Mereja

Author: Kok Siong Chen

  • Tamoxifen – Breast Cancer Treatment

    Tamoxifen plays an essential role as adjuvant drug in breast cancer treatment. Many people do not know about the mechanism how it functions to prevent the progression of breast cancer. I have found a lot of information about the Tamoxifen to share with all of you.
     

    Tamoxifen is Effective to Treat Breast Cancer

    As what we know, Tamoxifen works to occupy the estrogen receptor and blocks the estrogen. In fact, there is another mode of action to treat the breast cancer instead of just blocking the estrogen. It also works in estrogen-receptor negative breast cancer and progesterone-receptor positive breast cancer. Instead of just blocking the estrogen, it also blocks another type of signal known as Protein Kinase C (PKC). PKC is essential in regulation of activation of oncogenes. By blocking the PKC, the oncogenes will not be activated. Besides, PKC also regulates other signals that control the growth and transformation of cells.
     
    tamoxifen 300x196 Tamoxifen Breast Cancer Treatment

    Furthermore, Tamoxifen is able to interfere with the cell cycle too. This is another anti-cancer action of it. As we all know, cell cycle is a predetermined program that leading the cell goes through the division. Normally, the cell cycle will be stopped at the checkpoints to ensure everything is in normal condition. The checks will ensure that the abnormal cells do not replicate. However, the cancer cells have abnormal cell cycles where they lost those checkpoints. Therefore, the cancer cells can replicate without any barrier. Consequently, the traditional chemotherapy is to restore the checkpoint function in cancer cell to stop the cell cycle. Significantly, Tamoxifen is one of the good drugs to be used as chemotherapeutic agent as it can stop the cell cycle in cancer cells.
     
    In the previous post about the hormonal therapy for breast cancer treatment, I have mentioned that Tamoxifen can only work at 2 years. After 2 years, the drug will start to enhance the developing of tamoxifen-dependent cancer. We called this problem as Tamoxifen Resistance. Many cancer researches show that Tamoxifen Resistance is because of the permanent damage caused by the drug. It might damage the tumour suppressor gene, p53. p53 is a main role to stop the cell cycle and prevent the cancer cells to replicate. According to cancer research, p53 regulates the cell cycle when there are abnormal cells and cause them to apoptosis. Tamoxifen may stop p53 from working.
     
    In conclusion, Tamoxifen is an effective drug to regulate the development of breast cancer only with the appropriate used. We need to get the advices from the oncologist before consuming it.

    Tamoxifen – Breast Cancer Treatment is a post from: Cytogenetics and Cancer Research

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  • Hormonal Therapy to Treat Breast Cancer

    Breast cancer is a troublesome disease. There are many reasons that causing breast cancer. It has been clear that the hormone is one of the key factors of the development of breast cancer. Therefore, hormonal therapy is an important therapeutic strategy to control this cancer.
     

    Hormonal Therapy to Control Estrogen Level

    There are many cancer research on the removed tumours showing that the breast cancer is estrogen-receptor positive. Theoretically, this type of cancer should show response to hormonal therapy on estrogen. To manipulate the estrogen level in the body, the Tamoxifen has been introduced to the world.
     
    hormonal therapy to control estrogen level

    Hormonal Therapy Using Tamoxifen

    Tamoxifen is an adjuvant drug or antagonist of estrogen receptor in breast cancer cell. It helps in hormonal therapy to treat the breast cancer. However, several studies show that Tamoxifen may cause an increase of estrogen in the blood after 2 years hormonal therapy. This is because the breast cancer cells may become resistant to Tamoxifen hormonal therapy. Besides, the estrogen-receptor positive cells may easily mutate into new cancer cell type that can proliferate without the presence of estrogen. Thus, Tamoxifen fails to control cell proliferation after 2 years of hormonal therapy.
     
    Despite of this, the Tamoxifen hormonal therapy is suggested not to use beyond a two year period. Tamoxifen may cause serious side effects after 2 years. It can increase risk of abnormal blood clots too. The patients with Tamoxifen hormonal therapy must follow the Thrombosis Prevention protocol to minimize the risk of deep vein thrombosis.
     
    While taking Tamoxifen, women are recommended to take 4000 to 6000 IU of vitamin D3 and 3 to 50 mg of melatonin nightly. There are many clinical trials show that melatonin and vitamin D3 significantly enhance the efficiency of Tamoxifen. However, another side effect of taking vitamin D3 needs to be paid attention. Breast cancer patients may experience a high risk for developing blood calcium disorders causing kidney toxicity and abnormal calcium metabolism if taking high doses of vitamin D3. For all these reason, breast cancer patients who use therapeutic doses of vitamin D3 should carry out a regular blood chemistry panel to monitor the kidney toxicity and calcium imbalances before the problems become worse.
     
    In conclusion, hormonal therapy is a great way to control the progression of breast cancer though it brings many side effects. I will talk more about the Tamoxifen in my coming post especially the aspects we really need to know before using it. :)

    Hormonal Therapy to Treat Breast Cancer is a post from: Cytogenetics and Cancer Research

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  • Things to Know Before Breast Cancer Treatment

    Breast cancer is the fear of any woman in the world. It is not difficult to know that either a friend or a relative who has or had breast cancer. It has been the leading cause of death for women between the ages of 35 and 54. However, did every woman know the things before treatment of breast cancer? Thus, today’s post is all about the things to know before breast cancer treatment to help women understand about these.
     
    things to know before breast cancer treatment

    As we all know, all types of cancer cell can spread to the whole body from the origin. Most of the time, when the cancer has been detected the chance that the disease has spread is high. Once a lump has been detected on the breast, there may already be an average of 45 billion cancer cells present, and some of them have been metastasized to other parts of the body. Thus, the early detection of breast cancer is important to prevent the cancer cells from spreading. I have been covered the Early Detection of Breast Cancer in my previous post.
     
    Conventional medicine divides the stages of the breast cancer based on certain factors like tumour size, lymph node involvement, or distal spread. According to the stage of the cancer, the oncologist may suggest many options or even combinations from simple lumpectomy (breast-conserving surgery) to complete mastectomy (removal of one or both breast), radiation, and chemotherapy.
     
    Yet, not all the therapies are suitable for a particular patient. Usually, the oncologist will design the most suitable treatment to the patient. The use of radiation and chemotherapy will certainly weaken the immune system of the cancer patient. This leaves the cancer patient more vulnerable to the development of metastatic lesions in many of our body organs. Though, there are many successful cases that using the radiation and chemotherapy to improve the survival of breast cancer patients with appropriately dose.
     
    The oncologist will only give the best recommendations to the breast cancer patient according to the stages of the disease. The patient needs to make informed decisions whether which therapies to utilize. Therefore, the final decision is on the patient’s hand.
     
    In conclusion, we need to know a little bit about the breast cancer so that we will not panic when facing on this disease especially for the women. This is only an introduction of breast cancer treatment. I will cover the details in my future post in Cytogenetics and Cancer Research blog. :)

    Things to Know Before Breast Cancer Treatment is a post from: Cytogenetics and Cancer Research

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  • Genome Instability Causes Cancer

    Genome instability is an almost universal feature of cancer cells. The genome instability is probably necessary to enable a cell to accumulate enough mutations to develop to cancerous cell. There are two types of  genome instability which are chromosomal instability (CIN) and microsatellite instability (MIN). As tumours usually show either CIN or MIN but not both, therefore the instability is not a chance feature but is the result of selection.
     
    Genome instability

    Chromosomal Instability (CIN)

    Chromosomal Instability is the alterations in chromosome number in cancer cell genomes. Most of the chromosomal abnormalities seen in tumour cells occurred randomly.
     
    i. Spindle checkpoint

    The chromosomal abnormalities can occur at the spindle checkpoint. Tumour cells lose the spindle checkpoint. The spindle checkpoint plays a role to prevent chromosome segregation at mitosis until all chromosomes are correctly attached to the spindle fibers. APC gene is the only one known to be commonly mutated in cancer cell. It is involved in polyposis coli. APC encodes a very large multifunctional protein that is probably involved in a variety of cellular processes. In the colon CIN is observed even in very early adenomas, and APC-/- cells have abnormal mitotic spindles that lead to chromosomal instability.
     
    ii. DNA Replication with Damage DNA

    Furthermore, structural chromosome abnormalities can be a by-product of attempts at DNA replication or mitosis with damage DNA. Tumour cells are able to pass through the cell cycle despite having DNA damage. Initially, cells are trying to constantly repair all types of damage to their DNA. The normal response to such damage is to stop the cell cycle until the damage is repaired, yet cancer cell is loss of that control. A multiprotein machine called the BASC (BRCA1-associated genome surveillance complex), is involved, together with a raft of other proteins. Most of the cell defects have bad repairing at double-strand breaks.
     
    iii. Shorten of Telomeres

    Besides, the normal cells may transform to tumour cells when the telomeres become too short to protect chromosome ends. On the other hand, the tumour cells that have gross chromosomal abnormalities, have acquired excessive telomerase to maintain the telomeres which protect chromosome end and the tumour cells become immortal. This will cause the excessive cell division.
     

    Microsatellite Instability (MIN)

    Microsatellite Instability involves changes in thousands of microsatellite sequences scattered throughout a cell genome. There are many defects of DNA repairing system that cause cancer-prone genetic disorders.
     
    i. Nucleotide Excision Repair Defects

    One of them is nucleotide excision repair defects. When there are single-strand breaks and crosslinks in DNA that has been damaged by ionizing radiation, UV light or chemical mutagens, this repairing system will be activated before the next round of replication. However, the defect of this repairing system will cause cancer. For example, the xeroderma pigmentosum (XP) patients are homozygous for inherited loss of function mutations, and are unable to repair DNA damage caused by UV light. They are exceedingly sensitive to sunlight and develop many tumours on exposed skin.
     
    ii. Base Excision Repair Defects

    Another defect repairing system that will cause cancer is base excision repair defects. For instance, colon cancer is caused by defects in the MYH repair enzyme.
     
    iii. Double-strand Breaks Defects

    Moreover, the defect of double-strand break repair causes cancer too. The double-strand breaks are repaired by homologous recombination or nonhomologous end joining. The defect of replication error repair also causes cancer like colon cancer.
     

    Comparison between CIN and MIN

    CIN MIN
    Loss of heterozygosity (LOH) and causing the loss of whole chromosome. Loss of allele and not causing the loss of whole chromosome
    No nucleotide sequence alteration. Show nucleotide sequence alteration.
    Effective mechanism for changing cellular genome in a way that favours evolution toward neoplasm. Effective mechanism for changing cellular genome in a way that favours evolution toward neoplasm.

     

    p53 and Apoptosis

    Another major contributor to genomic instability is loss or mutation of TP53, the gene encoding the p53 transcription factor. This loss is probably the most common single genetic change in cancer. The p53 has been recognized as ‘the guardian of the genome. p53 is essential in controlling the apoptosis. If the damage of the cell is not repairable, apoptosis is triggered. Tumour cells that lack of p53 may continue to replicate damaged DNA and do not undergo apoptosis.
     
    In conclusion, the genome instability is an important factor to enable a cell to accumulate the mutations to develop to cancerous cell. Without breakdown of the various mechanisms responsible for maintaining the integrity of the genome, it seems like the mutation rate would be too slow to allow tumour progression to reach completion. Cancer research will certainly give some contributions to make us more understand about the tumour progression.

    Genome Instability Causes Cancer is a post from: Cytogenetics and Cancer Research

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  • Activation Proto-oncogenes Causing Cancer

    Oncogenes are genes that positively enhance the cell proliferation associated with cancer development. Proto-oncogenes are the normal nonmutant forms of oncogenes. When the proto-oncogenes are activated, the normal cell will transform to cancerous cell.
     
    There are many ways of activation of proto-oncogenes. Activation involves a gain of function. The activation can be quantitative which involve the increase of production of an unaltered product or qualitative which involve the production of a modified product as a result of a mutation. These alterations are dominant and only affect a single allele of gene. As far as the researchers know, only RET gene can be inherited to cause familial cancer when activated. The RET gene involve in multiple endocrine neoplasia and familial thyroid cancer.
     

    Activation of Proto-oncogenes via Amplification

    One of the ways of proto-oncogenes activation is via amplification. Many cancer cells contain multiple copies of structurally normal oncogenes. For examples, breast cancers amplify ERBB2 and sometimes MYC. The researchers use comparative genome hybridization (CGH) technique to reveal all regions of amplification in a single experiment.
     
    activation proto oncogenes

    Activation of Proto-oncogenes via Point Mutations

    Another ways of proto-oncogenes activation is via point mutations. For instance, specific point mutations in ras genes are frequently found in cells from varieties of tumours like colon, lung, breast and bladder cancers. The point mutations lead t amino acid substitutions and decrease the GTPase activity of the RAS protein. Consequently, the GTP-RAS signal is inactivated more slowly, leading to excessive cellular response to the signal from the receptor.
     
    Another example of proto-oncogenes activation by point mutations is RET. Mutations leading to amino acid substitutions at certain specific cysteine residues are found in multiple endocrine neoplasia type 2 and in medullary thyroid cancer.
     

    Activation of Proto-oncogenes by Chromosomal Translocations

    The proto-oncogenes can be activated by chromosomal translocations too. The best known example is Philadelphia chromosome, a very small acrocentric chromosome seen in 90% of patients with chronic myeloid leukemia. It is because of a balanced reciprocal 9;22 translocation. This is an example of activation by qualitative change. The breakpoint on chromosome 9 is within an intron of the ABL oncogene. The translocation joins most of the ABL genomic sequence on to a gene called breakpoint cluster region (BCR) on chromosome 22, creating a novel fusion gene. This chimeric gene is expressed to produce a tyrosine kinase related to the ABL product but with abnormal transforming properties.
     
    There are many other rearrangements are known which produce chimeric genes. The products are transcription factors. This has been one of the most satisfying stories to emerge from cancer research, with examples of clinical phenotypes being elegantly explained by a combination of cytogenetic and molecular genetic findings.
     

    Activation of Proto-oncogenes by Transposition to an Active Chromatin Domain

    On the other hand, Burkitt’s lymphoma is one of the example of tumour that caused by activation of proto-oncogenes by transposition to an active chromatin domain. It is an example of activation by quantitative change. The oncogene was put in an environment of chromatin which is actively transcribed in antibody-producing B cells. The Burkitt’s lymphoma translocations do not create novel chimeric genes. Usually, the exon of the MYC gene is not included in the translocated material.
     
    In conclusion, activating proto-oncogenes can cause cancer development. By knowing the ways of activation, maybe we can do something to prevent it via deeper cancer research.
     
    (Reference: Human Molecular Genetics from Tom Strachan and Andrew P. Read)

    Activation Proto-oncogenes Causing Cancer is a post from: Cytogenetics and Cancer Research

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  • Anti-angiogenic Therapy to Treat Cancer

    Anti-angiogenic therapy is a kind of cancer treatment that using drugs to stop tumor angiogenesis. This is a high potential approach to treat cancer. Today, I will share some of the basic knowledge about this kind of cancer treatment.
     
    What is angiogenesis? Angiogenesis is a multi steps process involving the growth of new blood vessels in our body. This process depends on the regulation of many distinct activities in many cell types. This process plays an essential role in many physiological and pathological conditions.
     
    tumor angiogenesis in anti-angiogenic therapy

    What is tumor angiogenesis? Tumor angiogenesis is the growth of new capillary blood vessels that penetrate into tumor and supply the nutrients and oxygen as well as removing waste products. The tumors need angiogenesis to grow and evade in our body. The tumor cells can get the necessary oxygen and nutrient supplies by passive diffusion when the tumor angiogenesis occur. Therefore, the anti-angiogenic therapy is a good approach to treat the tumor progression by stopping the tumor angiogenesis.
     

    Anti-angiogenic Therapy is Effective to Treat Cancer

    Anti-angiogenic therapy of cancer is a highly effective way for destroying the tumor cells. The tumors cannot grow and survive without angiogenesis. If the anti-angiogenic agents are applied before a tumor develops, it can be considered as a vaccine in preventing the tumor development. Yet, it is not a cure for cancer but just represents the treatment. If we really want to cure the cancer, we need to target the agents and pathways that cause cancer.
     

    Advantages of Anti-angiogenic Therapy

    i. Unlike the chemotherapy, anti-angiogenic therapy contains little or no toxic to our body. It is because it does not require the therapeutic drug enter any tumor cells. The therapeutic agent needs not to cross the blood brain barrier.
     
    ii. This treatment regulate the tumor growth regardless the growth fraction, tumor cell heterogeneity and tumor cell type.
     
    iii. This treatment does not induce acquired drug resistance.
     
    iv. As the normal vasculature of an adult is dormant, the specificity of angiogenic inhibitors can be applied. This allows the long-term and nontoxic treatment of tumors to the patients. This is the greatest advantage if compare to the nonspecific modalities of chemotherapy and radiation therapy to treat cancer.
     
    v. Anti-angiogenic agents aim not only DNA synthesis and cell division, but also the biologic feature of tumor cells.
     
    In conclusion, anti-angiongenic therapy has a great potential on treating the cancer and control the progression of tumor cells. Yet, there are some difficulties related to the clinical evaluation of the efficiency of these anti-angiogenic drugs. Sometimes, the therapy might works on the animal model but not in human. The cancer research on this therapy will be carried on to bring its potency into play.

    Anti-angiogenic Therapy to Treat Cancer is a post from: Cytogenetics and Cancer Research

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  • 3 Basic Ways to Relieve Cancer Pain

    Cancer can cause terrible pain to the patient. It is overwhelming that if the cancer patient suffers the pain without relief. Many people are dying because of suffering the terrible cancer pain everyday in hospitals and clinics around the world. To solve such problem, there are many drugs and techniques can relieve the cancer pain. Today, I will introduce to you about 3 basic ways to relieve cancer pain.
     
     

    3 Basic Ways to Relieve Cancer Pain

    1. Dealing with the Origin of the Pain

    Generally, people will choose to eliminate or modify the origin of the cancer pain. To do this, we can remove or shrink the cancer that caused the pain. Many cancer therapies are used to remove or shrink the cancer such as surgery, radiation, chemotherapy and hormonal therapy.
    relieve cancer pain
    Yet, there are many disadvantages by using this way to relieve the cancer pain. First, most of those cancer therapies possess some risk. The patients receive such therapies to relieve the cancer pain may take the risk to certain side effects. In addition, not all the cancer patients are suitable to use the surgery to relieve the cancer pain. For instance, if the cancer has spread or if a patient’s overall condition is weak, the surgery is not suitable for him. Furthermore, only some types of cancer respond well to radiation and chemotherapy. Most of these treatments can only reduce the pain slowly. Sometimes, the therapies may cause new pain as a side effect.
     

    2. Altering the Pain Message with Painkillers

    Another common way that we can use to relieve the cancer pain is to alter the perception of pain. When the message reaches the spinal cord and brain, we can use the painkillers or analgesics to change the message to relieve the pain. For example, Morphine is used to alter the perception of pain in a selective and reversible way to blunt the pain. This is an effective way as it will always function normally with proper use.
     

    3. Interrupting the Pain Signals

    The third way to relieve the cancer pain is to use a nerve block to interrupt the pain signal between the source of pain and the central nervous system. This is the least used way to relieve the cancer pain. In cancer research, these strategy have more risks and irreversible to blunt the pain. Therefore, it is only suitable to small amount of cancer patients.
     
    In conclusion, we can prevent the cancer pain by just applying some simple basic ways. Yet, before any of these approaches are applied, we should consult the medical expert so that the most appropriate treatment plan is established for optimum effect.
     
    (Reference: The Complete Guide to Relieving Cancer Pain and Suffering by Richard B. P. & Susan S. L.)

    3 Basic Ways to Relieve Cancer Pain is a post from: Cytogenetics and Cancer Research

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  • 3 Types of Pro-apoptotic Proteins

    Pro-apoptotic proteins are the proteins that induce and activate the apoptotic pathway. The antagonist of pro-apoptotic proteins are the anti-apoptotic proteins which inhibit and stop the apoptotic pathway. The pro-apoptotic and anti-apoptotic proteins can work together to maintain a dynamic balance between the survival and death of the cell. Today, we will discuss three types of pro-apoptotic proteins.
     

    Pro-apoptotic Protein – Bax

    The pro-apoptotic Bax protein is another major player in apoptosis (Mojgan et. al., 2002). Studies have proved that when Bax is activated, it creates discontinuity or pores in the outer mitochondrial membrane to regulate the release of cytochrome c. The intrinsic apoptotic pathway will not be activated in the absence of Bax-activating signals. In addition, cells lack of Bax protein will not undergo apoptosis even though there are death stimuli (Lei et. al., 2006).
     
    pro-apoptotic protein

    Pro-apoptotic Protein – Caspases

    Caspases are a family of cysteine proteases that play a crucial role in apoptosis. When the caspases are exposed to a pro-apoptotic signal, the zymogen forms of caspases will proteolytically cleave and activated. The initiator caspases like caspase 8, caspase 9, and caspase 10 can split other caspases. The executioner caspases such as caspase 3, caspase 6 and caspase 7 cleave the death substrates. All caspases consists of a single cysteine at the enzyme catalytic site (Byung et. al., 2002). Both intrinsic and extrinsic pathways trigger pro-apoptotic caspases or pro-caspases via a process called caspase cascade (Avi et. al., 2008).
     

    Pro-apoptotic Protein – p53

    The p53 protein is a transcription factor and pro-apoptotic protein. It proliferates the transcriptional expression of several genes that involved when react to genotoxic agents like ionizing radiation and chemical therapeutic drugs. The p53 protein initiates the cell cycle arrest and DNA damage repair. If the cells cannot be repaired, the p53 protein will activates cell death programs and the cells then go through the apoptosis. Hence, p53 protein is a tumor suppressor protein against cancer development. The effective ways to prevent tumor growth and discard cancers are inhibit the cell proliferation and promote the apoptosis in tumors. Conventionally, chemotherapeutic agents that used to induce apoptosis are mediated mostly via p53-dependent pathways. Yet, most of human tumors have p53 mutations and inactivation (Luo et. al., 2008). The p53 protein activates the expression of pro-apoptotic proteins, such as Bax and down regulates the expression of the anti-apoptotic protein like Bcl-2 (Byung et. al., 2002).
     
    In conclusion, many therapeutic strategies can be designed to treat the cancer by regulating the pro-apoptotic and anti-apoptotic proteins. Cancer research on apoptotic pathway will really help us to design the most effective cancer treatment.

    3 Types of Pro-apoptotic Proteins is a post from: Cytogenetics and Cancer Research

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  • Apoptotic Pathway – Our Cell is Going to Die

    It has been long time I did not update the Cytogenetics and Cancer Research blog. Recently, I am celebrating the Chinese New Year. I am so happy to receive a lot of “Ang Pow” from the elders. Today, I will put on some information about the apoptotic pathway in this blog so that the readers can know how our cells die.
     
    Apoptosis occurs in two signalling pathway which are extrinsic and intrinsic signalling pathway. The researchers try to look through the molecular pathways involved in the regulation of apoptosis in order to develop effective therapeutic approaches. There are many ways to induce apoptosis. One of it is to alter apoptosis threshold by modulating pro-apoptotic and anti-apoptotic members of Bcl-2 family.
     

    apoptotic pathway,intrinsic extrinsic pathway,apoptosis

    Figure 1: Apoptotic signalling pathways (Avi et. al., 2008).

    Any stimuli that cause oxidative stress, mitochondrial disturbances and DNA damage may stimulate the intrinsic pathway. For example, cancer therapeutic agents, hypoxia, and ionizing irradiation can trigger intrinsic pathway of apoptosis. When the mitochondrial damage, the outer membrane will become permeable and facilitates cytochrome c release into cytoplasm. Then, the cytochrome c will bind to the caspase adaptor, Apaf-1 (apoptotic protease-activating factor-1), and consequently triggering the apoptotic cascade by activating procaspase 9. The apoptosome complex is formed. This complex will activate many downstream effector caspases like caspase 3, caspase 6 and caspase 7, leading to DNA fragmentation and cell death. Therefore, caspases play essential role in intrinsic apoptotic pathway. Meanwhile, the Bcl-2 family is another group of key players in intrinsic apoptotic pathway. The Bcl-2 family consists of more than 20 members of pro-apoptotic proteins and anti-apoptotic proteins. Members of the Bcl-2 family function as agonists or antagonists to each other as they can form homo- or heterodimers. Pro-apoptotic members of Bcl-2 family such as Bax, Bak, Bok, Bid and Bim can induce the release of cytochrome c from mitochondria. While anti-apoptotic members like Bcl-2, Bcl-XL and so on can bind to Apaf-1 to inactivate the intrinsic pathway. However, the pro-apoptotic members can dissociate the complex of anti-apoptotic members and Apaf-1 to allow the Apaf-1 to activate the caspase 9 and lead to subsequent apoptotic process. At the same time, Bax and Bak can promote apoptosis by triggering the release of Smac/DIABLO protein from mitochondria and subsequently inactivate the inhibitors of apoptosis proteins (IAP).
     
    On the other hand, the extrinsic apoptotic pathway is induced by ligand binding of death receptors. The major ligand-death receptor system include tumor necrosis factor (TNF) with tumor necrosis factor receptor 1 (TNFR1), Fas ligand with Fas, and TRAIL with TRAIL receptors. The binding of the receptors with the ligands will induce the receptor oligomerization and recruitment of death signal adaptor proteins. These formed a complex termed DISC (death-inducing signalling complex), which can bind to initiator caspases like caspase 8 and caspase 10. Consequently, the caspase cascade will be triggered to activate the caspase 3, caspase 7 and caspase 9, and leading to apoptotic events.
     
    In conclusion, there is an extensive crosstalk exists between the intrinsic and extrinsic apoptotic pathways. The activation of caspase cascade is the crucial component in the death process in either pathway. The pro-apoptotic and anti-apoptotic proteins can work together to maintain a dynamic balance between the survival and death of the cell.

    Apoptotic Pathway – Our Cell is Going to Die is a post from: Cytogenetics and Cancer Research

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  • Cri du Chat Syndrome – Human with Cat-like Cry

    Cri du chat syndrome is a kind of genetic disorder that occurs when a small part of chromosomal material is missing from a particular region on chromosome 5.
     

    Overview of Cri du Chat Syndrome

    In 1963, Dr. Jerome Lejeune first described Cri du chat syndrome. It is named for the cat-like cry made by the patients with this genetic disorder. In French, Cri du chat means “cry of the cat”. Or we can call this syndrome as “5p minus syndrome”. This is because there is small deletion of genetic material from the short “p” arm of chromosome 5 to cause this unusual genetic disorder.
     

    Features of Cri du Chat Syndrome

    cri du chat syndrome, cat-like cry, mewing cry, 5p minus
    There are many unusual features for the infants with Cri du chat syndrome.

    i. Cat-like cry (the most classic feature)

    ii. Unusual facial features

    iii. Poor muscle tone (hypotonia)

    iv. Small head size (microcephaly)

    v. Mental retardation

    vi. Low birth weight

    vii. Slow growth

    viii. Congenital heart defects

    ix. Language difficulties

    x. Delayed motor skill development

    xi. Behavioral problems (childish)
     

    Genetic Basis of Cri du Chat Syndrome

    The high-pitched mewing cry during infancy is caused by defective development of the larynx (organ in the throat which produced voice). The deleted part of chromosome 5 is essential for normal development. As we all know, human have 46 chromosomes in every single cell of our body. At the same time, we should have two copies of chromosome 5. However, individuals with Cri du chat syndrome have lost a small part of chromosome 5. There is a small piece of material has been deleted from the “p” arm of one of the chromosome 5. On the other hand, the deleted chromosomal material consists of many important genes for normal development. Because of losing these essential genes, the larynx, brain and other parts of body cannot function normally. Generally, the deletion is sporadic (occurs irregularly).
     

    Diagnosis of Cri du Chat Syndrome

    Yet, the cat-like cry from children with Cri du chat syndrome will becomes less noticeable when they get older. Therefore, we can just identify and diagnose this syndrome if a child with younger age has this unusual mewing cry. Chromosome analysis or karyotyping can provide the definitive diagnosis of Cri du chat syndrome by staining the chromosome and examining them under a microscope. FISH (fluorescence in-situ hybridisation) is useful and effective to detect a small deletion in chromosome like Cri du chat syndrome.
     
    Unfortunately, there is still no cure for this syndrome. Nevertheless, the medical experts can still provide the supportive care and development therapy to the patients to make the things better. Once the unusual features are under controlled, most of them can live normally.
     
    In conclusion, although there is still no cure for Cri du chat syndrome, we can still lessen the symptoms by receiving the suitable therapy.
     
    I have to apologise as I seldom to update this Cytogenetics and Cancer Research blog recently. I’m busying doing my final year project in University of Malaya. However, I will try my best to keep on updating the blog. Thanks!

    Cri du Chat Syndrome – Human with Cat-like Cry is a post from: Cytogenetics and Cancer Research

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  • 9 Steps of Peritoneal Cancer Progression

    Peritoneal cancer is caused by carcinomatosis which occurs at the visceral and parietal peritoneal lining of the abdominal cavity. The tumour cells disseminate from their primary organ of origin to develop metastatic deposits on the visceral and parietal lining of the abdominal cavity. Therefore, it is important to find out the molecular events involved in peritoneal carcinomatosis to design the treatment to deal with the peritoneal cancer.
     
    For better understanding on the events involved in peritoneal carcinomatosis, we need to look deeply on every single process of peritoneal cancer progression. We called this series of steps as “Peritoneal Metastatic Cascade”. Yet, we have to bear in mind that each step in the metastatic cascade does not occur in isolation but occur in a continuous and interdependent process.
     

    Peritoneal Cancer Progression

    1. At first, the tumour cells from the primary organ must break away from the primary tumour mass and gain access to the peritoneal cavity.
     
    2. Then, the tumour cells free to disseminate around the peritoneal cavity.

    peritoneal cancer progression, peritoneal carcinomatosis, peritoneal metastatic cascade
     
    3. There are many factors that determine the final destination of these tumour cells.

    i. Gravity
     
    ii. Movement of the abdominal viscera
     
    iii. Flow of ascetic fluid
     
    4. The tumour cells will first enter the innermost layer of peritoneum which is our mesothelium.
     
    5. Next, the tumour cells will attach to the mesothelium.
     
    6. Consequently, the mesothelial monolayer and its basement membrane will penetrate to the submesothelial connective tissue. The penetration provides the chance to the tumour cells to access to the submesothelial connective tissue too.
     
    7. Continuously, the invasion of the underlying connective tissue gives the necessary scaffold for tumour proliferation and provides tumour-stromal interaction.
     
    8. The discrete metastatic tumour deposit starts to establish.
     
    9. Finally, the induction of angiogenesis to sustain tumour proliferation has enabled the further metastatic growth of peritoneal cancer cells.
     
    In conclusion, peritoneal cancer is a rare cancer that still needs a lot of research for further understanding. I decide to write about it in Cytogenetics and Cancer Research blog because it is interesting to look on. I will try to find out more information about peritoneal cancer and write it out here. Stay tuned! :)

    ( Resource: Cancer Treatment and Research by Steven T. Rosen)
     

    Have you heard about peritoneal cancer before? Any extra useful information to share with us?

    9 Steps of Peritoneal Cancer Progression is a post from: Cytogenetics and Cancer Research

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  • Human Genome Project – Find out Human Database

    The Human Genome Project (HGP) was an international effort and collaborative research program to map and understand the entire human genome. This is a dream project for me to look through of it. I decide to write a review on it in Cytogenetics and Cancer Research blog so that more people can access to this tremendous project.
     

    What is human genome?

    Human genome is the complete set of DNA (deoxyribonucleic acid) in human body. The DNA contained within each of body cells. The DNA carries the signals to build and maintain the body cells to function so that the heart will keep pumping, brain will keep thinking and bones will keep growing.
     

    Overview and History of Human Genome Project

    The Human Genome Project was the natural culmination of the history of genetic research. Alfred Sturtevant, an undergraduate student in Thomas Hunt Morgan’s laboratory, found that he could map the locations of fruit fly (Drosophila melanogaster) genes whose mutations the Morgan laboratory was tracking over generations. This is the tremendous start of gene mapping and finally leads to the human genome sequencing project.
     
    When the Human Genome Project started in 1990, the researchers had set a goal to complete the project within 15 years but completed it in 2003, with two years to spare. During that time, many volunteers gave blood to provide their DNA as a contribution for the HGP. However, the labels on the blood tubes were intentionally removed to protect the privacy of the donors. Therefore, the final human genome sequence which has been published in 2003 is a combination of many of the donors’ DNA. The researchers had found that 99.9% of everyone’s DNA sequence is exactly the same. However, there are still some tiny fractions of genome that varies among humans. These variations are very important and make all humans unique in physical appearance like colour of eyes and even influence the risk of disease and the response to drugs. Even so, the genome is just one part of the amazing puzzle of human. Lifestyle and environmental factors do influence humans’ health condition too.
     

    Contributions of Human Genome Project

    By knowing this, the successful of HGP to sequence human genome has made the job of finding genes that cause some genetic diseases easier. The researchers hope that they can find out the genetic basis of other diseases such as heart disease, diabetes and even mental illness so that the drugs and treatments that specifically target these diseases can be designed properly. For example, there are some genes that involved in cancer had already been identified and make the treatment designed much easier.

    human genome project
     

    What have been done in Human Genome Project?

    In Human Genome Project, the researchers have deciphered the human genome in three major ways:
     
    i. The sequence of all DNA bases in human genome.
     
    ii. Maps that show the locations of genes for major sections of human chromosomes.
     
    iii. Linkage maps which inherited traits especially those for genetic disease can be tracked over generations.
     
    There are about 20,500 human genes revealed in Human Genome Project. This finding appeared to be significantly fewer than previous estimates, which ranged from 50,000 genes to 140,000. This final human genome sequence has given the world a resource of detailed information about the structure, organization and function of the complete set of human genes. This can be considered as the basic set of inheritable information for the development and function of a human being.
     
    According to Francis Collins, the director of National Human Genome Research Institute (NHGRI), the genome could be imagine as a book with multiple uses. He said: “It’s a history book – a narrative of the journey of our species through time. It’s a shop manual, with an incredibly detailed blueprint for building every human cell. And it’s a transformative textbook of medicine, with insights that will give health care providers immense new powers to treat, prevent and cure disease.”
     
    The Human Genome Project had created many tools that can be used in characterize the genomes of other organisms used extensively in biological research. For examples, mice, fruit flies and flatworms are the model organism that can be used to identify the sequence or function of a homologous (similar) gene in human beings.
     
    In conclusion, the Human Genome Project might appear as a perfect project at the first glance. Most probably is the genome was successfully sequenced and the involvement of the government in the project. Yet, the ultimate success of HGP still remains unclear.
     
    Reference: National Human Genome Research Institute
     

    Is Human Genome Project really beneficial to humans? Leave your precious opinion to start the discussion.

    Human Genome Project – Find out Human Database is a post from: Cytogenetics and Cancer Research

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  • Angelman Syndrome – Angel-like Genetic Disorder

    Angelman syndrome (AS) was first described by Dr. Harry Angelman, who is an English physician. He noticed that there are 3 children under his care with similar developmental problems. They looked very happy and tend to flap their hands when excited. Therefore, Dr. Harry Angelman described these children in his paper called “Puppet Children” as these children’s characteristics just like the puppet.
     
    Angelman Syndrome is now a familiar genetic disorder to most clinical geneticists and child neurologists in Cytogenetics. It is a recognizable syndrome which related to mental retardation and infantile seizures. Unlike Prader-Willi syndrome that I described last week, individual with Angelman syndrome is because the loss of maternally inherited region 15q11 – q13 of chromosome 15. Simple to say, the AS individual does not inherit the region 15q11 – q13 of chromosome 15 from his/her mother but only from father.

    angelman syndrome - angel-like syndrome
     
    The Angelman syndrome clinical diagnosis is heavily dependent on the combination of some common behaviour like excessive laughter, apparent happiness with tremulous movements and gait ataxia (lack of coordination of muscle movement). Usually, the normal prenatal and birth history do not provides any clues in diagnosis of AS in Cytogenetics. CT scans, laboratory tests of blood and urine are usually normal including metabolic screening. Consequently, it is difficult for the clinical experts to encounter the AS especially when the child is less than 12 months of age. It is because the tremulous movements, ataxia and severe lack of speech may not be apparent during that time.
     
    There are many common features of Angelman syndrome.

    i. Severe speech deficit (usually absent speech)
     
    ii. Mental retardation
     
    iii. Microcephaly (small head)
     
    iv. Seizures (convulsions in which AS patient’s body shakes rapidly and uncontrollably)
     
    v. Developmental delay
     
    vi. Feeding problems
     
    vii. Hypopigmentation (the loss of skin color)
     
    viii. Frequently drooling
     
    ix. Tend to put objects in mouth
     
    The facial features general physical appearances are generally normal for the individual of Angelman syndrome. As the child with AS growing up, the correct diagnosis may become evident when speech is essentially absent and the attempts at walking are compromised because of sever ataxia. In addition, the seizures will occur more frequently after 1 year of age.
     
    In conclusion, the individual of Angelman syndrome may be hyperexcitable with excessive laughing, grabbing and pulling to engage others. They are just like the ‘Angels’ who always bring happiness to people. Usually, the parents may be the first to suggest the possibility of Angelman syndrome. Thus, earlier detection of this genetic disorder may help the children to overcome the learning problem through the assessment from the clinical experts.
     

    My ultimate hope is this Cytogenetics and Cancer Research blog can really help in increasing the awareness of people about the genetic disorders and cancer.

    Angelman Syndrome – Angel-like Genetic Disorder is a post from: Cytogenetics and Cancer Research

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  • Prader-Willi Syndrome – Genetic Disorder That Cause Obesity

    Prader-Willi syndrome or PWS syndrome is thought to be one of the most common genetic disorders. Prader-Willi syndrome and Angelman syndrome were the first examples in humans of genomic imprinting in Cytogenetics. Angelman syndrome has an entirely different clinical condition with PWS syndrome. I will explain about the Angelman syndrome in my future post.
     
    What is genomic imprinting? Imprinting is a type of marking process that has a memory. Genomic imprinting is where a segment of DNA is marked or imprinted during gametogenesis. This mark will be retained and recognized throughout the life of the individual. Maternal and paternal inherited alleles will be marked differently and are expressed differently in the offsprings. Therefore, the offspring with the same genetic material will have different appearances. The individual with Prader-Willi syndrome is because the loss of paternally inherited region 15q11 – q13 of chromosome 15. Simple to say, the PWS individual does not inherit the region 15q11 – q13 of chromosome 15 from his/her father but only from mother.

    prader-willi syndrome, pws

    Prader-Willi syndrome is the most common genetic cause of marked obesity in humans according to Cytogenetics. It is a complex disorder with cardinal features of
     
    i)    Infantile hypotonia (low muscle tone)
     
    ii)   Mild growth retardation
     
    iii)  Frequent occurrence of breech presentation (baby enters the birth canal with the buttocks or feet first)
     
    iv)  Small hands and feet with gracile and tapering fingers
     
    v)   Microcephaly (smaller head)
     
    vi)  Almond-shaped eyes
     
    vii) Mental deficiency (average IQ of 65)
     
    viii) Short stature and so on.
     
    From the age of about one and half years onward, hyperphagia becomes a serious problem, leading to gross obesity. Due to hyperphagia and gross obesity, diabetes often sets in during adolescence or later. Epilepsy is found in a minority of cases. Mental development is characterised by moderate to severe retardation with tendency to behaviour disorders, especially reactive to food deprivation. Patients with this syndrome may need specialists for assessment and treatment of their behavioural and learning problems, at the beginning of childhood. Prader-Willi syndrome is present in all races and ethnic groups and most cases are sporadic.
     
    In conclusion, Prader-willi syndrome is a genetic disorder that needs treatment and assessment to overcome the learning problem and obesity problem of the patients. I will write a series of Prader-Willi syndrome in this Cytogenetics and Cancer Research blog in order to give people a clear mind about this syndrome. Stay tuned! :)

    Prader-Willi Syndrome – Genetic Disorder That Cause Obesity is a post from: Cytogenetics and Cancer Research

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  • HepG2 – Human Liver Cancer Cell Line

    HepG2 cells derived from a human hepatocellular carcinoma line (We et al., 2006). Hepatoblastoma (HB) or hepatocellular carcinoma is an embryonal malignancy of hepatocellular origin and the most common primary liver tumor of childhood, usually presenting in the first year of life. I have described mcf-7, human breast cancer cell line before.
     
    HepG2 cell line has been the subject of significant confusion for almost 30 years (Dolores et al., 2009). It has been found to express a wide variety of liver-specific metabolic functions (Norman et al., 1992). Therefore, HepG2 has been widely used in varieties of fields like liver metabolism, development, oncogenesis and hepatoxicity at that time in cancer research (Dolores et al., 2009).

    hepG2 - liver cancer cell line
     
    HepG2 cell line has been introduced since 1979 (Norman et al., 1992). Until now, there are more than nine thousands HepG2 references can be found in the scientific literature (Dolores et al., 2009). HepG2 cell line is known to be capable of producing many plasma proteins for which there are antisera commercially available (Liu et al., 1985).
     
    This cell line has been proved to be an useful model of the human liver cell as there is high proportion of liver-specific proteins identified in the medium. The metabolic pathways that have been studied appear to simulate the behaviour of normal hepatocytes. Thus, those studies encourage a wider application of this HepG2 cell line to biologic problems that relate specifically to the role of the liver (Norman et al., 1992).
     
    Reference:

    Dolores L-T, Sau W. C., Milton J. F. & Barbara B. K. HepG2 is a        Hepatoblastoma-derived Cell Line. Oncology Stat, 1512 – 1515 (2009).
     
    Liu M-C, Yu S., Jose Sy, Colvin M. R. & Fritz L. Tyrosine Sulfation of Proteins      from the Human Hepatoma Cell Line HepG2. Proc Natl Acad Sci 82      (21), 7160 – 7164 (1985).
     
    Norman B. J. HepG2 Cells As a Resource for Metabolic Studies: Lipoprotein,       Choresterol, and Bile Acids.  The FASEB Journal 4, 161 – 168 (1992).

    HepG2 – Human Liver Cancer Cell Line is a post from: Cytogenetics and Cancer Research

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  • End of 2009 in Cytogenetics and Cancer Research Blog

    While celebrating the new coming year 2010, I am going to end up the year 2009 with my 30th blog post in this Cytogenetics and Cancer Research blog. I started this blog on 16th of October with the first post about What is Cytogenetics. I have put a lot of efforts to develop and organize this blog so that people around me can really get benefits from my writing. Today, I am going to make a roundup for this 2 months and 21 days old blog. :)

     

    3 ‘Top’ in Cytogenetics and Cancer Research Blog

     

    Top Commented Post

    15 Benefits of Smoking Cessation

    “Smoking cessation provides extensive health benefits for everyone including the smokers and non-smokers. There are 15 significant health benefits of quitting smoking.”
     
    There are 6 comments for this post. Although not much, it is an encouragement for me as a new blogger. I’m looking forward to listen to more comments for this Cytogenetics and Cancer Research blog.
     

    Top Searched Post

    Cancer Research: How Cancer Cell Spread to Other Cell?

    “Cancer research is the study of abnormal cells. The malignant cancer cells will harm to our body and invade to other adjacent cells. We discover that these malignant cells can infiltrate to the surrounding tissue through the lymphatics and blood vessels.”
     
    I noticed that people prefer to know how cancer cell spread to other cell in my blog. This topic is the top searched in my blog for almost every day. I will try to write more about this in 2010.
     

    Top Visited Post

    Top 10 Discoveries of Cancer Treatment in 2009

    “I have gathered the cancer research news from Google and NCI. Below are some of the new findings of cancer treatment which I found really benefits to the world.”
     
    I have used this post to participate the Group Writing Project organized by DailyBloggingTips.com. This is the top visited post that I have in my blog now. I get a lot of natural links from other websites since I posted this article.
     

    3 ‘Most’ in Cytogenetics and Cancer Research Blog

     

    Most Controversial Post

    Cigarette Smoking – Primary Risk Factor for Lung Cancer

    “Cigarette smoking is the primary risk factor for lung cancer. The cancer research shows that the risk of getting the lung cancer is higher among the cigarette smokers than the non-smokers.”
     
    I am so surprised that this post had been listed in the top 200 of controversial article in Reddit.com at the day I posted it. I don’t think this is good news for me. However, I am so happy that this article had been highlighted in the world and hopefully it can increase the awareness of people regarding to the lung cancer.
     

    Most Viewed Post

    3 Main Types of Cancer Diseases

    “Cancer is a complicated set of diseases which human still cannot really figure out what is going on. There are more than 200 types of diseases cause by cancer. Most of these cancer diseases possess the different properties and treatments.  There are three main types of cancer diseases.”
     
    I noticed that people tend to click on this post when they visit my blog. I think most of us wish to know more about cancer now.
     

    Most Favourite Post

    XXX Syndrome (Superwoman) | Birth Defect in Cytogenetics

    “Why a female with 47, XXX karyotype can be described as a ‘superwoman’ in Cytogenetics? Is she possesses any super power or advantage just like X-Men?”
     
    Personally, this is the favourite post that I like most in this blog. How about you? Do you like this post too?
     
    In conclusion, I will try to write more quality articles in year 2010 to reach the aim to increase the awareness of people around me regarding to cancer and genetic disorders. Thanks for your supporting! :)
     

    Which post you like the most in this Cytogenetics and Cancer Research blog? I would like to hear the feedback from you all. Come and share with me.

    End of 2009 in Cytogenetics and Cancer Research Blog is a post from: Cytogenetics and Cancer Research

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  • Autosomal Aneuploidy – Cytogenetic Abnormalities

    Cytogenetic abnormalities are what I have learnt during my internship in Hospital Kuala Lumpur. Today, I’m going to introduce Autosomal Aneuploidy in this Cytogenetics and Cancer Research blog.
     
    In Cytogenetics, the term aneuploidy refers to cytogenetic abnormalities in which all or part of one or more chromosomes is added or deleted. Autosomal aneuploidy is the abnormality that does not involve the sex chromosomes. Sometimes, the abnormalities can be either numerical or structural. Normally we only have pair of chromosomes which are structurally similar. Other than that, it can be recognized as abnormal. Those cytogenetic abnormalities can be present only in some cells which we called mosaicism or in all cells.

    autosomal aneuploidy | Cytogenetic abnormalities
     

    Meiotic Nondisjunction Causes Autosomal Aneuploidy

    The origin of autosomal aneuploidy is because of meiotic nondisjunction. The meiotic nondisjunction is random for all autosomes except for chromosome 21. Chromosome 21 has shown the highest frequency of autosomal aneuploidy.
     
    According to cytogenetic studies, the incidence of autosomal aneuploidy in spontaneous abortuses (die before birth) is much higher than incidences in newborns. So, what is the case for aneuploidy actually observed in spontaneous abortuses or liveborns? All trisomies for all autosomes have been reported in spontaneous abortuses. The fetal only can survive if and only if the trisomies are in mosaic form. However, there are still many exceptions for the trisomies 13, 18 and 21. Some of the foetus still can survive even though the trisomies 13, 18 or 21 are in nonmosaic form.
     
    Why the frequencies of trisomy for each chromosome might be similar at the time of conception but differ greatly among abortuses and liveborns especially for trisomy 21? It can be explained by the devastating effect of chromosomal imbalance. Most of the autosomal aneuploidies are very deleterious and lethal in the pre-embryonic stage. As a result, those abnormalities are unrecognized and, therefore, unstudied spontaneous abortions.
     
    Furthermore, the lethality of a particular autosomal aneuploidy is related to the gene content of the particular chromosome. Aneuploidies for the gene rich chromosomes are less likely to survive. However, the less gene rich chromosomes like chromosome 13, 18 and 21 are more likely to survive to term.
     
    Anyway, we will just focus on those observed in liveborns for the autosomal aneuploidy in Cytogenetics. I will talk more details about the monosomies and trisomies in my future post. Stay tuned! :)

    Autosomal Aneuploidy – Cytogenetic Abnormalities is a post from: Cytogenetics and Cancer Research

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  • Say No to Cancer! – 3 Approaches to Prevent Cancer

    Cancer prevention is a popular topic that people wish me to write more in my Cytogenetics and Cancer Research blog. Cancer prevention is the best possible way to reduce the death rate of cancer worldwide. According to Fundamentals of Cancer Prevention, written by David S. A. and Lisa M. H., cancer prevention research can be divided to 3 approaches to target different aspects in order to reduce cancer morbidity and mortality: Primary, Secondary and Tertiary prevention.
     

    Primary Cancer Prevention

    Primary cancer prevention is an approach to reduce the impact of carcinogens. We can do this through administration of a chemopreventive agent or remove the environmental carcinogens. The main aim of primary prevention is to prevent a cancer from the very beginning to the developing by reducing individual risk.

    Cancer prevention
     
    There are many primary cancer prevention methods which include the lifestyle modification or interventions that modify risk. These methods will become more effective if those cancers in which causes are known.
     
    Below are some of the factors that can help to reduce overall cancer incidence:

    i. Minimize the exposure to carcinogens. For example, we should avoid from consuming tobacco which contains carcinogen.
     
    ii. Dietary modification. For example, we should take balanced meal and reduce the consuming of salt, sugar and high cholesterol foods.
     
    iii. Increasing physical activity. For example, we should do some exercises during our daily life like jogging, swimming and so on to keep our body fit.
     
    As we all know, unhealthy diet and tobacco use are the leading risk factors for cancer. Smoking cessation is the best way to avoid ourselves from cancer developing. Benefis of quitting smoking begin within the first year of stopping and continue to increase. If you wish to know more about the benefits of smoking cessation, you may read the 15 Benefits of Smoking Cessation. In addition, the role of diet, nutrition and maintaining a healthy body weight is critical to lessen the cancer risk.
     

    Secondary Cancer Prevention

    Secondary cancer prevention is an approach to detect the abnormal changes at the beginning of the development of malignancy. It involves screening and early detection methods like mammogram, pap test and so on. This can help us to identify any abnormal changes of our body before they become cancerous. Therefore, it is effective to prevent cancer from fully developing. Sometimes, secondary cancer prevention can involve the treatment of precancerous lesions in an attempt to reverse carcinogenesis so that the lesion can regress.
     

    Tertiary Cancer Prevention

    Tertiary cancer prevention is an approach to control the cancer and prevention of disease-related complications. It involves a variety of aspects of patient care such as quality of life, adjuvant therapies, surgical intervention and palliative care.
     
    In conclusion, we can see that the primary cancer prevention is the main role of cancer prevention. Unfortunately, the primary prevention research and efforts are largely underfunded. This lack of prioritization cause the delays in improving and delivering early detection and prevention methods that can save millions of lives.
     

    Do you know any methods of cancer prevention? Come and share with us! Prevention is always better than cure!

    Say No to Cancer! – 3 Approaches to Prevent Cancer is a post from: Cytogenetics and Cancer Research

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  • MCF-7 – Human Breast Cancer Cell Line

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    MCF-7 is a human breast cancer cell line that i will use in my Cancer Research. I am going to share some knowledge about this breast cancer cell line. I’m so sorry for not updating the Cytogenetics and Cancer Research blog for a week time. I just came back from joining a camp. I will continue my lab work start from tomorrow. Let us explore about MCF-7 now!
     
    MCF-7 cell line was first derived from a pleural effusion of a post menopausal 69 years patient with metastatic breast cancer in 1970 (Rebecca et al., 2003). The MCF-7 cell line is the most widely used in cancer research and best characterized of all the human breast cancer cell lines (Dino et al., 2007).

    mcf 7 300x178 MCF 7 Human Breast Cancer Cell Line
     
    MCF-7 cell line is useful as an investigative tool in laboratories worldwide in cancer research. It possesses the abilities to undergo DNA fragmentation. It also has differential sensitivities to estrogens and anti-estrogens, differential expression of estrogens receptor (ER), ER mRNA, and progesterone receptor, and differences in tumorigenicity and proliferation rates (Matthew et al., 2003). MCF-7 cells is the first hormone-responsive breast cancer cell line (Amanda et al., 2003).
     
    The characteristics of MCF-7 cells like the estradiol-dependence for growth and low metastatic potential has led to the assumption that they represent an early epithelial adenocarcinoma of breast (John et al., 1995). MCF-7 cells are perfect model to study the pathway of malignant progression as they can be subjected to appropriate endocrinologic and physiologic selective pressures for the derivation of variants with more progressed phenotypes (Hans et al., 2007).
     
    The epithelial breast cancer derived MCF-7 cell line is one of the most frequently used model systems for clinical studies. The researchers used it for the studies of breast cancer treatment. The clinical studies have shown that therapeutic agents preventing the synthesis and activity of estrogens are essential in the breast cancer treatment. The addition of extradiol which is one of the fractions of estrogen to the medium of MCF-7 cells induces a proliferative response (Irene et al., 2003).
     
    There are apoptotic responses of MCF-7 cells to the apoptosis-inducing agents like tumor necrosis factor and anti-Fas antibody. The MCF-7 cells still remains as an excellent in vitro model for studying the mechanisms of chemoresistance because of its susceptibility to apoptosis (Richard et al., 2003).
     
    Sources:

    1. Rebecca S., Matthew B., Amanda P., Christopher W. & Barbara B. Apoptosis, Chemoresistance, and Breast Cancer: Insights from the MCF-7 Cell Model System. Exp Biol Med (Maywood) 228(9), 995-1003 (2003).

    2. John J. P., Jiang S. Y., Michael F. & Jordan V. C. An Estrogen-Independent MCF-7 Breast Cancer Cell Line Which Contains a Novel 80-Kilodalton
     

    Do you know anything about MCF-7? Please share with us.

    MCF-7 – Human Breast Cancer Cell Line is a post from: Cytogenetics and Cancer Research

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  • Top 10 Discoveries of Cancer Treatment in 2009

    Since 2009 is getting close to the end, I am going to join the Group Writing Project organized by DailyBloggingTips.com to write this article about the top 10 new discoveries of cancer treatment in 2009.
     
    I have gathered the cancer research news from Google and NCI. Below are some of the new findings of cancer treatment which I found really benefits to the world.
     

    1. Brachytherapy – New Cancer Treatment without Surgery

    On the 27th of January 2009, U.T.’s Health Science Centre unveiled a new promising cancer treatment that revolutionized the way to treat cancerous tumors in patients’ lungs. This new finding is called Brachytherapy, a new cancer treatment without surgery.

    After mild sedation, a catheter is inserted into patient’s throat and the lung near to the tumor. Radiation is released from a small seed at the end of the catheter and killed the tumor cells without killing the normal lung tissue. Therefore, the patient can still live normally after treatment. It only takes 3 to 4 minutes to undergo the Brachytherapy and the patient can leave the hospital a short time later without feeling sick.
     

    2. Linac – Machine Boots Cancer Treatment

    On 12th of June 2009, a new machine called Linac that can speed up cancer treatment for cancer patients has been unveiled at Velindre Cancer Centre. This machine enables an extra 200 radiotherapy cancer treatments to be carried out every week. Linac generate high intensity of radiation beams to kill cancer cells effectively.
     

    3. CD8+ Memory Stem Cells to Destroy Large Tumors

    On 14th of June 2009, the researchers at the National Cancer Institute found that a subset of immune cells, T lymphocytes called CD8+ memory stem cells, were capable of mediating strong anti-tumor immune response. These stem-like characteristics of CD8+ memory stem cells enable tiny numbers of T cells to stimulate the destruction of large melanoma tumors. The CD8+ memory stem cells have the enhanced ability to renew themselves, to proliferate, to differentiate and to kill tumor cells effectively.
     

    4. α-CbT – Compound Inhibited Nicotine Receptors for Cancer Treatment

    On 15th of June 2009, the compound α-CbT was found to inhibit the expression of nicotine receptors and increased apoptosis. As we all know, changes in genes encoding nicotine receptors can drive the urge to smoke and increase susceptibility to lung cancer as well. Exposure to nicotine will boost the expression of nicotine receptors which inhibits the apoptosis. Therefore, this new cancer treatment that targeted nicotine receptors by using α-CbT can prevent the developing of lung cancer. The α-CbT did not affect the noncancerous cells.
     

    5. microRNA – Help Identify and Cancer Treatment for Lung Cancer

    On 7th of October 2009, the scientists at National Cancer Institute (NCI) revealed that a small RNA molecule, known as microRNA, can help to identify liver cancer and respond well to cancer treatment with a biological agent called interferon. The researchers showed that miR-26 (microRNA) status in tumors may be useful indicator both to determine prognosis for patients with hematocelular carcinoma (HCC) and to inform the selection of patients who might benefit from treatment with interferon to prevent disease relapse.
     

    6. Suicide Gene – Induce Apoptosis on Tumor cells

    On 9th of October 2009, A group of researchers from National Cancer Institute (NCI) have used the suicide genes that cause a cell to kill itself through apoptosis to treat cancer. This new technique used the surviving gene promoter to induce the expression of suicide gene in cancer cells with a minimum effect on normal cells. When the survivin promoter-driven mutant bax was injected in to tumors of mice, the gene induced 60% of cancer cells in tumor tissue to undergo apoptosis. This slowed tumor growth significantly.
     

    7. Reduce Radiation Damage by Blocking the Expression of CD47

    On 21st of October 2009, the researchers at National Cancer Institute (NCI) once again showed their contribution to the cancer research by developing a method that protects healthy tissues from damaging effects of radiation cancer treatment. Previous cancer research showed that mice lacking CD47 are resistant to radiation damage. Therefore, the researchers injected an agent that suppressed the CD47 expression during the radiation. They proved that this can protect the normal cells from damage by radiation.
     

    8. Nicotine Patch and Nicotine Lozenge Works Best for Smoking Cessation

    On 2nd of November 2009, the researchers from National Cancer Institute (NCI) showed that the combination of nicotine patch and nicotine lozenge provided the great benefit for smokers to quit smoking effectively.
     

    9. PDF – Mushroom Extract that Shrink Tumors Effectively

    On 1st of December 2009, Dr. Brandon Louie and colleagues from Department of Urology at New York Medical College showed that a combination of interferon alpha (immunotherapy for bladder cancer) and PDF (mushroom extract) can reduce bladder cancer cell growth. However, it is too soon to claim that the PDF are a cure for cancer as the study provides no evidence that the mushrooms extract have health benefits in humans. Anyway, I still feel that this study has the further research value for cancer treatment in future.
     

    10. Lunasin – Fighting Leukemia and Blocking Inflammation

    On 2nd of December 2009, Elvira de Mejia, a professor of Food Science and Human Nutrition from University of Illinois claimed that lunasin, a soy peptide may have important benefits that fighting leukemia and blocking the inflammation that accompanies such chronic health conditions as diabetes, heart disease and stroke. Lunasin is a soy peptide often discarded in the waste streams of soy-processing plants.
     
    In conclusion, the cancer research on cancer treatment is still has a long way to go. The cancer research will continue to carry out to provide the greatest benefits to the world.
     

    Do you know any new discovery of cancer treatment in 2009 that I do not mentioned above? Please leave your comment to provide us a great resource of information.

    Top 10 Discoveries of Cancer Treatment in 2009 is a post from: Cytogenetics and Cancer Research

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