Backtracking technique is an important technique in leukemia research. There are many of the acquired genetic changes that causes the molecular pathogenesis of leukemia can be well characterized by using backtracking technique. The researchers can trace many of genetic events to fetal origins using sensitive amplification methods.

Why is Backtracking Easy to be done?

1. Simplicity

The relative simplicity of the tumor genetics of the common subtypes of leukemia permitted the tracing becomes easier.

2. Archived Neonatal Blood Spots

There are the archived material in archived neonatal blood spots (ANB or Guthrie cards) form enable the backtracking becomes easier.

Backtracking to Trace Back Mutation Occurred Before Birth

Backtracking is a great technique to trace back the mutation occurred before birth and causing cancer, especially for leukemia. Therefore, before we go any further, we need to know a little bit about the childhood cancer. As we all know, childhood cancer is totally different with most adult cancers. The childhood cancer is relatively short latencies. That means the time between the initiating mutation and clinically diagnosed tumor is very short. We can see this by looking at the difference between the age of the child at diagnosis and the embryonic origin of the organ or tissue from which the cancer arises. This is an advantage for the researcher to trace back the genetic event. As I mentioned before, the availability of ANB has increase the possibility to identify the early or initiating genetic events before the child birth.

Unlike other cancers, leukemia is present in the general circulation without metastasis. It is because leukemia is a liquid form tumor. Thus, the preleukemic stem cells and their differentiated clonal progeny may also present in circulation too. Those cells can be detected on a neonatal blood specimen during birth.

Importance of Backtracking

1. Backtracking helps the researchers to understand the natural history, pathophysiology, and genetic information of various type of childhood cancer. This is important for researchers to deepen the knowledge about childhood cancer especially for leukemia.

2. From backtracking, we can know the exact time period when the key mutational events occur for childhood cancer. This definitely helps the epidemiologic efforts to discover the origin and causes of leukemia.

3. Besides, the information of backtracking is a great resource to know about prenatal mutation. The prenatal mutation is a potential target for early screening and intervention in leukemia.

4. Last but not least, if we can get the positive result from this approach, it is possible for us to use the cord blood for transplantation purposes. It is because the assays mentioned here apply to ANB cards. ANB cards can be used in cord bloods studies.

In conclusion, backtracking is essential or leukemia research. There are so many advantages of using backtracking in leukemia research. This technique will be continuously used for childhood cancer research and also leukemia research. I will describe more about the backtracking in my forthcoming post.

(Reference: Leukemia edited by Chi Wai Eric So)

Introduction of Backtracking in Leukemia Research is a post from: Cytogenetics and Cancer Research

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A great thing to tell you all is I’m going to do a project about the cancer cytogenetics in University Malaya Medical Centre (UMMC). I will start off doing the research on leukemia first. To prepare myself for this project, I need to read as many books as I can to deepen my knowledge about leukemia. Thus, today I will write a simple introduction about acute leukemia to make sure that I really understand about that. At the same time, I wish to share with you all what I have learnt too.

What is Acute Leukemia?

Acute leukemia is a hematological malignancy that can be classified into various subtypes. The classification of the subtypes is according to the morphology and immunophenotype of leukemic blasts. There were many studies shown that most probably the acute leukemia disease is because of genetic information of the origin of leukemic stem cells. The genetic material of these leukemic stem cells determines the phenotype, aggressiveness, and prognosis of acute leukemia.

To find out more about this disease, the clinical and researchers developed a lot of molecular and cellular techniques to recognize and analyze the genetic appearances in all the patients. In addition, they tried to use the new technology and methodologies to understand the transformation mechanisms of acute leukemia.

The common chromosomal abnormalities that occur on the patients are important for characterizing the types of diseases, risk stratification and the treatment design. For instance, if there is the abnormalities occur on MLL gene, we might difficult to do the prognosis on the patients. Furthermore, the all-trans retinoic acid (ATRA) and arsenic trioxide treatment might not suitable for the patient with PML-RARα fusion which is associated with chromosomal translocation between chromosome 15 and chromosome 17.

Transcriptional Deregulation Causing Acute Leukemia

Transcription is an important process in protein synthesis. And the transcription process is regulated by various transcription factors. The researchers found out that most of the primary abnormalities in acute leukemia involve the transcription factors except the abnormalities that affecting ABL gene. From that, we can conclude that the transcriptional deregulation plays a vital role in causing acute leukemia. Thus, a lot of studies have been done on the transcriptional deregulation that involve in acute leukemia for further understanding the mechanism.

Summing up, there are too many things about acute leukemia that I need to know and share with you. It is impossible for me to put all the things in just an article. I will continuously post up some information about acute leukemia in this Cytogenetics Cancer Research blog.

(Reference: Leukemia edited by Chi Wai Eric So)

What is Acute Leukemia? is a post from: Cytogenetics and Cancer Research

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If you are really familiar with apoptotic pathway, I’m sure you will know how essential role are the apoptosis protein play in this programmed cell death. Today, I’m going to show you 4 apoptosis protein families in details which are pro-apoptosis protein, anti-apoptosis protein, caspases and p53 tumour suppressor protein.

Pro-apoptosis Protein

The pro-apoptosis protein is a protein family that promotes the apoptosis to occur. The pro-apoptosis Bax protein is one of the major players 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).

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).

P53 Tumour Suppressor Proteins

The p53 protein is a transcription factor and pro-apoptosis 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-apoptosis protein, such as Bax and down regulates the expression of the anti-apoptosis protein like Bcl-2 (Byung et. al., 2002).

Anti-apoptosis Protein

Anti-apoptosis protein is a protein family that discourages the apoptosis to occur. Bcl-2 protein can protect the cell against apoptosis. Many experiments have proven that Bcl-2 protein controls intracellular Ca²⁺ levels and disallows the ruined of mitochondrial membrane when induced by pro-apoptotic proteins. Some evidences have shown that Bcl-2 protein is an ion channel which controls the release of cytochrome c from mitochondrial. This ion channel may modulate the apoptosis by regulating the permeability of intracellular membranes and cytochrome c release from mitochondria. Therefore, many Bcl-2 anti-apoptotic mechanisms have been suggested. Yet, the overexpression of Bcl-2 protein can save the cells from death (Jong et. al., 2001). The high expression of Bcl-2 proteins in tumours is related to resistance to cancer therapy. This is a major obstacle for the cancer treatment when the cancer is surgically incurable (Huang et. al., 2005).

In conclusion, these families of apoptosis protein are crucial in apoptotic pathway. The regulation of these apoptosis protein families may help in cancer treatment. Further cancer research need to be carried out so that we can regulate these apoptosis protein families well.

4 Apoptosis Protein Families is a post from: Cytogenetics and Cancer Research

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Immortality or eternal life is a dream of most of the people since long time ago. Most of us wish to live eternally in the world, at least live for longer. However, do you know what will happen if our cells become immortal and will not die eternally? These immortal cells will cause a lot of problem to our health and body. These cells are the cancer cells, the name that we are more familiar with.

Relationship between Cancer and Apoptosis

Cancer is because of the uncontrolled proliferation of abnormal cells that possess many oncogenic mutations (Avi et. al., 2008). Why is it called abnormal cells? This is because these cells are immortal even though they are malfunction. As we all know, normally our body cells will be eliminated if there are abnormalities like abnormal genes number. When the regulation of the cell cycle is disturbed, the tumour starts to grow (Pongpun et. al., 2009). These cancer cells cannot be eliminated via apoptosis, the programmed cell death mechanism.

Apoptosis is an essential pathway that eliminates the abnormal cells which are a serious threat to the human’s life (Avi et. al., 2008). So, apoptosis kills most of the tumourigenic cells and provides an initial important barrier against cancer disease (Liang et. al., 2009). However, as the malignant cells start to progress with the cells acquiring additional mutations, it allows the tumour cells to avoid from apoptotic death (Avi et. al., 2008). As a result, this abnormal apoptosis contributes to cancer initiation, development and treatment failure. Therefore, the cancer cells will gain their immortality and live eternally in our body. They will keep on replicate in our body to form tumour.

As the consequence of apoptosis does not deduce inflammatory or immune responses, it is the best way to kill the cancer cell through various anticancer treatments. Identifying the blockage in apoptosis and consequently to selectively induce the programmed cell death in cancer cells is a promising therapeutic strategy for many cancers (Liang et. al., 2009).

Immortal Cells, Good or Not Good?

As we can see, if the cells transform to cancer cells and become immortal, they will cause us problem. According to cancer research, these cells will continue to replicate in our body. The accumulation of these immortal cells will block the functional normal cells to grow. Sooner or later, our body will full of these immortal cells and the deficient normal cells cannot sustain our life anymore.

In conclusion, immortal cells are not good for us. “Nothing in the universe is able to last long eternally unchanged”. No matter how strong we are, we still cannot fight with this universal truth. What we can do is to cherish what we have now. Cherish our time. Cherish our beloved. Cherish our health and body.

Can I Have Your Feedback?

Have you ever think of to have an immortal life? Can you share with us the reason why you think of it?

What Will Happen If Our Cells Become Immortal? is a post from: Cytogenetics and Cancer Research

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Apoptosis or type one programmed cell death is intrinsic death program of the cell (Simone et. al., 2006). Do you know that our body eliminates billions of unwanted cells via apoptotic pathway every day? That means there are billions of our cells will die everyday. The new born cells will take place to make our body functions.

Apoptosis is Important

Apoptosis plays an important role in the development and homeostasis of multicellular organisms (Pongpun et. al., 2009). It is important for organ development, tissue remodeling, immune response and tumour suppression (Liang et. al., 2009). According to cancer research, excessive occurrence of apoptosis will cause numerous pathological conditions like AID and neurodegenerative disorders like Alzheimer’s disease and Huntington’s disease. On the other hand, deficiency of apoptosis is the main factor to the progression of autoimmune diseases and cancer (Avi et. al., 2008). Therefore, the mechanism of apoptosis should not go extreme in our body. It is neither over do the work nor less do the work.

Apoptosis Signals

Apoptosis is important for tissue growth and maintenance. There are many conditions that give signal to the cell to undergo suicide. For example, the decrease in the local concentration of a critical tissue morphogen or growth factor, the severe tension to critical cellular components like DNA or cytoskeleton which are affected by heat shock, ionizing radiation, bacterial or viral infection and oncogenic transformation (Simone et. al., 2006).

Apoptosis Mechanism

When the cells undergo the apoptosis, there is ruffling, blebbing and condensation of the plasma and nuclear membranes, and continuous aggregation of the nuclear chromatin. At the same time, the mitochondria and ribosomes remain as their gross constitution. The cytoskeletal structure will also be corrupted. When the cell gets smaller, it breaks up into a group of apoptotic bodies and will rapidly be gulped by adjacent macrophages or phagocytic cells. There is no inflammatory response in this process (Byung et. al., 2002).

In conclusion, apoptosis, type one programmed cell death is essential to retain our body to function. The failure of apoptosis is one of the reasons that causes cancer progression. Thus, please take good care of your health as our body system is the best doctor for us.

This is a part of literature review of my final year project thesis. I wish to share with you all what i have done.

Apoptosis | How our Cell Die is a post from: Cytogenetics and Cancer Research

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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 and best characterized of all the human breast cancer cell lines (Dino et. al., 2007).

I have described to you about cancer cell lines in my previous post HepG2 Cell Line. You may read through it to get the idea of cancer cell lines.

MCF-7 – Breast Cancer Cell Line

MCF-7 cell line is the first hormone-responsive breast cancer cell line (Amanda et. al., 2003).  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). 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). 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 cell line 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).

It has been shown to possess the ability to go through DNA fragmentation. There are apoptotic responses of MCF-7 cell line to the apoptosis-inducing agents like tumour necrosis factor and anti-Fas antibody. The MCF-7 cells are also an excellent in vitro model for studying the mechanisms of chemo-resistance because of its susceptibility to apoptosis (Richard et. al., 2003).

In conclusion, MCF-7 cell line is another useful cell line that can be used in various cancer research especially in breast cancer research. I also used it in my final year project.

This is a part of literature review of my final year project thesis. I wish to share with you all what i have done.

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

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HepG2 cell line is 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 tumour of childhood, usually presenting in the first year of life.

Before we go any further, let us explore about what is cancer cell line first. Cancer cell lines are widely used as experimental models of neoplastic disease, and data interpretation depends on unambiguous attribution of the respective cell line to its original source (Walther et. al., 2005). The progress of cell culture techniques enable the researchers to establish varieties of human carcinoma cell lines from surgical and autopsy tissues, peritoneum effusion, biopsy specimens and so on. As the pure cells in cell cultures can be applied for many types of researches that cannot be performed using tissue specimens, the research of permanent cell lines established form human cancers plays an important contributing role to help us understand the biology of cancers (Ku et. al., 2002).

HepG2 – Liver Cancer Cell Line

Let us go back to talk about HepG2 cell line. HepG2 cell line was introduced since 1979 (Norman et. al., 1992). Until now, there are more than nine thousands HepG2 references found in the scientific literature. This cell line has been proven to be a useful model of the human liver cell as there is high proportion of liver-specific proteins identified in the medium, for which there are antisera commercially available (Liu et. al., 1985). The metabolic pathways that have been studied appear to simulate the behaviour of normal hepatocytes. Thus, the studies encourage a wider application of this HepG2 cell line to biological problems that relate specifically to the role of the liver (Norman et. al., 1992).

Therefore, HepG2 cell line has been widely used in varieties of fields like liver metabolism, development, oncogenesis and hepatoxicity (Dolores et. al., 2009).

In conclusion, HepG2 cell line is an useful cell line that can be used in variuos field of cancer research. I used it for my final year project too.

This is a part of the literature review of my final year project thesis. I wish to share with you all what i have done on it.

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

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Carcinogenesis or tumourigenesis is the process of which normal cells are transformed into cancer cells, where they acquired the ability to proliferate abnormally and invade surrounding tissues (Atif and Peter, 2006).

All about Carcinogenesis

Cancer is a group of diseases that are characterized by uncontrolled cellular growth, enhanced angiogenesis and reduced programmed cell death (David and Lisa, 2008). Because of carcinogenesis, cancer cells can spread to other locations throughout the body, where they grow and upset normal bodily functions. It is known as metastatic spread where the cells are dispersed around the blood stream that formed leukemia or the lymphatic system that formed lymphoma or when some of the cancer cells clump together to form solid tumours (Arthur and Gary, 2009). As part of carcinogenesis, the disruptive behaviours of cancer cells are because of the changes in their genomes and gene expression that result in disruption of normal regulatory signalling pathways (Atif and Peter, 2006).

According to cancer research, about 200 varieties of cancer disease have been described. The cancer diseases can be grouped in four main types: carcinomas, sarcomas, leukemias and lymphomas, and neuroectodermal. Carcinomas are solid cancers which arise from the epithelial cells that line the inner and outer surfaces. Sarcomas are solid cancers that developed from the connective tissue cells that form our body structures. Leukemias and lymphomas are cancers caused by white blood cells (Arthur and Gary, 2009). Neurodectodermal is another group of nonepithelial tumours which arise from cells that form various components of the central and peripheral nervous system.

There are many risk factors of cancer which include both external and internal factors. Some of the examples of external factors are tobacco, exposure to chemical, radiation, and infectious organisms that can induce the development of cancer cell. On the other hand, the internal factors such as inherited mutations, hormones, immune conditions, and mutations that involved metabolism are the risk factors that have been implicated with the development of cancer cells. These causal factors may act together or in sequence to initiate or promote carcinogenesis (American Cancer Society, 2008).

In conclusion, carcinogenesis will harm our body. However, we can still prevent it from happenning. Live healthy with balanced meal is one of the best way to get rid of carcinogenesis. Recently, many cancer researchers recommend people to consume more vegetables. I have converted myself to be a vegetarian since last year. You may do so. At least, reduce the amount of meat in your meal. May you be healthy and well always!

This is a part of the literature review of my final year project thesis. I wish to share with you all what i have done on it.

Introduction of Carcinogenesis is a post from: Cytogenetics and Cancer Research

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This is a guest post submitted by G. Garcia and written by Ben Stillwater. Ben Stillwater is a freelance writer for AsbestosNews.com, an online resource on malignant mesothelioma and asbestos cancer.

There has been some research on the relationship between genetics and the development of malignant mesothelioma.  While there is no conclusive body of work, there is some compelling evidence that genetic defects may result in a higher risk for the development of malignant mesothelioma.  Research reported in Cancer Genetics and Cytogenetics in 2001 found evidence of chromosomal defects aligned through a family with a history of cancer that included at least one malignant mesothelioma patient.

Frightening Story of Malignant Mesothelioma

There is also an intriguing and frightening story of three villages in Turkey where fifty percent of the deaths are caused by malignant mesothelioma.  This is a relatively rare disease, diagnosed perhaps 3,000 times a year in the United States, a nation of 300 million people.  The ostensible cause is exposure and inhalation or ingestion of asbestos fibers.  In the villages located in the Cappadocian area of Turkey residents were uniformly exposed to a fibrous material called erionite, similar in structure to the six types of fiber categorized as asbestos.  Erionite occurs naturally in other areas of Turkey however and the occurrence of malignant mesothelioma is fractional compared to the villages of Tuzkoy, Karain, and Sarihidir. 

A cancer study conducted by a collaboration of physicians and scientists from Turkey and the United States looked closely at this epidemic for evidence of genetic predisposition to mesothelioma cancer and reported their findings in the May, 2006 edition of Cancer Research.   They found no evidence of a different, more malicious type of erionite fiber among the villages with populations disposed to the development of malignant mesothelioma than in other Cappadocian villages.  Further, they found that occurrences of the disease were more frequent in some families than others.  And finally, epidemiological research showed that members of families with frequent malignant mesothelioma occurrence who married into families without the history of malignant mesothelioma carried an increased risk of the disease developing for their children and grandchildren.  The evidence of genetic predisposition is overwhelming.

Gene Therapy for Malignant Mesothelioma

One of the developments in cytogenetics with regard to malignant mesothelioma and other carcinomas has been the identification of chromosomal damage with the onset of tumor development.  Genetic evidence of damage has served as a source of markers for malignant growths.  Today the use of gene therapy applying targeted tumor-suppressant genes at malignant cells is in its nascent stage but promising a hopeful path to improved and effective treatment.  Gene therapy has been one of the sidelights in mesothelioma news as thoracic oncologists have cast about for more effective ways to target mesothelioma cells.  Chemotherapy combinations employing cisplatin, Pemetrexed and Onconase have been tested and retested in various combinations but the difficulty of targeting two distinct types of malignant cells remains.

Malignant mesothelioma is most commonly caused by an epithelial cell, but a sarcomatoid cell is a less frequent possibility and the presence of both occurs in up to twenty percent of all cases.  Experimental gene therapy models have been developed for both.  The use of gene therapy to slow the reproduction of epithelial cells has shown some effectiveness, while a method of genetic vaccination for sarcomatoid cells has been less conclusive.  A summation of recent gene therapy treatment for malignant mesothelioma appeared in the German medical journal Onkologie in 2008, detailing the clinical studies to that point.  Oncologists are accustomed to mixing chemotherapy drugs as a treatment option, mixing chemotherapy and radiotherapy for malignant mesothelioma treatment, and now are looking at incorporating gene therapy into treatment protocols for this lethal disease.

Genetics and Malignant Mesothelioma is a post from: Cytogenetics and Cancer Research

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Today, we will talk about the benefits of consuming whey protein to minimize the chemotherapy side effects to the patients. Before we go further, we need to know a little bit about glutathione, which is an antioxidant that protects cells from toxic compounds.

Glutathione Protects Cells Against Toxic

As I mentioned, glutathione plays an important role to protect cells against toxic compounds. Glutathione balance is very important for cancer patients as glutathione actually gives the cancer cells advantage to escape from the effect of chemotherapy. Cancer research showed that the concentration of glutathione in tumour cell is one of the determinants of the cytotoxicity of many chemotherapeutic agents and radiation. There will be drug resistance to chemotherapy if there is an increase of glutathione concentration in cancer cells.

Whey Protein Reduces Glutathione Levels in Cancer Cells

According to cancer studies, the researchers found that the presence of whey protein helps to reduce glutathione levels in cancer cells but enhance the concentration of glutathione in normal cells. By knowing this, the whey proteins are used in combination with glutathione to help in decreasing the concentrations of glutathione in cancer cells so that the cancer cells more vulnerable to chemotherapy. At the same time, the whey proteins can help to maintain or even increase glutathione concentration in normal healthy cells. Moreover, glutathione level in cancer and normal cells is negatively inhibited by its own synthesis. As glutathione level in cancer cells is higher than normal cells, it is much easier to achieve negative-feedback inhibition for glutathione synthesis in cancer cells.

According to Life Extension Foundation Protocols, chemotherapy patients should at least consuming 30 to 60 grams of whey protein a day for 10 days before initiation of chemotherapy, during chemotherapy and 10 days after the chemotherapy session is ended. Yet, this is only a theoretical statement and might not suitable to everyone. Please do not hesitate to seek the advice from the doctor before consuming the whey protein.

In conclusion, the relationship between cancerous cells, glutathione and whey protein is believed to be an important factor of chemotherapy resistance in cancer cells. It is essential to know that whey protein selectively decreases glutathione level in cancer cells, consequently making them more susceptible to chemotherapy. It also maintains and increase glutathione in normal cells to reduce chemotherapy side effects.

Whey Protein to Minimize Chemotherapy Side Effects (Part 3) is a post from: Cytogenetics and Cancer Research

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