Protists are a diverse group of organisms that includes many single-celled and multi-celled eukaryotes. They differ from typical eukaryotic organisms in several ways.
First, protists lack the complex cell structure found in plants, animals and fungi. For example, they do not have rigid cell walls or specialized organelles such as chloroplasts or mitochondria. This makes them more adaptable to varied environmental conditions than most other eukaryotic organisms.
Second, protists reproduce differently than other eukaryotes. Most commonly, they reproduce through binary fission – where one organism splits into two identical daughter cells with identical genetic material – instead of sexual reproduction which is common among higher eukaryotes. In some cases, however, protists may exchange genetic material through conjugation or transformation processes similar to those seen in prokaryotes.
In summary, there are a few key differences between protistans and other typical Eukaroyticorganisms: Protistans lack certain cellular structures present in most higher order euarkyotes; They also rely primarily on binary fission for reproduction instead of sexual reproduction; Finally their metabolic pathways are much more versatile compared to standard aerotbic respiration used by plants and animals .
Protists are a diverse group of single-celled or multi-cellular organisms that do not fit into any of the other categories of eukaryotic organisms. These include algae, protozoans, fungi, and slime molds. They differ from typical eukaryotic organisms in several ways.
First, many protists are unicellular while most other eukaryotes are multicellular. This means that only one cell makes up a protist’s body, while multiple cells work together to form the body of more advanced species like humans and animals.
The basic aim of the personalized medicine is applying right therapy to the right population of people by defining disease at the moecular level. So, identifying differences among the individuals support the new treatment methods and pharmaceutical companies to develop new cancer drugs. Patients who have similar clinical outcome and histological tumor type can give different response to the same drug(17). Prediction of who will be a nonresponders reduces the harmfull effect of drug on nonresponders like a potential toxic effect of drug and cost effect. Also when drug companies develop new drug, they focus on the patient population that benefit from drug to increase positive responds(17).
U.S. Food and Drug Administration bringed development about targeted therapy. For example, to treat chronic myeloid leukemia and gastrointestinal stromal tumor(18) ,imatinib mesylate is used and to treat breast cancer(19), trastuzumab (Herceptin) is used. Molecular characteristics of these cancer types that are abnormal protein tyrosine kinase activity in chronic myeloid leukemia and gastrointestinal stromal tumor and HER-2 receptor in breastcancer is used as a predictive biomarker. By using these markers only individuals which have these molecular alteration is selected and it means they are favorable for the treatment. Using this way some cancer types’ survival rate is shifted from 0 to 70%(17).
This application is used in non-small cell lung cancer treatment with using of mutations screeing. In this cancer type mutation occurs in kinase domain of EGFR. Gefitinib (Iressa) and erlotinib are tyrosine kinase inhibitors drug are used to treat and patients give a higher response to the treatment(20). Also if patient that is never smoked Asian females have adenocarcinomas, these drugs efficient on them(21). On the other hand, if the mutatuions occur at downstream effector KRAS, patient is resistant to to erlotinib(22). Also mutations that is at KRAS have a resistance to cetuximab (Erbitux) and panitumumab (Vectibix) drugs in colon cancer patients. If the KRAS is wild type, these these drugs is effective on the patients(23). These responses that are specific and different are based on molecular profile. Some molecular test are done before the using of cetuximab or panitumumab to a colon cancer patient. Lung and colon cancer is concerned with targeted therapy that is guide to patient about treatment by understanding the structure of cancer(24).
Pharmacogenomics and treatment safety
Genes that have genetical variation encode enzymes which metobolize drug, drug transporters, or drug targets. Variation in genes that can predict dose and safety of treatment for different types of cancer patient can have harmful influence on these patients’ treatment(25). For instance, polymorphism where in cytochrome P450 enzymes could cause to metabolite to drug slowly or very fast. So patient give an overdose symptoms or no response to drug by changing the pharmacokinetics of drug metabolism, also it may cause an adverse drug reaction(26). Thereby , forecasting optimal dose of drug , inducing the harmful side effects can be provided by using polymorphism(27). In familial breast cancer, patients shows low survival rate to treatment with tamoxifen that is chemotherapeutic drug because of genetic variation in CYP2D6 that is seen as a poor metabolizer (28). There are some studies abour genetic testing on drug label including test for CYP450 polymorphisms.
Prognosis
Insteaf of using clinicopathologic parameters as a biomarker in biochemical testing for prognosis and selection of therapatic way for cancer patient , Genotyping or gene expression profiling by microarray and protein analysis by mass spectrometry is used for prognostic biomarkers with the understanding of the molecular mechanism of cancer subtypes(29).
Biomarkers can be used alone or with combination of other parameters for classify subgroups according to their risk rate and for leading to therapy decision. For example, tissue microarray analysis with combining molecular and clinical biomarker is more efficient than the clasical cl
