… those who saw a palliative care specialist stopped chemotherapy sooner, entered hospice far earlier, experienced less suffering at the end of their lives—and they lived 25 percent longer. In other words, our decision making in medicine has failed so spectacularly that we have reached the point of actively inflicting harm on patients rather than confronting the subject of mortality. If end-of-life discussions were an experimental drug, the FDA would approve it.

JWT Brazil introduces: “Superformula” to fight cancer.

The first step in the fight against cancer is believing in the cure. But the chemotherapy treatment is difficult, especially for a child. To help them believe, we worked with the A.C.Camargo Cancer Center and another client of the agency, Warner Bros., to create an idea capable of changing their negative perception of the treatment:

Transform the chemotherapy into a “Superformula.”

We made covers for intravenous bags based on characters from the ‘Justice League.’ Creating, for the first time, a child-friendly version of the treatment. Co-developed with doctors, the covers are easy to sterilize and handle and meet all hospital hygiene standards. To give these covers a more powerful meaning, we started to produce a special series of cartoons and comic books in which the superheroes go through experiences similar to those of kids with cancer, and recover their strength, thanks to this “Superformula.”

An experience that went far beyond the covers by also providing a new look to the entire Children'sWard: the game room was turned into the Hall of Justice, corridors and doors were decorated in the same theme, and the exterior acquired an exclusive entrance for these little heroes.

An idea which, since it has been up and running, is helping the children in their own struggle against one of the real world’s greatest villains.

Italian scientists unravel brain tumour growth process.

Scientists have discovered the mechanism that allows the survival of cancer stem cells in glioblastoma, the most aggressive and lethal type of brain tumour. A key element in the process is the protein ID2, which can trigger off a chain of events leading to both the onset and progression of glioblastomas. The discovery has been reported in an article in the journal Nature by a group of researchers from Columbia University in New York, led by Antonio Iavarone and Anna Lasorella. The scientists believe that by “inactivating” the protein, it will be possible to block tumour growth.

The protein ID2 promotes the reproduction of the cancer stem cells at the root of tumours, and encourages their growth by continuing to generate further new cells. These are difficult to eradicate, even using highly aggressive treatments such as radiotherapy and chemotherapy. The importance of this study lies in its identification of the mechanisms that activate ID2, but also in the discovery of how the protein ID2, when activated in human cancer, encourages the uncontrolled growth of cancer stem cells. By blocking ID2 activation mechanisms, researchers aim to contain the spread of tumours or prevent their reappearance after surgery. Glioblastoma is the most common and malignant form of brain tumour, and affects individuals of all ages including children, although it is most common between the ages of 45 and 70.

Unfortunately, surgery, combined with radiotherapy and chemotherapy, is not yet effective against this type of cancer, and the life expectancy of sufferers is usually under two years. This is why an increased understanding of the mechanisms that cause glioblastoma to develop and make it so difficult to treat is the only way it can be combated more effectively. The ID2 protein is known to be an inhibitor of cell differentiation in the embryo, when the active division and subsequent differentiation of the stem cells of various tissues is necessary for the formation of organs specialising in a variety of functions (brain, muscles, bones, etc.). Under normal conditions, ID2 is released when cells stop dividing and start to differentiate, but in the case of glioblastoma, ID2 is activated abnormally.

“Our study found that ID2 remains active due to reduced oxygen concentration in the growing tumour. In the “inappropriately active” form, ID2 is capable of blocking the system which destroys two proteins called Hypoxia Inducible Factor (HIF) alpha 1 and 2, whose action is particularly important for the survival of cancer stem cells in the absence of adequate levels of oxygen and nourishment. In practice, ID2 allows more malignant glioblastoma cells to adapt and survive even in extremely unfavourable conditions, and to continue to multiply without losing their stem-cell identity,” said Anna Lasorella, professor of pediatrics and pathology at Columbia University, who, together with Professor Antonio Iavarone, heads the team of scientists behind the study.

Antonio Iavarone explained that “By inactivating ID2, we obviously deprive the tumour of a process essential to its preservation. Understanding the sequence of events that glioblastoma, and possibly other human cancers rely on to survive, this is an important step towards new therapeutic strategies. Nevertheless, this is not yet a cure, and further studies are required before the new discovery can be translated into treatment.”


World’s first pelvis transplant carried out in Italy.

The Centre for Orthopaedic Trauma (CTO) in Turin, Italy, has performed the world’s first pelvis transplant, an operation that saved the life of an 18-year-old suffering from osteosarcoma. The condition was considered inoperable and the boy responded quite well to 16 cycles of chemotherapy, but the doctors didn’t stop at the traditional treatment, racking their brains to find a definitive solution.

Osteosarcoma is a cancerous tumor in a bone. Specifically, it is an aggressive malignant neoplasm that arises from primitive transformed cells of mesenchymal origin (and thus a sarcoma) and that exhibits osteoblastic differentiation and produces malignantosteoid. Osteosarcoma is the most common histological form of primary bone cancer and it is most prevalent in children and young adults. It tend to occur at the sites of bone growth, presumably because proliferation makes osteoblastic cells in this region prone to acquire mutations that could lead to transformation of cells (RB gene and p53 gene are commonly involved).

In an 11.5-hour operation, surgeons removed half the patient’s pelvis along with part of his hip affected by the cancer, replacing them with a prosthetic made in the United States from titanium covered in tantalum, a non-corrosive metal mainly used in electronics components.

The operation had “an excellent outcome” and the patient is now undergoing intensive therapy to help him adapt to his new pelvis, the hospital said in a statement.

(Picture by Alexey Kashpersky).

Cancer-fighting viruses win approval
US regulators clear a viral melanoma therapy, paving the way for a promising field with a chequered past.

This is pretty exciting. The approved treatment uses a virus named Talimogene laherparepvec, (often referred to as T-VEC) that has been genetically engineered to attack tumor cells.

It has been modified to only attack rapidly dividing cells, which means that it preferentially attacks cancer cells and leaves normal cells alone. The treatment involved injecting the virus into tumors, where it kills the cancerous cells and lyses, or splits them open. The virus releases a chemical called GM-CSF that summons the immune system to the scene. The immune cells identify the broken-open cancer cells as a threat, and spread throughout the body and kill other cells with the same pattern, effectively wiping out any cancer that might have spread:

The linked article goes into a lot more detail on the approval process, and covers some of the history of anti-cancer viruses. This wikipedia article on T-VEC gives some information about how the virus was modified from the original to make it an effective cancer-fighter.

Image Credit for virus action Wikimedia user CaptainVivacious

Gene editing saves girl dying from leukaemia in world first.

It’s got all the elements of a movie script — a dying baby, desperate parents, and a team of doctors with a completely untried and highly experimental treatment. With nothing to lose, they try it on the baby. And…it works. Maybe. Maybe not. But one-year-old Layla Richards is better, and everyone involved is elated.

Layla was diagnosed with acute lymphoblastic leukemia when she was just three months old, a disease in which cancerous stem cells in the bone marrow release vast numbers of immature immune cells into the blood. She was immediately taken to Great Ormond Street to start the standard treatment of chemotherapy followed by a bone marrow transplant to restore the immune system.

In older children, this treatment is usually successful, says Sujith Samarasinghe, a leukaemia specialist at the hospital and one of Layla’s doctors. But for children as young as Layla, the cure rates are only 25 per cent. Layla was one of the unlucky ones. Cancerous cells were still detectable after the chemotherapy. Despite this, it was decided to go ahead with a bone marrow transplant. “We hoped for a graft-versus-leukaemia reaction,” says Paul Veys, head of bone marrow transplants at the hospital. This is where immune cells in the donor bone marrow attack the cancer – but this failed too.

The approach is called gene editing. It’s a way to modify the body’s cells in a very precise way — much more precise than old-fashioned gene therapy, in which new genes are inserted somewhat haphazardly into a cell’s nucleus.

In this case, the team at Great Ormond Street Hospital in London had developed a batch of immune system cells called T-cells that are precisely snipped in just the right way to prevent them from attacking the patient’s own cells. They’re also modified to resist chemotherapy drugs. And they’re boosted to attack leukemia cells.

Unlike approaches being used by other teams, which modify a patient’s own T-cells, this allows for a donor’s cells to be used in a patient. It worked, the team is preparing to tell a meeting of the American Society of Hematology next month. “The treatment was highly experimental and we had to get special permissions, but she appeared ideally suited for this type of approach,” said Waseem Qasim, the researcher at Great Ormond Street Hospital who led the experiment.

(To read more).

Patho-morphology of Heart:

1 :- Heart injured by bullet
2:- Heart of patient with atrial myxoma
3:- Heart of teen with drug addiction
4:- Heart of patient with high fat/cholesterol

Do you want to share this with your ❤️ friends? So, please tag him/her……

#heart #cardiology #pathology #anatomy #cardiologist #tumor #oncology #physiology #usmle #university #usmlestep1 #usmlestep2 #doctor #doctordconline #nhs #premed @doctordconline #nurse #nursing #amc #plab #medicine #medstudent #medlife #hospital #patient


Oncologist Jim Olson received a standing ovation at PopTech 2013 yesterday after he delivered a moving talk about working in pediatric oncology and what inspired his creation of “tumor paints” to light up and locate cancerous cells during surgery.


The black liquid was aspirated from a growing mass on the shoulder of a 2y.o. male neutered crossbreed dog. After sending the sample to the labs, it was suspected to be a pigmented basal cell carcinoma, so we made the quick decision to book him in for surgical excision.

After removing the mass, we sent the mass to the labs again for histopathology analysis, which came back and said it was a benign follicular cyst!

This highlights the importance to always perform histopathology on masses you remove!


A Dangerous TransitionAnne Weston

Just as embryonic cells undergo an epithelial to mesenchymal transition during gastrulation, cancer cells can reactivate this developmental program to become motile and metastasize to other tissues. During this “EMT,” adherens junction components, such as E-cadherin and β-catenin, are targeted for destruction, while the activation of the GTPases Cdc42 and Rac1 favors the formation of lamellipodia and filopodia, migration, and invasion.

Bone cancer cell (nucleus in light blue)

This image shows an osteosarcoma cell with DNA in blue, energy factories (mitochondria) in yellow and actin filaments, part of the cellular skeleton, in purple. One of the few cancers that originate in the bones, osteosarcoma is extremely rare, with less than a thousand new cases diagnosed each year in the United States.

Image courtesy of Dylan Burnette and Jennifer Lippincott-Schwartz, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health. Part of the exhibit Life:Magnified by ASCB and NIGMS.


An Ependymoma is a glial tumour which originate from the ependymal cells that line the ventricles of the brain, or the central canal of the spinal cord. These tumours typically account for 10% of all paediatric brain tumours, and 33% of brain tumours in the under 3 age category - with the mean age of diagnosis being 6 years old. The symptoms of ependymoma tend to be associated with raised intracranial pressure, and can present as headaches, nausea and vomiting, vision or balance disturbances or personality changes. Treatment and prognosis of these tumours depends on the grade and location.

A scanning electron micrograph of ovarian cancer cells forming a small tumor. Image courtesy of the University of Gothenburg.

Potential New Way to Suppress Tumor Growth Discovered

Researchers at the University of California, San Diego School of Medicine, with colleagues at the University of Rochester Medical Center, have identified a new mechanism that appears to suppress tumor growth, opening the possibility of developing a new class of anti-cancer drugs.

Writing in this week’s online Early Edition of the Proceedings of the National Academy of Sciences (PNAS), Willis X. Li, PhD, a professor in the Department of Medicine at UC San Diego, reports that a particular form of a signaling protein called STAT5A stabilizes the formation of heterochromatin (a form of chromosomal DNA), which in turn suppresses the ability of cancer cells to issue instructions to multiply and grow.

Specifically, Li and colleagues found that the unphosphorylated form of STAT promotes and stabilizes heterochromatin, which keeps DNA tightly packaged and inaccessible to transcription factors. “Therefore, genes ‘buried’ in heterochromatin are not expressed,” explained Li.

Phosphorylation is a fundamental cellular function in which a phosphate group is added to a protein or molecule, causing it to turn it on or off or to alter its function. An unphosphorylated STAT lacks this phosphate group. 

More here