page contents

sites

Monday, 4 February 2013

What Is Blood Cancer


Source(google.com.pk)
What Is Blood Cancer Biography
Blood cancer is a form of cancer which attacks the blood, bone marrow, or lymphatic system. There are three kinds of blood cancer: leukemia, lymphoma, and multiple myeloma. These malignancies have varying prognoses, depending on the patient and the specifics of the condition, but overall survival rates with blood cancer increased radically in the late 20th century with the development of advanced treatments. When caught early, blood cancer can be very manageable in some cases, which is one very good reason to make regular trips to the doctor a priority for people of all ages.

In the case of leukemia, the cancer interferes with the body's ability to make blood. Leukemia attacks the bone marrow and the blood itself, causing fatigue, anemia, weakness, and bone pain. It is diagnosed with a blood test in which specific types of blood cells are counted. Treatment for leukemia usually includes chemotherapy and radiation to kill the cancer, and in some cases measures like bone marrow transplants may be required. There are several different types of leukemia, including chronic myelogenous leukemia, acute lymphoblastic leukemia, and hairy cell leukemia.

Swiss API quality at Asian prices. www.dolder.com/bendamustine
Lymphomas are blood cancers which involve the lymphocytes, a type of white blood cell. They are divided into Hodgkin's and non-Hodgkin's types. Lymphoma often involves swollen lymph nodes in addition to the symptoms for leukemia listed above, and it is also treated with chemotherapy and radiation. Multiple myeloma is a type of blood cancer which primarily appears in older people, involving the plasma, another type of white blood cell. Chemotherapy, radiation, and other drug treatments can be used to manage multiple myeloma.

The goal in treating blood cancer is to achieve remission, a situation characterized by the absence of symptoms. Even in remission, a blood cancer can still start up again, so people who have experienced blood cancer may need to attend regular follow-up medical appointments and annual checkups to check for a recurrence of the cancer. Blood cancer does not appear to be preventable, but like other cancers, the risk seems to be reduced among people who eat a healthy diet, exercise, and maintain good mental health.

People diagnosed with blood cancer can work with an oncologist, a doctor who specializes in cancer, or a hematologist, a doctor who specializes in diseases of the blood. Some patients work with both, attempting to develop a treatment plan which will be as effective as possible. Because individual cases can be quite varied, patients often benefit from second opinions to confirm the diagnosis and treatment plan.

Blood Cancer

Source(google.com.pk)
Blood Cancer Biography

Oncologist Siddhartha Mukherjee was treating one of his patients, a woman with advanced abdominal cancer who had relapsed multiple times, when she asked him what seemed like a simple question.

"She said, 'I'm willing to go on, but before I go on, I need to know what it is I'm battling,' " Mukherjee tells NPR's Terry Gross.

But, as Mukherjee explains, describing his patient's illness wasn't so simple. Defining cancer, he says, is something doctors and scientists have been struggling to do since the disease's first documented appearance thousands of years ago.

The Emperor of All Maladies: A Biography of Cancer
By Siddhartha Mukherjee
Hardcover, 592 pages
Scribner
List price: $30
"Cancer is not just a dividing cell," he says. "It's a complex disease: It invades, it metastasizes, it evades the immune system. So there are many, many other stages of [defining] cancer which are still in their infancy."

Mukherjee's new book, The Emperor of All Maladies: A Biography of Cancer, grew out of his desire to better understand the disease he treats, through examining the way cancer has been described and treated throughout history. He chronicles the ways therapies evolved, particularly in the 20th century, as more treatment options became available and scientists worked to understand the underlying genetic mutations that caused the disease.

Enlarge image
Siddhartha Mukherjee is a staff oncologist at Columbia University Medical Center.

Deborah Feingold via Scribner
"If there's a seminal discovery in oncology in the last 20 years, it's that idea that cancer genes are often mutated versions of normal genes," he says. "And the arrival of that moment really sent a chill down the spine of cancer biologists. Because here we were hoping that cancer would turn out to be some kind of exogenous event — a virus or something that could then be removed from our environment and our bodies and we could be rid of it — but [it turns out] that cancer genes are sitting inside of each and every one of our chromosomes, waiting to be corrupted or activated."

As the genetic understanding of cancer evolves, Mukherjee says, oncologists will be able to integrate that knowledge to develop more targeted treatment options — particularly as they find commonalities between different types of cancer.

"A breast cancer might turn out to have a close resemblance to a gastric cancer," he says. "And this kind of reorganization of cancer in terms of its internal genetic anatomy has really changed the way we treat and approach cancer in general."

Dr. Siddhartha Mukherjee is an assistant professor of medicine at Columbia University and a staff cancer oncologist at Columbia University Medical Center. His articles have been published in Nature, The New England Journal of Medicine, and The New York Times.

Excerpt: 'The Emperor Of All Maladies'
On the morning of May 19, 2004, Carla Reed, a thirty-year-old kindergarten teacher from Ipswich, Massachusetts, a mother of three young children, woke up in bed with a headache. "Not just any headache," she would recall later, "but a sort of numbness in my head. The kind of numbness that instantly tells you that something is terribly wrong."

Something had been terribly wrong for nearly a month. Late in April, Carla had discovered a few bruises on her back. They had suddenly appeared one morning, like strange stigmata, then grown and vanished over the next month, leaving large map-shaped marks on her back. Almost indiscernibly, her gums had begun to turn white. By early May, Carla, a vivacious, energetic woman accustomed to spending hours in the classroom chasing down five- and six-year-olds, could barely walk up a flight of stairs. Some mornings, exhausted and unable to stand up, she crawled down the hallways of her house on all fours to get from one room to another. She slept fitfully for twelve or fourteen hours a day, then woke up feeling so overwhelmingly tired that she needed to haul herself back to the couch again to sleep.

Carla and her husband saw a general physician and a nurse twice during those four weeks, but she returned each time with no tests and without a diagnosis. Ghostly pains appeared and disappeared in her bones. The doctor fumbled about for some explanation. perhaps it was a migraine, she suggested, and asked Carla to try some aspirin. The aspirin simply worsened the bleeding in Carla's white gums.

Outgoing, gregarious, and ebullient, Carla was more puzzled than worried about her waxing and waning illness. She had never been seriously ill in her life. The hospital was an abstract place for her; she had never met or consulted a medical specialist, let alone an oncologist. She imagined and concocted various causes to explain her symptoms — overwork, depression, dyspepsia, neuroses, insomnia. But in the end, something visceral arose inside her — a seventh sense — that told Carla something acute and catastrophic was brewing within her body.

On the afternoon of May 19, Carla dropped her two children with a neighbor and drove herself back to the clinic, demanding to have some blood tests. Her doctor ordered a routine test to check her blood counts. As the technician drew a tube of blood from her vein, he looked closely at the blood's color, obviously intrigued. Watery, pale, and dilute, the liquid that welled out of Carla's veins hardly resembled blood.

Carla waited the rest of the day without any news. At a fish market the next morning, she received a call.

"We need to draw some blood again," the nurse from the clinic said.

"When should I come?" Carla asked, planning her hectic day. She remembers looking up at the clock on the wall. A half-pound steak of salmon was warming in her shopping basket, threatening to spoil if she left it out too long.

In the end, commonplace particulars make up Carla's memories of illness: the clock, the car pool, the children, a tube of pale blood, a missed shower, the fish in the sun, the tightening tone of a voice on the phone. Carla cannot recall much of what the nurse said, only a general sense of urgency. "Come now," she thinks the nurse said. "Come now."

I heard about Carla's case at seven o'clock on the morning of May 21, on a train speeding between Kendall Square and Charles Street in Boston. The sentence that flickered on my beeper had the staccato and deadpan force of a true medical emergency: Carla Reed/New patient with leukemia/14th Floor/Please see as soon as you arrive. As the train shot out of a long, dark tunnel, the glass towers of the Massachusetts General Hospital suddenly loomed into view, and I could see the windows of the fourteenth floor rooms.

Carla, I guessed, was sitting in one of those rooms by herself, terrifyingly alone. Outside the room, a buzz of frantic activity had probably begun. Tubes of blood were shuttling between the ward and the laboratories on the second floor. Nurses were moving about with specimens, interns collecting data for morning reports, alarms beeping, pages being sent out. Somewhere in the depths of the hospital, a microscope was flickering on, with the cells in Carla's blood coming into focus under its lens.

I can feel relatively certain about all of this because the arrival of a patient with acute leukemia still sends a shiver down the hospital's spine — all the way from the cancer wards on its upper floors to the clinical laboratories buried deep in the basement. Leukemia is cancer of the white blood cells — cancer in one of its most explosive, violent incarnations. As one nurse on the wards often liked to remind her patients, with this disease "even a paper cut is an emergency."

For an oncologist in training, too, leukemia represents a special incarnation of cancer. Its pace, its acuity, its breathtaking, inexorable arc of growth forces rapid, often drastic decisions; it is terrifying to experience, terrifying to observe, and terrifying to treat. The body invaded by leukemia is pushed to its brittle physiological limit — every system, heart, lung, blood, working at the knife-edge of its performance. The nurses filled me in on the gaps in the story. Blood tests performed by Carla's doctor had revealed that her red cell count was critically low, less than a third of normal. Instead of normal white cells, her blood was packed with millions of large, malignant white cells — blasts, in the vocabulary of cancer. Her doctor, having finally stumbled upon the real diagnosis, had sent her to the Massachusetts General Hospital.

In the long, bare hall outside Carla's room, in the antiseptic gleam of the floor just mopped with diluted bleach, I ran through the list of tests that would be needed on her blood and mentally rehearsed the conversation I would have with her. There was, I noted ruefully, something rehearsed and robotic even about my sympathy. This was the tenth month of my "fellowship" in oncology — a two-year immersive medical program to train cancer specialists — and I felt as if I had gravitated to my lowest point. In those ten indescribably poignant and difficult months, dozens of patients in my care had died. I felt I was slowly becoming inured to the deaths and the desolation — vaccinated against the constant emotional brunt.

There were seven such cancer fellows at this hospital. On paper, we seemed like a formidable force: graduates of five medical schools and four teaching hospitals, sixty-six years of medical and scientific training, and twelve postgraduate degrees among us. But none of those years or degrees could possibly have prepared us for this training program. Medical school, internship, and residency had been physically and emotionally grueling, but the first months of the fellowship flicked away those memories as if all of that had been child's play, the kindergarten of medical training.

Cancer was an all-consuming presence in our lives. It invaded our imaginations; it occupied our memories; it infiltrated every conversation, every thought. And if we, as physicians, found ourselves immersed in cancer, then our patients found their lives virtually obliterated by the disease. In Aleksandr Solzhenitsyn's novel Cancer Ward, Pavel Nikolayevich Rusanov, a youthful Russian in his midforties, discovers that he has a tumor in his neck and is immediately whisked away into a cancer ward in some nameless hospital in the frigid north. The diagnosis of cancer—not the disease, but the mere stigma of its presence—becomes a death sentence for Rusanov. The illness strips him of his identity. It dresses him in a patient's smock (a tragicomically cruel costume, no less blighting than a prisoner's jumpsuit) and assumes absolute control of his actions. To be diagnosed with cancer, Rusanov discovers, is to enter a borderless medical gulag, a state even more invasive and paralyzing than the one that he has left behind. (Solzhenitsyn may have intended his absurdly totalitarian cancer hospital to parallel the absurdly totalitarian state outside it, yet when I once asked a woman with invasive cervical cancer about the parallel, she said sardonically, "Unfortunately, I did not need any metaphors to read the book. The cancer ward was my confining state, my prison.")

As a doctor learning to tend cancer patients, I had only a partial glimpse of this confinement. But even skirting its periphery, I could still feel its power—the dense, insistent gravitational tug that pulls everything and everyone into the orbit of cancer. A colleague, freshly out of his fellowship, pulled me aside on my first week to offer some advice. "It's called an immersive training program," he said, lowering his voice. "But by immersive, they really mean drowning. Don't let it work its way into everything you do. Have a life outside the hospital. You'll need it, or you'll get swallowed."

But it was impossible not to be swallowed. In the parking lot of the hospital, a chilly, concrete box lit by neon floodlights, I spent the end of every evening after rounds in stunned incoherence, the car radio crackling vacantly in the background, as I compulsively tried to reconstruct the events of the day. The stories of my patients consumed me, and the decisions that I made haunted me. Was it worthwhile continuing yet another round of chemotherapy on a sixty-six-year-old pharmacist with lung cancer who had failed all other drugs? Was is better to try a tested and potent combination of drugs on a twenty-six-year-old woman with Hodgkin's disease and risk losing her fertility, or to choose a more experimental combination that might spare it? Should a Spanish-speaking mother of three with colon cancer be enrolled in a new clinical trial when she can barely read the formal and inscrutable language of the consent forms?

Immersed in the day-to-day management of cancer, I could only see the lives and fates of my patients played out in color-saturated detail, like a television with the contrast turned too high. I could not pan back from the screen. I knew instinctively that these experiences were part of a much larger battle against cancer, but its contours lay far outside my reach. I had a novice's hunger for history, but also a novice's inability to envision it.

About Leukemia

Source(google.com.pk)
About Leukemia Biography

Leukemia is a cancer of the bone marrow and blood. There are four main types of leukemia. These are: acute lymphocytic leukemia (ALL), chronic lymphocytic leukemia (CLL), acute myelogenous leukemia (AML), and chronic myelogenous leukemia (CML). MLL stands for “mixed lineage leukemia” and means that the leukemia comes from both the myeloid and the lymphoid cell progenitors (Robien and Ulrich, 2003). The cause of leukemia is currently still unknown. It often arises as a result of DNA translocations, inversions, or deletions in genes regulating blood cell development or homeostasis. In all types of leukemia, genetic translocations, inversions, or deletions cause dysfunctional cells to replace normal hematopoietic cells in the bone marrow (Robien and Ulrich, 2003). A leukemia patient will usually die from anemia or infection because of the lack of red blood cells and immune cells (Sompayrac, 1999).

Leukemia stem cells (LSC) are thought to have been derived from haematopoietic stem cells (HSC), which are CD34+CD38-. During leukemogenesis, the LSC expresses shared surface characteristics with the HSC. It also has the capacity for producing both the clonogenic leukemic progenitors and the non-clonogenic blast cells, which make up the bulk of the leukemia (Huntly, et al. 2005). In the bone marrow there are two types of hematopoietic stem cells. In someone who does not have leukemia, the myeloid progenitor is the parent cell to granulocytes and macrophages, and the lymphoid progenitor is the parent cell to T-cells and B-cells (Janeway, et al., 1999). In adults, 85% of all leukemia cases are myeloid, with 15% being lymphoid. In children the opposite is true, with 80% of all cases being lymphoid (ALL) and only 20% being myeloid (Greaves, 2000).

In people with acute leukemia, a mistake is made in the action of the VDJ recombinase enzyme, which normally creates antibody and T-cell receptor diversity. Proto-oncogene, a gene that promotes growth and spread, is inappropriately turned on and it activates other proto-oncogenes and deactivate anti-oncogenes, which normally protect cells against cancer-causing mutations (Sompayrac, 1999). Chronic leukemias may be caused when mistakes in recombination activate genes that either cause the cell to proliferate, or cause it not to die by apoptosis or increased activity of stem cells or abnormal committed progenitor cells (Marley and Gordon, 2005). The increased life span of the cell increases the chance that enough mutations will accumulate to cause cancer (Sompayrac, 1999).

Mutations that increase the risk of leukemia can be caused by radiation, extremely low frequency electromagnetic fields, pesticides, benzene, other carcinogens, viral infections, and recombination errors that occur throughout life (Sompayrac, 1999). Cigarette smoke, high altitude, or other factors that increase exposure to radiation can be accelerating factors for cancer (Sompayrac, 1999). Rates of leukemia may also be greater following periods of population mixing. During periods of population mixing, individuals are exposed to new infectious agents. A similar hypothesis is that children who were not exposed to common infectious agents at a young age would also have higher rates of leukemia. The infectious agents would be new to their system, causing a strong and inappropriate immune response that might trigger leukemia. Studies on daycare attendance as a measure of exposure to infectious agents have had mixed results (Robien and Ulrich, 2003).

Immuno-suppressed people such as patients being treated with chemotherapy or patients who have AIDS have higher rates of leukemia, but they do not have higher rates of other types of cancer (Sompayrac, 1999). Some cells in the immune system may protect against the development of cancer. Macrophages are cells that eat and destroy old or damaged red blood cells. The macrophages recognize the cells because a fat molecule called phospotidyl-serine flips to the outside of the cell as it ages (Sompayrac, 1999). Macrophages can also destroy cancer cells, but only when they are hyperactivated. Usually when there is no inflammatory reaction in the body, the macrophages will remain resting and will not attack the cancer cells, but natural killer cells secrete cytokines when cancer cells are present and the cytokines cause the hyperactivation of the macrophages (Sompayrac, 1999). The immune system has evolved to protect against leukemia by destroying cancerous cells, but in a person whose immune system is weakened or is being exposed to many new pathogens, it is not as effective at getting rid of damaged cells.

Specific Types of Leukemia
ALL is a disease of B or T lymphocyte lineage. Childhood ALL is of the B lineage. One of the most common translocations in B-precursor childhood ALL is suggested to be t(1;19)(q23;p13). The deletion of 9p has been suggested to be an evolutionary aspect of the progression of ALL but it is also thought to play a primary role in some cases of leukemogenesis (Forestier, et al., 2000). In ALL, it seems likely that leukemia develops in two stages: a pre-natal genetic alteration that predisposes the infant to developing leukemic precursor cells, and a post-natal event that triggers this latent disease. This has been suggested by several studies, including a number of "twin studies," which compare the incidence of diseases in identical (monozygotic) and fraternal (dizygotic) twins, in order to determine the relative importance of genetics and the environment as causal factors in a specific disease. Many twin studies have shown that identical twins have high "concordance" levels for leukemia, meaning that they share the disease. Concordance has often been taken as proof that a disease is genetic. However, in this case, it may be because they share a very similar environment during their fetal development: more than half of identical twins share a placenta, while no fraternal twins do (Greaves, 1999). The leukemic genetic alteration most likely takes place in one twin and spreads to the other through the placenta. This suggests that in non-twin children, the leukemic alteration may also take place in utero, as indicated by positive results from blood samples taken soon after birth (Greaves, 1999). Concordance rates near 100% would imply that the initial leukemic genetic alteration is the sole and sufficient cause for the development of leukemia. This is the case with another type of leukemia, MLL. However, in ALL, the concordance rate is closer to 10%. This suggests that the initial genetic alteration is not enough to cause leukemia in the absence of a second genetic alteration caused by the post-natal environment (Greaves, et al, 2003).

CML is caused by the reproduction of cells that have not matured properly, but continue to reproduce (Marley and Gordon, 2005). It has a distinguishing inherited characteristic called the Philadelphia chromosome (No. 22), a genetic abnormality in the blood cells that is referred to as the Ph-chromosome.  The breakage on the chromosome is referred to as "BCR" (breakpoint cluster region). A breakage on chromosome 9, known as "ABL" (Abelson) has also been noted. These two mutated genes fuse together, forming a gene called BCR-ABL.  This gene can still function properly. However, in CML patients, the protein that is produced is abnormal, causing unregulated myeloid cell production. Evidence has pointed to this abnormal protein production as the cause of the leukemic conversion of the hematopoietic stem cell (Leukemia and Lymphoma Society, 2005). Normally stem cells divide in the bone marrow to replace themselves and create differentiating cells. In CML, either the stem cells or progenitor cells are increasing at all times (Marley and Gordon, 2005).

The most common genetic abnormality in CLL is 13q14 deletion, observed in 50% of all cases. (Caporaso et al., 2004)

In addition to the four basic types of leukemia, there are a variety of other forms. Different types of leukemia are characterized by different patterns of nonrandom chromosomal aberrations, but the frequencies with which the various karyotypic subtypes are seen differ amongst geographic regions. In areas where children are not sufficiently exposed in early youth to childhood infections, there is a greater risk of developing leukemia from an abnormal immune system response.

What Is Leukemia

Source(google.com.pk)
What Is Leukemia Biography

Maya Scholars, in Mexico, Guatemala, Belize, Honduras, El Salvador and North America, have been watching with amusement and dismay as self-styled experts proclaim that ancient Maya prophets foretold an earth-shattering happening to occur December 21, 2012. This predicted phenomenon gets described in contradictory but often cataclysmic fashion--as an ecological collapse, a sunspot storm, a rare cosmic conjunction of the earth, sun, and the galactic center, a new and awesome stage of our evolution, and even a sudden reversal of the Earth's magnetic field which will erase all our computer drives. One even predicts the earth's initiation into a Galactic Federation, whose elders have been accelerating our evolution with a "galactic beam" for the last 5000 years. In sum, the world as we know it will suddenly come to a screeching halt.

These predictions are alleged to be prophecies by so-called "Ancient Mayans" whose "astronomically precise" calendar supposedly terminates on that date. According to such accounts, these mysterious Maya geniuses appeared suddenly, built an extraordinary civilization, designed in it clues for us, and then suddenly, inexplicably, vanished, as if they had completed their terrestrial mission. These same experts claim special credibility for the Maya prophecies by asserting that these historic sages, with their possible extraterrestrial origins, had tapped into an astonishing esoteric wisdom.

Could any of this be true?
The credibility of those claims deserves rational attention-which is what I intend to provide. Neither mystic nor prophet, I am a Mayanist. More specifically, I am a professional art historian and an epigrapher (less formally, a glypher), one who can read and write Maya hieroglyphs. For over a decade, I have focused my scholarly research specifically on Maya culture and writing, making some surprising discoveries that can present a more definitive perspective on the prophecies of the ancient Maya seers. As we approach the critical year, it is time to offer a more viable account of the Maya prophecy and expose both the fallacies and ethnocentricism tainting the current sensational accounts.

Here I intend to explain what we actually know about (1) Maya knowledge and attitudes, both ancient and modern, (2) the date 13.0.0.0.0. and (3) their many Creation stories and prophecies. I shall draw from recent decipherment, ethnography, interviews with Maya priests and knowledge-keepers, and especially from their surviving prophetic literature. That literature includes The Books of Chilam Balam, among others, the pre-Columbian Codices, and ancient inscriptions. The evidence is sometimes fragmentary and often puzzling to us moderns, at least at first. But I believe the effort will be worth it.

First, let me affirm that the year 2012 does hold particular significance in Mayan scholarship. Those of us who study the ancient and modern Maya — anthropologists, archaeologists, art historians, linguists, historians, amateurs, collectors — have been anticipating the end of the Maya Great Cycle for some time. We write it 13.0.0.0.0 4 Ajaw 3 K'ank'in. We have known for half a century that this date probably correlates to December 21 (or December 23) in the year 2012 in the Gregorian calendar.

Leukemia

Source(google.com.pk)
Leukemia Biography

Leukemia, a malignant cancer of the blood, was named in 1847 by Dr. Rudolf Virchow, a German politician whose wide-ranging interests led him to significant discoveries in cell biology, pathology and anthropology. Although Dr. Virchow’s name appeared often in The New York Times, mostly in the late 19th century, his discovery of leukemia was not mentioned until Feb. 22, 1970, in an article by Dr. Lawrence K. Altman.
Enlarge This Image

Of course, that was not the first time the disease was mentioned in the paper. That happened on Dec. 6, 1899, when Maj. Samuel T. Armstrong, surgeon of the 32nd Infantry, died in Manila. “The cause of death,” the brief obituary said, “is given as leukemia.”

By 1913, several types of leukemia were known, although none were treatable. On Dec. 2 of that year, The Times mentioned the illness in a report on the death of a Cornell student “suffering from a grave blood disease described by the hospital authorities as acute lymphatic leukemia.” This was also the first mention of an attempt to treat the disease — with a blood transfusion from the patient’s twin brother.

The next failed treatment noted in the paper was radium. On May 3, 1915, The Times reported that radium “has also been found effective in leukemia,” but then acknowledged that “patients might even succumb to the poisons released into the system.” Still, this was the first mention of a treatment, radiation therapy, that today remains one of the treatments for the illness.

The disease began to get significant public recognition only in the late 1920s. On March 5, 1927, The Times reported that a “Dutch gentleman” had offered an award of 25,000 guilders “for the most satisfactory treatise on the treatment of leukemia.” On April 3, 1934, in an article about a dying 4-year-old girl, a reporter described the disease as “an overabundance of white corpuscles in the blood,” adding that “its cure is infrequent.”

Throughout the 1930s, leukemia was frequently mentioned as a cause of illness and almost inevitable death, often in connection with heroic blood donations and transfusions in ultimately futile attempts to cure it. The disease, discovered almost a century before, had now become part of the public discourse.

The first suggestion to readers of The Times that a chemical approach might work was on April 13, 1946, when an anonymous reporter noted that because some of the chemicals tested and rejected for malaria treatment “destroy white blood cells, they may yet have their uses in leukemia.”

Today, more than 100 years after the first mention of the disease in The Times, treatment is complex, involving the skills of many specialists — hematologists, medical and radiation oncologists, pediatric leukemia specialists, nurses and dietitians. The many types of leukemia can be successfully treated, and sometimes cured, with chemotherapy, stem cell transplants and biological therapies that enhance the body’s immune system.

A Lymphoma

Source(google.com.pk)
A Lymphoma Biography
I started a new treatment in March, a week late, as I had to help move my grandma, since only one of her 6 children (plus 5 spouses) would help. My bf was going to help, but she changed the moving date, and he had already booked a day off for moving her.
So my mother and I were the only ones there to move her.

In April, I woke up with a swollen face, for no particular reason. Or at least, no reason was found.

I got a hickman line for my treatment, because my veins are so small, etc. I feel sorry for the nurses who have to find my veins. I have freaked a few out, causing them to poke and search numerous times for ONE IV insertion.

In May, the line got infected… I took a road trip to Wichita, Kansas from Buffalo, NY. 20 hour drive! With the stops for food, gas, rest, etc. it took 24 hours. I was very excited that my time estimation was right on! And I over estimated the fuel costs, so we had a good trip overall.

I woke up again beginning of June, with a swollen face. This time it was more intense, and went down to my throat. It was so bad that it altered my voice! I went to the local urgent care, and got a shot of Benedryl and a steroid shot. One in each buttock! OUCH!
I ended up in hospital for a week in June, for an undetermined infection. That was “fun”! It was during the 2nd week of my daughter’s summer visit. But I called her everyday, a few times a day. My friend was also going through a rough time, due to domestic abuse.

My hickman line was removed in July. That took a while to heal, due to the infection.

August was pretty uneventful, thankfully. August was also the end of my treatment.

First weekend of September, I spiked a fever of 105! Again I was admitted to hospital for a week. The doctor I had that time was insane, inconsiderate and useless. She did some of the stupidest things. Didn’t give me blood until 3 days after being there, when I went in with a low hemoglobin, and it dropped further the next day. Then she gave me something after the blood to help flush the excess fluids… this was at MIDNIGHT! The next day I had to take medical transport 2 hours away to go see my oncologist, so due to the medication she gave me to flush the fluids, we had to stop, so we were late. Didn’t help that the transport arrived to pick me up late, AND we had to stop for GAS! Crazy people!

October was somewhat crazy, because I was moving, and no one showed up to help, so it took my bf and I 2 weeks to move our stuff across the street. We were supposed to have the last 2 weeks of September to move our things into the new place, but the maintenance guy didn’t finish things until the last week, and left such a huge mess, that it took me 2 days to clean up after him! OH! To add to the stress of moving, I’d had a spot on my leg for over a month, that initially I thought was a mosquito bite, but it wasn’t itchy, so I eventually forgot about it. Well, suddenly, one day at the beginning of October, it started to itch, then a day later, it got sore. The next day it started to swell! I went to the urgent care again, for this. The doctor’s assumption was an ingrown hair. She told me that she could not be sure, without cutting it open. But she gave me antibiotics (At this point, I’d pretty much been on some form of antibiotics for the past 4-6 months!). A couple days later, it had swollen to the size of a quarter, and was at least half an inch high. It could barely walk (oh yeah, it was just to the front of my inner thigh). Finally, I’d had enough. I burst it open, because the pressure was SO intense! Oh my goodness, the nasty puss that came out of that thing, and the amount of it. WOW! Immediate relief from the pressure. But now I had to keep it clean, by flushing with saline solution. Thankfully, I had some left from when I’d had the hickman line. There is still a mark, I don’t think it will ever go away.

November was ok. December was my birthday and Christmas. And the year is done. We are not doing any testing beyond blood work, unless/until my symptoms return.

OH, and after all the years of chemotherapy, radiation, stem cell transplant, etc. I am finally gone into menopause. These hot flashes and mood swings are awful, and I feel very sorry for my wonderful boyfriend. Thankfully, he is wonderful; he has been amazing through all this stuff. I appreciate him more than I could ever express.

Lymphoma And

Source(google.com.pk)
Lymphoma And Articles
The TNF receptor superfamily members are all type I membrane glycoproteins with typical homology in the extracellular domain of variable numbers of cysteine-rich repeats (overall homologies, 25% to 30%). In contrast, the TNF ligand superfamily members (with the exception of LT alpha) are type II membrane glycoproteins with homology to TNF in the extracellular domain (overall homologies, 20%). TNF and LT alpha are trimeric proteins and are composed of beta-strands forming a beta-jellyroll. The homology of the beta-strand regions for the TNF ligand superfamily members suggest a similar beta-sandwich structure and possible trimeric or multimeric complex formation for most or all members. A genetic linkage, as evidence for evolutionary relatedness, is found by chromosomal cluster of TNFR p80, CD30, 4–1BB, and OX40 for 1p36; TNFR p60, TNFR-RP, and CD27 for 12p13; TNF, LT alpha, and LT beta for 6 (MHC locus); CD27L and 4–1BBL for 19p13; and FASL and OX40L for 1q25. Of the TNF ligand superfamily, TNF, LT alpha, and LT beta and their receptors (TNFR p60, TNFR p80, and TNFR-RP) interact in a complex fashion of cross-binding. However, the other family members presently have a one ligand/one receptor binding principle (CD27/CD27L, CD30/CD30L, CD40/CD40L, 4–1BB/4–1BBL, OX40/gp34, and FAS/FASL). In general, the members of the TNF ligand superfamily mediate interaction between different hematopoietic cells, such as T cell/B cell, T cell/monocyte, and T cell/T cell. Signals can be transduced not only through the receptors but also through at least some of the ligands. The transduced signals can be stimulatory or inhibitory depending on the target cell or the activation state. Taken together, TNF superfamily ligands show for the immune response an involvement in the induction of cytokine secretion and the upregulation of adhesion molecules, activation antigens, and costimulatory proteins, all known to amplify stimulatory and regulatory signals. On the other hand, differences in the distribution, kinetics of induction, and requirements for induction support a defined role for each of the ligands for T-cell-mediated immune responses. The shedding of members of the TNF receptor superfamily could limit the signals mediated by the corresponding ligands as a functional regulatory mechanism. Induction of cytotoxic cell death, observed for TNF, LT alpha, CD30L, CD95L, and 4–1BBL, is another common functional feature of this cytokine family. Further studies have to identify unique versus redundant biologic and physiologic functions for each of the TNF superfamily ligands.(ABSTRACT TRUNCATED AT 400 WORDS)

Epstein-Barr virus (EBV)-specific DNA sequences were detected by polymerase chain reaction analysis in 15 of 47 (32%) DNA extracts prepared from CD30-positive (Ki-1 antigen-positive) anaplastic large cell (ALC) lymphomas. EBV-encoded RNA (EBER) transcripts could be detected by in situ hybridization in the tumor cells of 9 of 11 EBV DNA- positive cases. Twenty-eight cases were examined by immunohistology on cryostat sections for the presence of the EBV-encoded latent membrane protein (LMP), the nuclear antigen 2 (EBNA2), the BZLF1 transactivator protein, and the late viral glycoprotein gp350/250. A distinct LMP- specific membrane and cytoplasmic staining was detected exclusively in lymphoma cells of five cases (18%); two of these cases additionally expressed EBNA2. BZLF1 protein and gp350/250 immunoreactivity was absent in all instances. All LMP-positive cases contained EBV DNA and EBER sequences. The pattern of EBV latent protein expression in ALC lymphomas showed heterogeneity with respect to EBNA2 expression: LMP- positive/EBNA2-negative cases displayed a pattern previously described for undifferentiated nasopharyngeal carcinomas and Hodgkin's disease, whereas LMP-positive and EBNA2-positive cases showed parallels to lymphoblastoid cell lines. Because the LMP gene has transforming potential, our findings support the concept of a pathoetiologic role for EBV in a proportion of CD30-positive ALC lymphomas.


OBJECTIVE: To review recent studies of systemic therapy for mycosis fungoides and the S�zary syndrome (cutaneous T-cell lymphomas).

DATA SOURCES: English-language articles indexed in MEDLINE from 1988 through 1994.

STUDY SELECTION: All therapeutic studies were selected.

DATA EXTRACTION: The data were abstracted without judgments on response criteria or patient numbers. Data quality and validity were assessed by independent author reviews.

DATA SYNTHESIS: No systemic therapy cures patients with cutaneous T-cell lymphomas. Single and combined chemotherapeutic agents produce high response rates. Whether any of these is preferred is not established. A randomized trial comparing combination chemotherapy plus radiation therapy with topical therapy showed no survival benefit for the combination. Several adenosine analogs and retinoids were active, but their optimal use is uncertain. Interferons are as active as chemotherapeutic agents and may be less toxic. Interferon combined with psoralen plus ultraviolet A light therapy produces high complete response rates and long-lasting remissions. Combinations with other systemic therapies do not increase response rates. Photopheresis therapy should be regarded as experimental. Promising preliminary results were seen with interleukin-2 fusion toxins and several antibody conjugates.

CONCLUSIONS: Systemic therapy should be considered effective and palliative. The principles of treating all low-grade lymphomas can be applied. Randomized trials are needed to evaluate new agents (such as a comparison of psoralen plus ultraviolet light with or without interferon), and large phase II trials are needed for new agents such as photopheresis, interleukin-2 fusion toxin, temozolomide, and others.