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Cancer Cells Be Described

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Last Updated: 16 October 2020

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The Cancer Biology portion of the site contains in - depth information about the structure and function of normal cells and cancer cells. Changes that make normal cells turn into cancer cells are describe. Topics covered include: biological Building Blocks - Information on molecules that are found in living things. Include proteins, carbohydrates, lipids and nucleic acids. Cell Structure - discusses functional parts of cells called organelles. Organelles cover include nucleus, ribosomes, mitochondria and cytoskeleton Cell Cycle - look at the clock - like flow that cells go through when they are growing and dividing. Cell Division - Covers control of normal Cell Division and defects seen in cancer cells. Gene Function - discuss way genetic information is used in cells. Mutation - Describes types and causes of changes to genes that can result in Cancer. Cancer Genes - describe types of genes that are altered in cancer. Some key examples are given for each type of gene. Contain section on microRNAs and their role in Cancer. Cancer Epigenetics - Changes in DNA can be subtle, but have huge impacts on the way cells behave. Epigenetics is a study of these small - but - important changes. Causes of Cancer - include details about causes of cancer, including chemicals, radiation and viruses. Cancer Development - Cancer progresses in a stepwise manner, often taking years to become detectable. Learn about that process here. Cancer Metabolism - All cells need energy and oxygen to survive. Cancer cells need a lot of energy to reproduce. Often, cancer cells don't get their energy in the same way normal cells do, and this can impact their growth and their response to cancer treatments. Cancer Cell Death - Most cancer drugs are designed to kill cancer cells. Death of cancer cells is a key step in stopping growth, and it happens in a very orderly fashion. Angiogenesis - Animations and text describe how tumors develop blood supply. Include discussions of drugs that fight cancer by blocking this critical process. Metastasis - The majority of cancer deaths are caused by the spread of disease from its orginal location. This section covers how and why cancer spread. Also covered are attempts to interefere with process in cancer patients. Tumor - Host Interactions - There are many interactions between different cells in tumor. This section covers some of the key cell types and ways that they influence growth of tumor. Microbiome - We are covered with tiny organisms that influence our health for better or worse. Learn about how these bacteria influence cancer growth and treatment responses. Immune System - Immune System is involved in guarding our bodies from internal and external threats, including cancer. Because of the important role of Immune cells in preventing and possibly contributing to Cancer, as well as the use of Immune cells and products in treating Cancer, subject is treated here in detail. Cancer in Domesicated Animals and Pets - Animals other than humans get Cancer and this section examines a few types of cancer in dogs and cats. Cancer in Wild Animals - For millions of years, wild animals have been getting cancer, including some strange ones that spread when animals bite each other or mate.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Characteristics of Cancer Cells

Malignant Cells are characterized by: acceleration of Cell Cycle; genomic Alterations; invasive growth; increased cell mobility; chemotaxis; changes in cellular surface; secretion of lytic factors, etc. Morphological and functional characteristics of malignant Cell.S Morphologically, cancerous cells are characterized by large nucleus,ss having irregular size and shape, nucleoli are prominent, cytoplasm is scarce and intensely colorful or, in contrast is pale. The nucleus of neoplastic cells plays through its changes main role in assessment of tumor malignancy. Changes concern its surface, volume, nucleus / cytoplasm ratio, shape and density, as well as structure and homogeneity. Ultrastructural characteristics are related to nucleus segmentation, invaginations, changes in chromatin, such as heterochromatin reduction, increase of interchromatin and perichromatin granules, increase of nuclear membrane pores, formation of inclusions, etc. The nucleolus is characterized by hypertrophy, macro - and microsegregation, its movement towards membrane, numerical increase and formation of intranuclear canalicular systems between nuclear membrane and the nucleolus. Mitoses are characteristic of malignant cells. The number of mitoses increases, atypical mitosis forms with defects in mitotic spindle appear, which results in triple or quadruple asters and dissymmetrical structures and atypical forms of chromosomes. Nuclear changes explain the presence of different cell clones and genetic anomalies associated with these changes. In intensely Anaplastic tumors, presence of gigantic nuclei and multinucleate cells express abnormal divisions. These morphological characteristics reflect changes occurring at the metabolic level, with augmentation of structures in relation to Cell Division and attenuation of structures associated with other metabolisms. Cytoplasm also undergoes changes, New structures appear or normal structures disappear. Accumulation of ribosomal and messanger RNA in cytoplasm makes it basophilic. Malignant cells have small cytoplasmic amount, frequently with vacuoles. The granular endoplasmic reticulum has appearance of simplified structure. Amorphous, granular of filamentous material can accumulate in cisternae. Fragmentation and degranulation are frequently find, with interruption of connections between granular endoplasmic reticulum and mitochondria. Fingerprint like formations are not uncommon. The decrease of granular endoplasmic reticulum from tumor cells occurs concomitantly with an increase of free ribosomes and polysomes, which show enhanced production of proteins necessary for the cell growth process. Agranular endoplasmic reticulum is, during the initiation phase, hyperplastic, without being correlated with functional hyperactivity. In other malignancy phases, endoplasmic reticulum undergoes reduction. Golgi apparatus in malignant cells is generally poorly develop, which involves positive correlation with lack of tumor cell differentiation. Cells that have completely lost differentiation sporadically exhibit Golgi apparatus. Mitochondria decrease in volume with tumor development. Mitochondria show high variability of shape and volume, and huge mitochondria can be observe. The abnormal glycolysis process occurs in mitochondrial membranes, known in literature as the Warburg phenomenon. Changes in mitochondrial crystals occur, inclusions are present in matrix, and pyknotic images can appear. Longitudinal distribution of mitochondria involves cytochrome oxidase insufficiency.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Benign and malignant growth

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ImageImageImage
An X-ray showing a tumor that has caused a saucer-like erosion in the end of the thighbone.A bone tumor in the middle of the femur exhibiting a combination of characteristics is displayed in an X-ray.A fracture through a tumor in the middle of the upper arm bone shown on X-ray.

Tumors grow because of malfunction in cells ' DNA, mainly in genes that regulate cells ' ability to control their growth. Some damaged genes may also prevent bad cells from killing themselves to make room for new, healthy cells. Regulation of cell death so important, dr. Garcia say. If your programmed cell death is alter, cells do not know when it's time to die and persists. If cell learn how to block that, and it develop the ability to proliferate, tumors grow more rapidly. Some of these mutations lead to rapid, unchecked growth, producing tumors that may spread quickly and damage nearby organs and tissue. Malignant cells have the ability to produce enzymes that dissolve native tissue. This is known as invasiveness, Dr. Garcia say. Other mutations are less aggressive, forming slow - growing tumors that are not cancerous. Benign tumors don't generally invade, Dr. Garcia say. They usually push normal tissue to the side. Many people carry Benign Tumors their entire life. Nevi, or moles, are types of Benign Tumors that may never need treatment. Other types of Benign Tumors include: adenomas: these bumps form on the surfaces of the G - I tract. Colon polyp, classic adenoma, has only a 1 percent chance of becoming cancer in a patient's lifetime, say Jeffrey Weber, MD, Gastroenterologist at our hospital near Phoenix. Fibromas: these tumors of connective tissue may be found in any organ. Fibroid Tumors are named for where they form in the body, such as uterine fibroids. Desmoid tumor: these are often more aggressive than most benign tumors and may invade nearby tissue and organs. But they do not metastasize. Hemangiomas: These tumors are collection of blood vessel cells in skin or internal organs. They may appear on skin as birthmark - like discoloration and often disappear on their own. Lipomas: these soft, round, fatty tumors are often found on the neck or shoulders. Leiomyomas: most common gynecologic tumors in the United States, These may be found in the uterus. Their growth is fuelled by hormones.


Whats a premalignant tumor?

Benign tumors dont necessarily turn into malignant tumors. Some have the potential, though, to become cancerous if abnormal cells continue to change and divide uncontrollably. These terms describe some unusual characteristics of potentially premalignant tumors: hyperplasia. Normal - looking cells are reproducing faster than normal. Atypia. Cells appear slightly abnormal. Metaplasia. Cells look normal but certain types of cells are usually found in this area of the body. Since it is difficult to know which tumors will progress, following types of masses must be carefully monitored or treat: dysplasia. Cells appear abnormal, are reproducing faster than normal, and are arranged normally. Carcinoma in situ. Cells are extremely abnormal but haven't yet invaded nearby tissue. This is sometimes called stage 0 cancer. Colon polyps, for example, are often precancerous. Even though it can take 10 or more years to develop into cancer, theyre usually removed as a precaution.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

General characteristics

Treatment of animals or cells in culture with carcinogenic agents is a means of studying discrete biochemical events that lead to malignant transformation. Studies of cell transformation in vitro, however, have many pitfalls. These tissue - culture artifacts include overgrowth of cells not characteristic of the original population of cultured cells, selection of small population of variant cells with continued passage in vitro, or appearance of cells with abnormal chromosomal number or structure. Such changes in characteristics of cultured cell populations can lead to spontaneous transformation that mimic some of the changes seen in populations of cultured cells treated with oncogenic agents. Thus, it is often difficult to sort out critical malignant events from noncritical ones. Malignant transformation can also be induced in vivo, by treatment of susceptible experimental animals with carcinogenic chemicals or oncogenic viruses or by irradiation, but identification of critical biochemical changes in vivo is even more tenuous because it is difficult to discriminate toxic from malignant events and to determine what role myriad factors, Such as nutritional state of animal, hormone levels, or endogenous infections with microorganisms or parasites, might have on in vivo carcinogenic events. Moreover, tissues in vivo are a mixture of cell types, and it is difficult to determine in which cells critical transformation events are occurring and what role the microenvironment of tissue plays. Most studies that are designed to identify discrete biochemical events occurring in cells during malignant transformation have therefore been DO with cultured cells, because clones of relatively homogeneous cell populations can be studied and the cellular environment defined and manipulate. The ultimate criterion that establishes whether or not cells have been transform, however, is their ability to form tumor in appropriate host animal. Recently developed ability to generate immortalized normal cell lines of give differentiated phenotype from human embryonic stem cells has enhanced the ability to study cells of normal genotype from a single source. 27 Such cell lines may also be generated by transfection of Telomerase gene into cells to maintain chromosomal length. Over the past 60 years, much scientific effort has gone into research aimed at identifying phenotypic characteristics of in vitro - transformed cells that correlate with growth of Cancer in vivo. This research has tremendously increased our knowledge of the biochemistry of cancer cells. However, many of biochemical characteristics initially thought to be closely associated with malignant phenotype of cells in culture were subsequently found to be dissociable from the ability of those cells to produce tumors in animals. Furthermore, individual cells of malignant tumors growing in animals or in humans exhibit marked biochemical heterogeneity, as reflected in their cell surface composition, enzyme levels, immunogenicity, response to anticancer drugs, and so on. This has made it extremely difficult to identify essential changes that produce malignant phenotype.


Hallmarks of cancer

In normal tissue there is a balance between generation of new cells via cell division and loss of cells through cell death. Old cells become damaged over time and then go through a process called apoptosis, form of programmed cell death. Apoptosis is one form of cellular suicide. Apoptosis is a very orderly process in which the genome of a cell, all of its genetic information, is broken down, cell is fragmented into smaller pieces and debris is taken in and digested by nearby cells. 5 this process is normal and necessary for us to refresh our bodies with new, healthy cells. When cells are reproducing, they go through a series of predictable events. Together, these events are called cell cycle. Like one could find in a factory, there are checkpoints built into the cell cycle that stop process when damage is present or something has gone wrong. Checkpoints can trigger death of cells that are dividing in an abnormal way and are responsible for preventing development of cancer. The balance between life and death for cells depends on the amounts and activity of two different types of signals. There are some proteins whose function is to keep cells alive and there is another set that works to trigger cell death. There are several ways that cancer cells can avoid death by apoptosis. One way is to make too many pro - survival proteins. These work as shields and prevent cells from dying when they should. Another way is to produce inactive or defective pro - death proteins. This can happen when genes that produce these proteins become mutated or silence. Avoidance of cell death, coupled with continued cell division leads to growth of tumor. Most of the chemotherapy drugs discussed in the Cancer Treatments section work by causing cancer cells to die by apoptosis. The process of apoptosis, including nuclear fragmentation and formation of many small cell fragments, is shown in the animation below. The image below shows human cancer cells treated with the chemotherapy agent camptothecin. Cells that are undergoing apoptosis appear yellow and show characteristic membrane blebbing seen in cells dying via apoptosis.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

The type of cancer

There are more than 100 types of cancer. Types of cancer are usually named for organs or tissues where cancers form. For example, lung cancer starts in cells of the lung, and brain cancer starts in cells of the brain. Cancers can also be described by the type of cell that forms them, such as epithelial cells or squamous cell.S You can search the NCIs website for information on specific types of cancer based on Cancers location in the body or by using our to Z List of Cancers. We also have collections of information on childhood cancers and cancers in adolescents and young adults. Here are some categories of cancers that begin with specific types of cells:

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What is oncology?

The branch of medicine dedicated to diagnosing, treating and researching cancer is know as oncology, while physicians who work in the field are called oncologist.S Some oncologists focus solely on particular cancer types or treatments. Depending on the type, stage and location of cancer, multiple oncology specialists may be involved in patient care. The field of oncology has three main specialtiesmedical,: surgical and radiationand numerous sub - specialties. A medical oncologist is a licensed physician trained in diagnosing, staging and treating cancer. This specialist also leads the development of cancer patients ' treatment plan, which may include surgery, chemotherapy, immunotherapy, target therapy or hormone therapy, while also coordinating with other oncology specialists and clinicians who may have a role in patient care. Medical oncologists is also doctor cancer patients will continue to see after treatment, for checkups over the long - term. A surgical oncologist is a surgeon who specializes in performing biopsies and removing cancerous tumors and surrounding tissue, as well as other cancer - related operations. Radiation oncologists specialize in treating cancer with radiation therapy to shrink or destroy cancer cells or to ease cancer - related symptoms. Many cancer types are treated by oncology sub - specialty. Gynecologic oncologists, for example, are trained to treat cancers of the female reproductive system such as those affecting the uterus, cervix, or ovaries, while hematologic oncologists specialize in diagnosing and treating blood cancers. Neuro - oncologists treat cancers of the brain, spine and peripheral nerves.

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Cell Cycle in Cancer

Cancer comprises many different diseases caused by a common mechanism: uncontrolled cell growth. Despite redundancy and overlapping levels of cell cycle control, errors do occur. One of the critical processes monitored by cell cycle checkpoint surveillance mechanism is proper replication of DNA during S phase. Even when ALL of cell cycle controls are fully functional, small percentage of replication errors will be passed on to daughter cells. If changes to DNA nucleotide sequence occur within the coding portion of a gene and are not correct, gene mutation results. All cancers start when gene mutation give rise to faulty protein that play key role in cell reproduction. Change in cells that results from malformed protein may be minor: perhaps slight delay in binding of CDK to cyclin or RB protein that detaches from its target DNA while still phosphorylated. Even minor mistakes, however, may allow subsequent mistakes to occur more readily. Over and over, small uncorrected errors are passed from parent cell to daughter cells and amplified as each generation produces more non - functional proteins from uncorrected DNA damage. Eventually, pace of the cell cycle speeds up as the effectiveness of control and repair mechanisms decreases. Uncontrolled growth of mutated cells outpaces growth of normal cells in area, and tumors can result.

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* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

How Do They Start?

Precancerous cells may look abnormal and similar to cancer cells but are distinguished from cancer cells by their behavior. Unlike cancer cells, precancerous cells do not have the ability to spread to other regions of the body. An often confusing condition is that of carcinoma - in - situ. Carcinoma in situ consists of cells with abnormal changes found in cancer cells, but since they have not spread beyond their original location they are not technically cancer. Since CIS can turn into cancer, it is usually treated as early cancer.

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Cancer Cells Keep Changing

Until now, little was known about mechanisms involved in these changing processes in tumour. There is a particularly intriguing way in which a tumour that initially presents solid state, attaches to nearby cells, afterwards becomes semiliquid mass, detaches from tissues and more flexible. A team lead by Manel Esteller, director of Cancer Epigenetics and Biology Program at Bellvitge Biomedical Research Institute, professor of Genetics at University of Barcelona and ICREA researcher, has identified a mechanism that explains this change. Tumours shed their skin because molecular switches called microRNAs - responsible for maintaining epithelial appearance of cells - turn off. The finding has been published this week in the online version of the international scientific journal Oncogene, Nature. We have discovered that some microRNAs, group called microRNA - 200S, undergo chemical inactivation and inhibit their expression. When these cellular appearance drivers are not present, tumour cells change, stretch, stop their inhibition and thus the tumour progresses, explains Dr. Esteller, adding that results from research show that this is a very dynamic process. Change involves appearance of tumour to onset of metastasis, but if we change environmental circumstances that influence these cells, process reverses. Dr Esteller compares the process with small planet in Darwinian evolution, but in an expedited manner. The study was conducted mainly on breast and colon tumours. Besides serving to better understand disease, results are important because they predict that external intervention is possible in the process. In this sense, drug treatments can reverse the process and move from highly evolved tumour form to more primitive form, which would be associated with slower progression of disease.

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A Collection of Related Diseases

Cancer, is a group of more than 100 distinct diseases characterized by uncontrolled growth of abnormal cells in the body. Though cancer has been known since antiquity, some of the most significant advances in scientists ' understanding of it have been made since the middle of the 20th century. Those advances led to major improvements in cancer treatment, mainly through development of methods for timely and accurate diagnosis, selective surgery, radiation therapy, chemotherapeutic drugs, and targeted therapies. Advances in treatment have succeeded in bringing about a decrease in cancer deaths, though mainly in developed countries. Indeed, cancer remains a major cause of sickness and death throughout the world. By 2018, number of new cases diagnosed annually had risen to more than 18 million, more than half of them in less - developed countries, and the number of deaths from cancer in 2018 was 9. 6 million worldwide. About 70 percent of cancer deaths are in low - and middle - income countries. The World Health Organization has estimated that the global cancer burden could be reduced by as much as 30 to 50 percent through prevention strategies, particularly through avoidance of known risk factors. In addition, laboratory investigations aimed at understanding causes and mechanisms of cancer have maintained optimism that the disease can be control. Through breakthroughs in cell biology, genetics, and biotechnology, researchers have gained fundamental understanding of what occurs within cells to cause them to become cancerous. Those conceptual gains are steadily being converted into actual gains in practice of Cancer diagnosis and treatment, with notable progress toward personalized Cancer medicine, in which therapy is tailored to individuals according to biological anomalies unique to their disease. Personalized cancer medicine is considered the most - promising area of progress yet for modern cancer therapy.


Tumour nomenclature

In the majority of cases, benign tumours are named by attaching suffix - oma to the name of tissue or cell from which cancer arose. For example, tumour that is composed of cells related to bone cells and has structural and biochemical properties of bone substance is classified as osteoma. That rule is followed with a few exceptions for tumours that arise from mesenchymal cells. Benign tumours arising from epithelial cells are classified in a number of ways and thus have a variety of names. Sometimes classification is based on cell of origin, whereas in other cases it is based on tumours ' microscopic architectural pattern or gross appearance. Term adenoma, for instance, designates a benign epithelial tumour that either arises in endocrine glands or forms glandular structure. Tumours of ovarian epithelium that contain large cysts are called cystadenomas. When a tumour gives rise to mass that projects into lumen, it is called a polyp. Most polyps are epithelial in origin. Strictly speaking, term polyp refers only to benign growths; malignant polyp is referred to as polypoid cancer in order to avoid confusion. Benign tumours build up of fingerlike projections from skin or mucous membranes are called papillomas.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

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"Drivers" of Cancer

Errors in DNA replication can alter cells ' DNA sequence. If such alterations occur early enough in embryonic development, changes are inherited by all organism cells. But if alterations arise later in adult life, it is more difficult to track such changes in small number of cells in specific tissue, so the extent of these alterations in normal tissues is poorly understood. It is thought that cancer is initiated when cells acquire the minimum compendium of genetic alterations needed to trigger tumour formation. Understanding when such initiating mutations occur in normal cells is crucial for enabling reconstruction of early events that lead to Cancer. Yokoyama et al. 1, writing in Nature, and Martincorena et al. 2, writing in Science, have analyse extent of mutations in human epithelial tissue from healthy oesophagus, and how this relates to processes that drive cancer development. Read paper: Age - related remodelling of oesophageal epithelia by mutated Cancer drivers Martincorena and colleagues sequence 74 Cancer - associate genes in 844 tissue samples taken from the upper oesophagus of 9 healthy donors who differed in gender, age and lifestyle. For 21 of these samples, authors also determined whole - genome sequences. Previous study 3 assessing mutations in healthy skin cells reported between two and six mutations per million nucleotides of DNA. By contrast, Martincorena and colleagues report that mutations in oesophageal cells arose at a roughly tenfold lower rate than that reported for skin. This difference is unsurprising, because skin cells are exposed to more DNA - damaging agents, such as ultraviolet light, than are oesophageal cells. Instead, surprise is that, compared with healthy skin, healthy oesophagus has more mutations in cancer - associate genes. Moreover, at least subset of these altered genes was under strong positive selection, meaning that genetic alterations promote cell proliferation, leading to formation of cell clones. Compared with samples from younger people, overall number of mutations, number of mutations in Cancer - associate genes and size of clones were all greater in samples from older people. Authors found that donors samples had an average of about 120 different mutations in NOTCH1, known Cancer - associate gene, per square centimetre of normal oesophageal tissue. Several of these mutations were of the same type as those seen in cancer of the upper oesophagus called oesophageal squamous cell carcinoma. Yet despite these similarities, there were striking differences between expansion of cell clones in normal oesophageal tissue and in OSCC. Normal and cancerous clones seem to be driven by mutations in different genes. Notch1 was the most frequently mutated gene in healthy oesophageal samples, whereas previous study 4 reported that NOTCH1 was mutated in only around 10% of OSCCs. Mutations in Cancer - promoting gene TP53 are found in more than 90% of OSCC cases 4, but were present at much lower frequency in normal oesophageal samples. In normal cell clones, Martincorena et al.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

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Sources

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