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Posts Tagged ‘hormone’


Reporter and Curator: Dr. Sudipta Saha, Ph.D.

 

The majority of living forms depend for their functioning upon two classes of biocatalysts, the enzymes and the hormones. These biocatalysts permit the diverse chemical reactions of the organism to proceed at 38°C with specificity and at rates frequently unattainable in vitro at elevated temperatures with similar reactants. The physiologic importance of enzymes and hormones is evident not only under normal circumstances, but is reflected clinically in the diverse descriptions of errors of metabolism, due to lack or deficiency of one or more enzymes, and the numerous hypo and hyper functioning states resulting from imbalance of hormonal supply.

 

In as much as both enzymes and hormones function, with rare exception, to accelerate the rates of processes in cells, investigators have sought possible interrelationships and interactions of enzymes and hormones, particularly as a basis for the mechanism of hormonal action. It has seemed logical to hypothesize that hormones, while not essential for reactions to proceed but never the less affecting the rates of reactions, may function by altering either the concentration or activity of the prime cellular catalysts, the enzymes. This proposed influence of hormones on enzymatic activity might be a primary, direct effect achieved by the hormone participating as an integral part of an enzyme system, or an indirect influence based upon the hormone altering the concentration of available enzyme and/or substrate utilized by a particular enzyme. Many publications have described alterations in the activity of enzymes in various tissues following administration in vivo of diverse hormonal preparations. However, it is not possible to judge, in the in vivo experiments, whether the reported effects are examples of direct enzyme-hormone interaction, or an indirect influence of the hormone mediated via one or more metabolic pathways, and therefore other enzyme systems whose activities are not being measured. Data from in-vivo studies of this type are thus not pertinent to a discussion of direct hormone-enzyme interaction.

 

Enzyme hormone interaction, as seen, for example, in the profound role of the enzymes of the liver in the metabolism of certain hormones, is of paramount importance in determining the effectiveness of these hormones. The ability of the organic chemist to prepare synthetic hormonal derivatives which are relatively resistant to enzymatic processes in the liver has been of outstanding value for approaches to oral hormonal therapy. Largely unexplored as yet is the possibility that enzyme-hormone interactions may lead to the production of physiologically more active substances from compounds normally synthesized and secreted by a particular endocrine gland. It may be said at the outset that in no instance has a hormone been demonstrated to influence the rate of a cellular reaction by functioning as a component of an enzyme system.

 

It is plausible that enzymes in a pathway might be structurally conserved because of their similar substrates and products for linked metabolic steps. However, this is not typically observed, and sequence analysis confirms the lack of convergent or divergent evolution. One might postulate that, if the folds or overall structures of the enzymes in a pathway are not conserved, then perhaps at least pathway-related active site similarities would exist. It is true that metal-binding sites and nucleotide-binding sites are structurally conserved. For example, cofactor-binding motifs for zinc, ATP, biopterin and NAD have been observed and biochemically similar reactions appear to maintain more structural similarity than pathway-related structural motifs. In general, ‘horizontal’ structural equivalency is prevalent in that chemistry-related structural similarities exist, but ‘vertical’ pathway-related structural similarities do not hold.

 

For metabolic pathways, protein fold comparisons and corresponding active site comparisons are sometimes possible if structural and functional homology exists. Unfortunately, with the current structural information available, the majority of active sites that can be structurally characterized are not similar within a metabolic pathway. Other examples exist of nearly completed pathways, for example, the tricarboxylic acid (TCA) cycle, and similar observations are observed. Situations in which different metals are incorporated in enzyme active sites lead to inherently different catalytic portions of the active sites. Slight differences in the ligand-binding portions of the respective active sites must lead to the observed differences in pathway-related enzyme specificities. These modifications in enzymatic activity are similar to what Koshland and co-workers previously observed. They showed that very minor active site perturbations to isocitrate dehydrogenase had drastic effects on catalysis.

 

Molecular level understanding of chemical and biological processes requires mechanistic details and active site information. The current knowledge regarding enzyme active sites is incomplete. Even in situations in which ATP-, ADP- or NAD(P)+-binding domains are observed or in situations in which similar folds are found (e.g. even for related kinases or for proteins involved in the immune system), structural comparisons do not yield specific details about active sites and it is not possible to predict where the substrate binds or to identify determinants of active site substrate specificity. Therefore, in this era of structural genomics, there should be major continued emphasis on completing structural information for important metabolic pathways. This will require improved efforts to obtain structures for enzyme complexes with appropriate cofactors, substrates or substrate analogs, as well as with inhibitors and regulators of activity. Then and only then will we have complete structural knowledge and facilitated structure-based drug design efforts. Structural genomics efforts promise to provide structural data in a high-throughput mode. However, we need to ensure that much of this focus is placed on completing the picture of metabolic pathways and enzyme active sites.

 

The availability of the human genomic sequence is changing the way in which biological questions are addressed. Based on the prediction of genes from nucleotide sequences, homologies among their encoded amino acids can be analyzed and used to place them in distinct families. This serves as a first step in building hypotheses for testing the structural and functional properties of previously uncharacterized paralogous genes. As genomic information from more organisms becomes available, these hypotheses can be refined through comparative genomics and phylogenetic studies. Instead of the traditional single-gene approach in endocrine research, we are beginning to gain an understanding of entire mammalian genomes, thus providing the basis to reveal subfamilies and pathways for genes involved in ligand signaling. The present review provides selective examples of postgenomic approaches in the analysis of novel genes involved in hormonal signaling and their chromosomal locations, polymorphisms, splicing variants, differential expression, and physiological function. In the postgenomic era, scientists will be able to move from a gene-by-gene approach to a reconstructionistic one by reading the encyclopedia of life from a global perspective. Eventually, a community-based approach will yield new insights into the complexity of intercellular communications, thereby offering us an understanding of hormonal physiology and pathophysiology. Many cellular signaling pathways ultimately control specific patterns of gene expression in the nucleus through a variety of signal-regulated transcription factors, including nuclear hormone receptors. The advent of genomic technologies for examining signal-regulated transcriptional responses and transcription factor binding on a genomic scale has dramatically increased our understanding of the cellular programs that control hormonal signaling and gene regulation. Studies of transcription factors, especially nuclear hormone receptors, using genomic approaches have revealed novel and unexpected features of hormone-regulated transcription, and a global view is beginning to emerge.

 

Source References:

 

http://pediatrics.aappublications.org/content/26/3/476.abstract

 

http://www.ncbi.nlm.nih.gov/pubmed/13499378

 

http://endo.endojournals.org/content/54/5/591.long

 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC528661/

 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1196745/

 

http://www.ncbi.nlm.nih.gov/pubmed/11114510

 

http://www.ncbi.nlm.nih.gov/pubmed/23516625

 

http://www.annualreviews.org/doi/abs/10.1146/annurev.bi.50.070181.002341

 

http://www.sciencedirect.com/science/article/pii/S0016648098971258#

 

http://www.interactive-biology.com/3931/basics-of-hormone-classification/

 

http://en.wikipedia.org/wiki/Category:Hormones_by_chemical_structure

 

http://www.annualreviews.org/doi/abs/10.1146/annurev-physiol-021909-135840

 

http://www.ncbi.nlm.nih.gov/pubmed/16423812

 

http://edrv.endojournals.org/content/23/3/381.full.pdf

 

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Treatment for Endocrine Tumors and Side Effects

Reporter and Curator: Dr. Sudipta Saha, Ph.D.

Surgery

The purpose of surgery is typically to remove the entire tumor, along with some of the healthy tissue around it, called the margin. If the tumor cannot be removed entirely, “debulking” surgery may be performed. Debulking surgery is a procedure in which the goal is to remove as much of the tumor as possible. Side effects of surgery include weakness, fatigue, and pain for the first few days following the procedure.

Chemotherapy

Chemotherapy is the use of drugs to kill tumor cells, usually by stopping the cells’ ability to grow and divide. Systemic chemotherapy is delivered through the bloodstream to reach tumor cells throughout the body. A chemotherapy regimen (schedule) usually consists of a specific number of cycles given over a set period of time. A patient may receive one drug at a time or combinations of different drugs at the same time. The side effects of chemotherapy depend on the individual and the dose used, but they can include fatigue, risk of infection, nausea and vomiting, loss of appetite, and diarrhea. These side effects usually go away once treatment is finished.

Radiation therapy

Radiation therapy is the use of high-energy x-rays or other particles to kill tumor cells. The most common type of radiation treatment is called external-beam radiation therapy, which is radiation given from a machine outside the body. When radiation treatment is given using implants, it is called internal radiation therapy or brachytherapy. A radiation therapy regimen usually consists of a specific number of treatments given over a set period of time. Side effects from radiation therapy may include fatigue, mild skin reactions, upset stomach, and loose bowel movements. Most side effects go away soon after treatment is finished.

Hormone therapy

The goal of hormone therapy is often to lower the levels of hormones in the body. Hormone therapy may be given to help stop the tumor from growing or to relieve symptoms caused by the tumor. In addition, for thyroid cancer, hormone therapy will be given if the thyroid gland has been removed, to replace the hormone that is needed by the body to function properly.

Immunotherapy

Immunotherapy (also called biologic therapy) is designed to boost the body’s natural defenses to fight the tumor. It uses materials made either by the body or in a laboratory to bolster, target, or restore immune system function. Examples of immunotherapy include cancer vaccines, monoclonal antibodies, and interferons. Alpha interferon is a form of biologic therapy given as an injection under the skin. This is sometimes used to help relieve symptoms caused by the tumor, but it can have severe side effects including fatigue, depression, and flu-like symptoms.

Targeted therapy

Targeted therapy is a treatment that targets the tumor’s specific genes, proteins, or the tissue environment that contributes to cancer growth and survival. This type of treatment blocks the growth and spread of tumor cells while limiting damage to normal cells, usually leading to fewer side effects than other cancer medications.

Recent studies show that not all tumors have the same targets. To find the most effective treatment, the doctor may run tests to identify the genes, proteins, and other factors in the tumor. As a result, doctors can better match each patient with the most effective treatment whenever possible.

Depending on the type of endocrine tumor, targeted therapy may be a possible treatment option. For instance, targeted therapies, such as sunitinib (Sutent) and everolimus (Afinitor), have been approved for treating advanced islet cell tumors. Early results of clinical trials (research studies) with targeted therapy drugs for other types of endocrine tumors are promising, but more research is needed to prove they are effective.

Recurrent endocrine tumor

Once the treatment is complete and there is a remission (absence of symptoms; also called “no evidence of disease” or NED). Many survivors feel worried or anxious that the tumor will come back. If the tumor does return after the original treatment, it is called a recurrent tumor. It may come back in the same place (called a local recurrence), nearby (regional recurrence), or in another place (distant recurrence). When this occurs, a cycle of testing will begin again to learn as much as possible about the recurrence. Often the treatment plan will include the therapies described above (such as surgery, chemotherapy, and radiation therapy) but may be used in a different combination or given at a different pace. People with a recurrent tumor often experience emotions such as disbelief or fear. Patients are encouraged to talk with their health care team about these feelings and ask about support services to help them cope.

Metastatic endocrine tumor

If a cancerous tumor has spread to another location in the body, it is called metastatic cancer. A treatment plan that includes a combination of surgery, chemotherapy, radiation therapy, hormone therapy, immunotherapy, or targeted therapy may be recommended if required.

In addition to treatment to slow, stop, or eliminate the cancer (also called disease-directed treatment), an important part of cancer care is relieving a person’s symptoms and side effects. It includes supporting the patient with his or her physical, emotional, and social needs, an approach called palliative or supportive care. People often receive disease-directed therapy and treatment to ease symptoms at the same time.

Source References:

http://www.cancer.net/cancer-types/endocrine-tumor/treatment

 

http://www.macmillan.org.uk/Cancerinformation/Cancertypes/Endocrine/Endocrinetumours.aspx

 

http://cancer.osu.edu/patientsandvisitors/cancerinfo/cancertypes/endocrine/Pages/index.aspx

 

http://cancer.northwestern.edu/cancertypes/cancer_type.cfm?category=8

 

http://www.cancervic.org.au/about-cancer/cancer_types/endocrine_cancer

 

http://www.oncolink.org/types/types1.cfm?c=4

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Women

 

Author: Jukka Karjalainen, MD, PhD

 

Sorry ladies, you will be seduced, pheromones make it impossible for you to resist men, no matter how dreadful the man wearing the pheromones may be.

Wait, please don’t panic. Sadly, the pheromone marketing craze may be causing us to turn a blind eye to an interesting discovery. As far as I see it’s like hearing about vitamins for the first time from a hard core drug dealer. When you get over your encounter with Mr. Dealer, you are not going to think of vitamins in the same way as a person who had heard about vitamins from GNC or Vitamin World. I believe the same thing is happening with marketers and pheromones. With that in mind let’s take a deeper look at pheromones.
Most people still believe pheromones are no different from X-ray glasses sold in the back of comic books. Some have been using them for years. To be sure, they are used heavily by government agencies worldwide. Business uses them daily, you may even use them. Of course I’m talking about insect and animal pheromones.
It was well known by the late 70s that females of the insect and animal kingdom produced chemicals for attracting males of the same species. Several examples were presented in literature. By the late 70s pheromones were already being manufactured for pest control. Indeed, pheromones were being used to attract or repel bugs and animals. Pheromones were already protecting crops from damage. Roaches were checking in and not checking out. At the same time scientist were working hard to find and prove the existence of human pheromones. This evidence was found in the mid 70s but did not reach the public with any power until the mid 80s.

Human pheromones made front page news in 1986 when Researchers at the Monell Chemical Senses Center of Philadelphia released their findings to the scientific journal Hormones and Behavior, as well as to the public by way of:

  • Time Magazine: “Studies find that male pheromones are good for women’s health.”
  • News week: “The Chemistry Between People: Are Our Bodies Affected by Another Person’s Scent?”
  • USA Today: “The Real Chemical Reaction between the Sexes.”
  • The Washington post: “Pheromones Discovered in Humans.”

The human pheromone was big news in the 80s. It was found that women’s health was directly affected by male pheromone. Interestingly, Monell Chemical Senses Center of Philadelphia reported that women who work or live together tend to get their menstrual cycles in sync. That curious phenomenon known for years by scientists and many ordinary folk, has long been suspected as an indication that humans, like insects and some mammals, communicate subtly by sexual aromas known as pheromones. (1)

In 1986 Dr. Winnifred Cutler, a biologist and behavioral endocrinologist, co discovered pheromones in our underarms. She and her team of researchers found that once any overbearing underarm sweat was removed, what remained were the odorless materials containing the pheromones. The approach to test the hypothesis was interesting: women and men emitted pheromones into the atmosphere and the authors showed that extracted pheromones could be collected, frozen for over a year, thawed and then applied topically above the upper lip of recipients to mimic some of the pheromonal effects found in nature. Dr. Cutler’s original studies in the ’70s showed that women who have regular sex with men have more regular menstrual cycles than women who have sporadic sex. Regular sex delayed the decline of estrogen and made women more fertile. This led the research team to look for what the man was providing in the equation. By 1986 they realized it was pheromones. (1, 2, 3).
Male scents play a role in maintaining the health of women, particularly the health of the female reproductive system. Pheromones help to maintain the health of women. To be more exact, they keep a woman’s reproductive system healthy. They found that women who have sex with men at least once a week are more likely to have normal menstrual cycles, fewer infertility problems and a milder menopause than celibate women and women who have sex rarely or sporadically. A healthy testosterone rich male pheromone signature somehow encouraged a woman’s body to keep itself healthy and young.

The scent of a good man may be music to a woman’s nose. Researchers also found that exposure to the male pheromones also prompted a shift in blood levels of a reproductive hormone called luteinizing hormone (LH). Levels of this hormone typically surge before ovulation, but women also experience small surges during other times in the menstrual cycle. It also can stabilize the menstrual cycle and reduce the symptoms of PMS. Pheromones could lift a woman’s mood actually alleviating depression, even postpone and then alleviate menopause health. (1, 2)
How did we get from health benefits to wild seduction products? People can’t resist a fast buck. If it’s about money, maybe we should be using pheromone products to make women’s lives better. Strike that. We should instead be using pheromone products to make people’s lives better. Provide pheromones that do the things mentioned above. Help to enable pheromone research that will gain more knowledge related to health and longevity. I don’t have anything against attracting the opposite sex. I think that’s a good idea. It’s just sad to see a good thing, or potentially good thing, be lost because of a poorly focus on health.

There is always more to the story than meets the eye. The person who does not ask questions has either been beaten down low by the people who know-it-all, or, they are the people who know-it-all. Keep asking questions. You will keep finding better answers.

REFERENCES: 
1. Biology of Reproduction, June 2003. News release, University of Pennsylvania.
2. Cutler WB, Preti G, Krieger A, Huggins GR, Garcia GR, Lawley HJ. Human axillary secretions influence women’s menstrual cycles: the role of donor extract of men. Horm Behav 1986; 20: 463473.
3. McCoy and Pitino. Pheromonal influences on sociosexual behavior in young women. Physiology & Behavior 2002; 75: 367-375.

 

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Author: Ritu Saxena, Ph.D.

Recently, two world renowned innovators, Steve Jobs-the CEO of Apple Inc. and Dr. Steinman-winner of 2011 Nobel prize in Physiology or medicine lost their life battle against Pancreatic cancer. Although both Jobs and Steinman suffered from the same disease, they were diagnosed with two fundamentally different forms of cancer of pancreas.

Steve lived with the disease for 8 years, a relatively long time for Pancreatic cancer patients to survive. The reason is attributed to the rare form of cancer of pancreas he suffered from-referred to as pancreatic neuroendocrine tumor. Steinman, on the other hand died due to a more common form of pancreatic cancer, the adenocarcenoma.

Neuroendocrine tumors arise from islands of hormone-producing cells (islets), that happen to be in that organ. Jobs learned in 2003 that he had an extremely rare form of this cancer, an islet-cell neuroendocrine tumor. In his email to  Apple employees in 2004, Steven Jobs wrote “I have some personal news that I need to share with you, and I wanted you to hear it directly from me,” Jobs said in the message, which he sent from his hospital bed. “I had a very rare form of pancreatic cancer called an islet cell neuroendocrine tumor, which represents about 1 percent of the total cases of pancreatic cancer diagnosed each year, and can be cured by surgical removal if diagnosed in time (mine was). I will not require any chemotherapy or radiation treatments.”

About 2,500 cases of pancreatic islet cell tumors are seen in the United States each year, according to the University of Southern California’s Center for Pancreatic and Biliary Diseases. These tumors, which are derived from neuroendocrine cells, tend to be slow growing and are treatable even after they have metastasized, said the center’s Web site.  http://www.sfgate.com/cgi-bin/article.cgi?f=/c/a/2004/08/02/MNGMJ816F41.DTL&ao=all

The management strategy of neuroendrocrine tumors (NET) like any other disease is supposed to be curative where possible. As suggested by several researchers including Ramage et al (http://www.ncbi.nlm.nih.gov/pubmed/15686165, ), surgery is the only curative option currently available for NETs. The updated guidelines published for the NET management state the over the past few years, there have been advances in the management of neuroendocrine tumours, which have included clearer characterisation, more specific and therapeutically relevant diagnosis, and improved treatments. However, because of the uncommon nature of the disease, there remain few randomised trials in the field, hence all evidence mentioned in the research article is considered relatively weak compared with other more common cancers. For patients who are diagnosed early enough to be candidates for surgery, the aim is to keep the patient disease- and symptom-free for as long as possible. For patients suffering from advanced-stage NETs, operative therapy is rarely curative and chemotherapy could be used on metastasized NETs. http://www.ncbi.nlm.nih.gov/pubmed/22052063.

As reported in a story covered by CNN in 2008, there was a lot of speculation when he appeared rail-thin at the unveiling of the new iPhone. Jobs eventually said in January 2009 that doctors said he dropped so much weight because of “a hormone imbalance that has been ‘robbing’ me of the proteins my body needs to be healthy. Sophisticated blood tests have confirmed this diagnosis.” http://tech.fortune.cnn.com/2008/06/13/steve-jobs-life-after-the-whipple/ This statement explains how symptoms of hormonal excess in NET patients must be controlled before surgical procedure is followed. Also, recommended management of the symptoms of hormonal hypersecretion depends on the hormone secreted. For example, glucose levels in patients with insulinomas should be stabilized with diet and/or diazoxide. Gastrin hypersecretion in patients with gastrinomas may be managed with proton pump inhibitors (PPIs). http://www.neuroendocrinetumor.com/health-care-professional/net-treatment-options.jsp

Steinman, on the other hand, suffered from adenocarcenoma that arises from the pancreatic cells themselves, referred to as the “far more common form of pancreatic cancer” by Jobs. He further wrote in his memo “…(adenocarcenoma) is currently not curable and usually carries a life expectancy of around one year after diagnosis. I mention this because when one hears ‘pancreatic cancer’ (or Googles it), one immediately encounters this far more common and deadly form, which, thank God, is not what I had.”

Dr. Steinman won the 2011 Nobel Prize for Medicine or Physiology for his early-career landmark discovery about the immune system in the 1970s when he first described ‘dendritic cells’ with the help of his mentor Zanvil Cohn at Rockefeller University. Unfortunately, he died just three days before the official announcement. http://www.scientificamerican.com/article.cfm?id=steinman-nobel-laureate-explains-discovery-dendritic-cells. He had been suffering from pancreatic cancer for four years, had been undergoing treatment using a pioneering immunotherapy based on his own research. Dendritic cells from his body were deployed to mount an assault on his cancer. His early research at Rockefeller, began as an attempt to understand the primary white cells of the immune system — the large “eating” macrophages and the exquisitely specific lymphocytes, which operate in a variety of ways to spot, apprehend and destroy infectious microorganisms and tumor cells. Steinman’s subsequent research pointed to dendritic cells as important and unique accessories in the onset of several immune responses, including clinically important situations such as rejection of graft, resistance to tumors, autoimmune diseases and infections including AIDS. http://newswire.rockefeller.edu/2011/10/03/rockefeller-university-scientist-ralph-steinman-honored-today-with-nobel-prize-for-discovery-of-dendritic-cells-dies-at-68/

The standard of care in the United States for the treatment of locally advanced pancreatic cancer is a combination of low-dose chemotherapy given simultaneously with radiation treatments to the pancreas and surrounding tissues. Radiation treatments are designed to lower the risk of local growth of the cancer, thereby minimizing the symptoms that local progression causes (back or belly pain, nausea, loss of appetite, intestinal blockage, jaundice). http://www.medicinenet.com/pancreatic_cancer/page6.htm#advanced

Research Efforts on Pancreatic Cancer: The untimely passing of the geniuses reminds us how important research in the area of pancreatic cancer is which lead to finding new therapeutic targets that might stem reliable therapies. A recent example is the report published in Science Daily stating that the protein RGL2 might be a promising therapeutic target for pancreatic cancer. http://www.sciencedaily.com/releases/2010/11/101105101400.htm. The conclusion was derived via research published in November in the Journal of Biological Chemistry by a team led by Channing Der, PhD from UNC Lineberger Cancer Center. http://www.jbc.org/content/285/45/34729.long   For almost three decades, scientists and physicians have known that a gene called the KRAS oncogene is mutated in virtually all pancreatic cancers, making it an important target for scientists looking for a way to stop the growth of pancreatic cancer tumors. The problem is that the KRAS gene triggers cancer cell growth in numerous ways, through multiple cell signaling pathways, and scientists have had difficulty determining which one will be the most promising to block — an important first step in designing a drug for use in patients. Dr. Der said that “We are particularly optimistic about RGL2 because we know that this protein is a critical component of KRAS signaling to another class of proteins called Ral GTPases, which are essential for the growth of almost all pancreatic tumors.”

Another groundbreaking research was published in the journal Nature talks about discovering the link between a gene and the prognosis of Pancreatic Ductal Adenocarcenoma. The team found that when a gene involved in protein degradation is switched-off through chemical tags on the DNA’s surface, pancreatic cancer cells are protected from the bodies’ natural cell death processes, become more aggressive, and can rapidly spread. Their research study proposed USP9X to be a major tumour suppressor gene with prognostic and therapeutic relevance in pancreatic cancer. http://www.sanger.ac.uk/about/press/2012/120429.html http://www.nature.com/nature/journal/vaop/ncurrent/pdf/nature11114.pdf

Although, most of the research efforts are concentrated on the more common form of cancer, pancreatic adenocarcenoma, similar research efforts are needed for developing cure for the uncommon form, the one Steve Jobs suffered from, neuroendocrine cancer.

What we lost to the disease is more than the two geniuses, we lost the possibility of further innovation that might have changed the world in ways we could not imagine. The loss, though, sheds light on the importance of finding a cure for the disease and its different types. Hope the research community is able to interpret and find answers to the enigma of Pancreatic cancer and its diverse forms in which it strikes.

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