NK Cells|url=http://student.ccbcmd.edu/courses/bio141/lecguide/unit4/innate/nkcell.html|access-date=2010-12-01|agency=Community College of Baltimore County|archive-url=https://web.archive.org/web/20100727063451/http://student.ccbcmd.edu/courses/bio141/lecguide/unit4/innate/nkcell.html|archive-date=2010-07-27}}{{Cite journal |last1=Coënon |first1=Loïs |last2=Geindreau |first2=Mannon |last3=Ghiringhelli |first3=François |last4=Villalba |first4=Martin |last5=Bruchard |first5=Mélanie |date=2024-08-23 |title=Natural Killer cells at the frontline in the fight against cancer |journal=Cell Death & Disease |language=en |volume=15 |issue=8 |page=614 |doi=10.1038/s41419-024-06976-0 |pmid=39179536 |pmc=11343846 |issn=2041-4889}}{{Cite journal |last1=Abel |first1=Alex M. |last2=Yang |first2=Chao |last3=Thakar |first3=Monica S. |last4=Malarkannan |first4=Subramaniam |date=2018-08-13 |title=Natural Killer Cells: Development, Maturation, and Clinical Utilization |journal=Frontiers in Immunology |volume=9 |doi=10.3389/fimmu.2018.01869 |doi-access=free |pmid=30150991 |issn=1664-3224|pmc=6099181 }}

DNA repair and mutation

When a cell is deficient in the capacity to repair DNA damages, such damages tend to be retained within the cell at an increased level. These damages, upon replication of the cell’s DNA, may cause replication errors, including mutations that lead to cancer. Numerous inherited DNA repair disorders have been described that increase cancer risk (see Wikipedia article DNA repair-deficiency disorder). In addition, particular DNA repair enzymes have been found to be deficient in multiple cancers.{{Cite journal |last1=Alhmoud |first1=Jehad F. |last2=Woolley |first2=John F. |last3=Al Moustafa |first3=Ala-Eddin |last4=Malki |first4=Mohammed Imad |date=2020-04-23 |title=DNA Damage/Repair Management in Cancers |journal=Cancers |language=en |volume=12 |issue=4 |pages=1050 |doi=10.3390/cancers12041050 |doi-access=free |pmid=32340362 |pmc=7226105 |issn=2072-6694}}{{Cite journal |last1=Torgovnick |first1=Alessandro |last2=Schumacher |first2=Björn |date=2015-04-23 |title=DNA repair mechanisms in cancer development and therapy |journal=Frontiers in Genetics |volume=6 |doi=10.3389/fgene.2015.00157 |doi-access=free |issn=1664-8021|pmc=4407582 }} For example, deficient expression of the DNA repair enzyme O-6-methylguanine-DNA methyltransferase is observed in several kinds of cancer.

Although a DNA repair deficiency can predispose a cell lineage to develop cancer, increased (rather than decreased) expression of a repair capability may also emerge in the progression of cancer cell lineages, and this capability may be clinically important as reviewed by Lingg et al.{{cite journal|pmid=35251135 |date=2022 |last1=Lingg |first1=L. |last2=Rottenberg |first2=S. |last3=Francica |first3=P. |title=Meiotic Genes and DNA Double Strand Break Repair in Cancer |journal=Frontiers in Genetics |volume=13 |page=831620 |doi=10.3389/fgene.2022.831620 |pmc=8895043 |doi-access=free }} For instance, the DNA repair gene DMC1 encodes a protein that is normally expressed only in cells undergoing meiosis where it helps maintain an undamaged germ-line. However, DMC1 is also expressed in various cancer cell lines including cervical, breast, and lymphoma cancer cell lines. Expression of meiotic DNA repair genes such as DMC1 may promote tumor cell growth by dealing with endogenous DNA damage within the tumor, and may also diminish the effectiveness of anticancer therapy, such as radiation therapy.

Pathology

Cells playing roles in the immune system, such as T-cells, are thought to use a dual receptor system when they determine whether or not to kill sick or damaged human cells. If a cell is under stress, turning into tumors, or infected, molecules including MIC-A and MIC-B are produced so that they can attach to the surface of the cell. These work to help macrophages detect and kill cancer cells.{{Cite journal |last=Pan |first=Xing-Qing |date=2012-11-13 |title=The mechanism of the anticancer function of M1 macrophages and their use in the clinic |url=http://www.cjcsysu.cn/abstract_AOP.asp?id=12-046 |journal=Chinese Journal of Cancer |doi=10.5732/cjc.012.10046|doi-broken-date=24 February 2025 }}

Discovery

Early evidence of human cancer can be interpreted from Egyptian papers (1538 BCE) and mummified remains.{{cite journal | vauthors = David AR, Zimmerman MR | title = Cancer: an old disease, a new disease or something in between? | language = En | journal = Nature Reviews. Cancer | volume = 10 | issue = 10 | pages = 728–733 | date = October 2010 | pmid = 20814420 | doi = 10.1038/nrc2914 | s2cid = 10492262 }} In 2016, a 1.7 million-year-old osteosarcoma was reported by Edward John Odes (a doctoral student in Anatomical Sciences from Witwatersrand Medical School, South Africa) and colleagues, representing the oldest documented malignant hominin cancer.{{cite journal| vauthors = Odes EJ, Randolph-Quinney PS, Steyn M, Throckmorton Z, Smilg JS, Zipfel B, Augustine TN, De Beer F, Hoffman JW, Franklin RD, Berger LR |display-authors=6 |title= Earliest hominin cancer: 1.7-million-year-old osteosarcoma from Swartkrans Cave, South Africa |journal=South African Journal of Science|volume=112|issue=7/8|doi=10.17159/sajs.2016/20150471|language=en|issn=1996-7489|year=2016|page=5 |doi-access=free}}

The understanding of cancer was significantly advanced during the Renaissance period and in the Age of Discovery. Sir Rudolf Virchow, a German biologist and politician, studied microscopic pathology, and linked his observations to illness. He is described as “the founder of cellular pathology”.{{Cite web |url=http://www.uib.no/med/avd/miapr/arvid/MOD2/Arvid/Patofysiologi/history_of_cancer.pdf |title=History of cancer | work = University of Bergen | date = 23 March 1999 |access-date=2010-11-30 |archive-url=https://web.archive.org/web/20120314090145/http://www.uib.no/med/avd/miapr/arvid/MOD2/Arvid/Patofysiologi/history_of_cancer.pdf |archive-date=2012-03-14 |url-status=dead }}{{Cite web |title=International Online Medical Council (IOMC) |url=https://www.iomcworld.org/medical-journals/circulating-tumor-cells-42986.html |access-date=2025-02-24 |website=International Online Medical Council |language=en}} In 1845, Virchow and John Hughes Bennett independently observed an abnormal increase in white blood cells in patients. Virchow correctly identified the condition as a blood disease, and named it leukämie in 1847 (later anglicised to leukemia).{{cite journal | vauthors = Degos L | title = John Hughes Bennett, Rudolph Virchow... and Alfred Donné: the first description of leukemia | journal = The Hematology Journal | volume = 2 | issue = 1 | pages = 1 | year = 2001 | pmid = 11920227 | doi = 10.1038/sj/thj/6200090 }}{{cite journal | vauthors = Kampen KR | title = The discovery and early understanding of leukemia | journal = Leukemia Research | volume = 36 | issue = 1 | pages = 6–13 | date = January 2012 | pmid = 22033191 | doi = 10.1016/j.leukres.2011.09.028 }}{{cite book| vauthors = Mukherjee S |author-link=Siddhartha Mukherjee|title=The Emperor of All Maladies: A Biography of Cancer|url=https://books.google.com/books?id=5rF_31RVTnMC|access-date=6 September 2011|date=16 November 2010|publisher=Simon and Schuster|isbn=978-1-4391-0795-9}} In 1857, he was the first to describe a type of tumour called chordoma that originated from the clivus (at the base of the skull).{{cite journal| vauthors = Hirsch EF, Ingals M |title=Sacrococcygeal chordoma|journal=JAMA: The Journal of the American Medical Association | date = May 1923 |volume=80 |issue=19 |pages=1369 |doi=10.1001/jama.1923.02640460019007}}{{cite journal | vauthors = Lopes A, Rossi BM, Silveira CR, Alves AC | title = Chordoma: retrospective analysis of 24 cases | journal = Sao Paulo Medical Journal = Revista Paulista de Medicina | volume = 114 | issue = 6 | pages = 1312–1316 | year = 1996 | pmid = 9269106 | doi = 10.1590/S1516-31801996000600006 | doi-access = free }}

Telomerase

Cancer cells have unique features that make them “immortal” according to some researchers.{{Cite journal |last1=Duesberg |first1=Peter |last2=McCormack |first2=Amanda |date=March 1, 2013 |title=Immortality of cancers: A consequence of inherent karyotypic variations and selections for autonomy |journal=Cell Cycle |language=en |volume=12 |issue=5 |pages=783–802 |doi=10.4161/cc.23720 |pmid=23388461 |pmc=3610726 |issn=1538-4101 }} The enzyme telomerase is used to extend the cancer cell's life span.{{Cite journal |last=Shay |first=Jerry W. |date=2016-06-01 |title=Role of Telomeres and Telomerase in Aging and Cancer |journal=Cancer Discovery |language=en |volume=6 |issue=6 |pages=584–593 |doi=10.1158/2159-8290.CD-16-0062 |pmid=27029895 |pmc=4893918 |issn=2159-8274}} While the telomeres of most cells shorten after each division, eventually causing the cell to die, telomerase extends the cell's telomeres. This is a major reason that cancer cells can accumulate over time, creating tumors.File:Cancer stem cells.svg targeted and conventional cancer therapies]]

Treatment

In February 2019, medical scientists announced that iridium attached to albumin, creating a photosensitized molecule, can penetrate cancer cells and, after being irradiated with light (a process called photodynamic therapy), destroy the cancer cells.{{cite news |author=University of Warwick |title=Simply shining light on dinosaur metal compound kills cancer cells |url=https://www.eurekalert.org/pub_releases/2019-02/uow-ssl013119.php |date=3 February 2019 |work=EurekAlert! |access-date=3 February 2019 |author-link=University of Warwick }}{{cite journal | vauthors = Zhang P, Huang H, Banerjee S, Clarkson GJ, Ge C, Imberti C, Sadler PJ | title = Nucleus-Targeted Organoiridium-Albumin Conjugate for Photodynamic Cancer Therapy | journal = Angewandte Chemie | volume = 58 | issue = 8 | pages = 2350–2354 | date = February 2019 | pmid = 30552796 | pmc = 6468315 | doi = 10.1002/anie.201813002 }}

See also

References

{{Reflist}}

Further reading

  • {{cite journal|pmc=2908063|year=2010 |last1=Schwarzer |first1=K. |last2=Foerster |first2=M. |last3=Steiner |first3=T. |last4=Hermann |first4=I. M. |last5=Straube |first5=E. |title=BCG strain S4-Jena: An early BCG strain is capable to reduce the proliferation of bladder cancer cells by induction of apoptosis |journal=Cancer Cell International |volume=10 |page=21 |doi=10.1186/1475-2867-10-21 |doi-access=free |pmid=20587032 }}