Category Archives: Cell Medicine

A study led by researchers at the University of Arizona Health Sciences discovered new information about the inner workings of the immune system that could have a profound impact on T cell therapies for cancer and other diseases.

T cells are a type of white blood cell essential to the immune system and defending the body against infection. The CD4 molecule is found on the surface of many T cells and has historically been thought to only play a supporting role in the cells functions. The paper, Enhancing and inhibitory motifs regulate CD4 activity, published in eLife, shows CD4 plays a more active role in regulating T cell receptor signaling.

The study took a unique evolutionary approach to the immune system by examining the ways T cells have changed or remained the same over time. Michael Kuhns, PhD, associate professor in the UArizona College of Medicine Tucsons Department of Immunobiology, and Koenraad Van Doorslaer, PhD, assistant professor in the UArizona College of Agriculture and Life Sciences School of Animal and Comparative Biomedical Sciences, assembled a team that focused on the evolution and function of CD4.

This study is giving us a better appreciation for how CD4 works in concert with the T cell receptor to naturally direct T cells, said Dr. Kuhns who serves on theCenter for Advanced Molecular and Immunological Therapies advisory committee. CD4 is very much a co-equal player in antigen recognition and T cell activation.

The findings allow researchers to paint a more accurate evolutionary blueprint of the mechanisms within CD4 that could allow for even more powerful versions of T cell therapy. Chimeric antigen receptor (CAR) T cell therapy is already being used for some forms of cancer. Dr. Kuhnsandresearchers at the Harvard Medical School-affiliated Joslin Diabetes Center, are currently testing genetically engineered five-module CAR T cells as a possible treatment for Type 1 diabetes.

Drs. Kuhns and Van Doorslaer, both members of theBIO5 Institute, looked at CD4 from several different species, from fish to human, to explore more than 400 million years of the molecules evolution. They identified regions in CD4 that are unique to mammals.

We looked at what amino acids in these proteins changed, and what amino acids in these proteins stayed the same, Dr. Van Doorslaer said. The idea being, if they didn't change, they could be important for the function of the protein.

The research team discovered conserved sequences of amino acids, called motifs, then worked to find out how the motifs enhanced or inhibited CD4 activity. They designed genes with mutated motifs and introduced them into a T cell system, then looked at the proteins response where it went in the cell, what it interacted with, and how it impacted signaling events and outcomes. They found different combinations of motifs resulted in varying degrees of upregulation and downregulation.

If you think about T cells as being driven by molecular machines, what we do is take the machines apart to figure out how they were built, Dr. Kuhns said. CD4 seems to be really important to the function of T cells, because evolution doesn't want it to change. We went in and changed it, which is like looking at how the car works in the absence of the tires.

More work needs to be done to measure the differing contributions the motifs make to CD4 function. Eventually, the research could lead to the engineering of more finely tuned synthetic receptors for T cell therapies.

The research reported on in this release was supported in part by the National Institute of Allergy and Infectious Diseases (R01AI101053).

Read the original:
Study Uncovers Possible Path for Improving T Cell Therapies - University of Arizona

-- 3.2 Month Survival Benefit Demonstrated in Patients who had Already Received Prior Endocrine-based Therapy and at Least Two Prior Chemotherapies --

-- Trodelvy Now Shows a Survival Benefit in both Pre-treated HR+/HER2- Metastatic Breast Cancer and Second-Line Metastatic Triple-Negative Breast Cancer --

FOSTER CITY, Calif.--(BUSINESS WIRE)--Gilead Sciences, Inc. (Nasdaq: GILD) today announced the positive overall survival (OS) results from the Phase 3 TROPiCS-02 study evaluating Trodelvy (sacituzumab govitecan-hziy) versus comparator chemotherapy (physicians choice of chemotherapy, TPC) in patients with HR+/HER2- metastatic breast cancer who received endocrine-based therapies and at least two chemotherapies. In the study, Trodelvy demonstrated a statistically significant and clinically meaningful improvement of 3.2 months in OS compared to TPC (median OS: 14.4 months vs. 11.2 months; hazard ratio [HR]=0.79; [95% confidence interval [CI]: 0.65-0.96]; p=0.02). OS was a key secondary endpoint of the trial.

These findings will be presented on Friday, September 9 at 4:20pm CEST during the European Society for Medical Oncology (ESMO) Congress 2022 as a late-breaking oral presentation (#LBA76) in the Brest Auditorium, Paris Expo Porte de Versailles.

Other key secondary endpoints including objective response rate (ORR) demonstrated statistically significant improvement in favoring Trodelvy versus TPC. Time to deterioration (TTD) of Global Health Status/Quality of Life (QoL) and Fatigue scale per EORTC-QLQ-C30 also favored Trodelvy versus TPC (QoL: 4.3 months vs. 3.0 months, p=0.006; Fatigue: 2.2 months vs. 1.4 months, p=0.002). No statistically significant difference in TTD on the Pain Scale was observed.

It is outstanding to see a clinically meaningful survival benefit of over three months for patients with pre-treated HR+/HER2- metastatic breast cancer, said Hope S. Rugo, MD, Professor of Medicine and Director, Breast Oncology and Clinical Trials Education at the University of California San Francisco Comprehensive Cancer Center, U.S. Nearly all patients with HR+/HER2- metastatic breast cancer will develop resistance to endocrine-based therapies even in combination with targeted agents, so these data are welcome news for the breast cancer community. The results of TROPiCS-02 highlight the potential for sacituzumab govitecan in patients with pre-treated HR+/HER2- metastatic breast cancer.

The safety profile for Trodelvy was consistent with prior studies, with no new safety signals identified in this patient population.

With these data from TROPiCS-02, Trodelvy has now demonstrated a survival benefit in both pre-treated HR+/HER2- metastatic breast cancer and second-line metastatic TNBC two difficult-to-treat forms of breast cancer, said Bill Grossman, MD, PhD, Senior Vice President, Therapeutic Area Head, Gilead Oncology. Our Gilead Oncology ambition is to transform care for people with cancer, and the meaningful improvement in survival benefit seen in the TROPiCS-02 study with Trodelvy is another step forward in pursuing this ambition for patients.

The TROPiCS-02 study met its primary endpoint of progression-free survival earlier this year; detailed results were presented during the 2022 American Society of Clinical Oncology (ASCO) Annual Meeting.

Trodelvy has not been approved by any regulatory agency for the treatment of HR+/HER2- metastatic breast cancer. Its safety and efficacy have not been established for this indication. Gilead has submitted a supplemental Biologics License Application (sBLA) to the U.S. Food and Drug Administration (FDA) based on data from TROPiCS-02; these data will also be shared with health authorities outside the U.S.

Sacituzumab govitecan-hziy is currently included in the National Comprehensive Cancer Network (NCCN) Clinical Practice Guidelines in Oncology (NCCN Guidelines)i. This includes a Category 1 recommendation for use in adult patients with second-line metastatic triple-negative breast cancer (defined as those who received at least two prior therapies, with at least one line for metastatic disease). It also has a Category 2A preferred recommendation for investigational use in HR+/HER2- advanced breast cancer after prior treatment including endocrine therapy, a CDK4/6 inhibitor and at least two lines of chemotherapy.

Trodelvy has a Boxed Warning for severe or life-threatening neutropenia and severe diarrhea; please see below for additional Important Safety Information.

About HR+/HER2- Breast Cancer

Hormone receptor-positive/human epidermal growth factor receptor 2-negative (HR+/HER2-) breast cancer is the most common type of breast cancer and accounts for approximately 70% of all new cases, or nearly 400,000 diagnoses worldwide each year. Almost one in three cases of early-stage breast cancer eventually become metastatic, and among patients with HR+/HER2- metastatic disease, the five-year relative survival rate is 30%. As patients with HR+/HER2- metastatic breast cancer become resistant to endocrine-based therapy, their primary treatment option is limited to single-agent chemotherapy. In this setting, it is common to receive multiple lines of chemotherapy regimens over the course of treatment, and the prognosis remains poor.

About the TROPiCS-02 Study

The TROPiCS-02 study is a global, multicenter, open-label, Phase 3 study, randomized 1:1 to evaluate Trodelvy versus physicians choice of chemotherapy (eribulin, capecitabine, gemcitabine, or vinorelbine) in 543 patients with HR+/HER2- metastatic breast cancer who were previously treated with endocrine therapy, CDK4/6 inhibitors and two to four lines of chemotherapy for metastatic disease. The primary endpoint is progression-free survival per Response Evaluation Criteria in Solid Tumors (RECIST 1.1) as assessed by blinded independent central review (BICR) for participants treated with Trodelvy compared to those treated with chemotherapy. Secondary endpoints include overall survival, overall response rate, clinical benefit rate and duration of response, as well as assessment of safety and tolerability and quality of life measures. In the study, HER2 negativity was defined per American Society of Clinical Oncology (ASCO) and the College of American Pathologists (CAP) criteria as immunohistochemistry (IHC) score of 0, IHC 1+ or IHC 2+ with a negative in-situ hybridization (ISH) test. More information about TROPiCS-02 is available at https://clinicaltrials.gov/ct2/show/NCT03901339.

About Trodelvy

Trodelvy (sacituzumab govitecan-hziy) is a first-in-class Trop-2 directed antibody-drug conjugate. Trop-2 is a cell surface antigen highly expressed in multiple tumor types, including in more than 90% of breast and bladder cancers. Trodelvy is intentionally designed with a proprietary hydrolyzable linker attached to SN-38, a topoisomerase I inhibitor payload. This unique combination delivers potent activity to both Trop-2 expressing cells and the microenvironment.

Trodelvy is approved in more than 35 countries, with multiple additional regulatory reviews underway worldwide, for the treatment of adult patients with unresectable locally advanced or metastatic triple-negative breast cancer (TNBC) who have received two or more prior systemic therapies, at least one of them for metastatic disease. Trodelvy is also approved in the U.S. under the accelerated approval pathway for the treatment of adult patients with locally advanced or metastatic urothelial cancer (UC) who have previously received a platinum-containing chemotherapy and either programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor.

Trodelvy is also being developed for potential investigational use in other TNBC and metastatic UC populations, as well as a range of tumor types where Trop-2 is highly expressed, including hormone receptor-positive/human epidermal growth factor receptor 2-negative (HR+/HER2-) metastatic breast cancer, metastatic non-small cell lung cancer (NSCLC), metastatic small cell lung cancer (SCLC), head and neck cancer, and endometrial cancer.

U.S. Indications for Trodelvy

In the United States, Trodelvy is indicated for the treatment of:

U.S. Important Safety Information for Trodelvy

BOXED WARNING: NEUTROPENIA AND DIARRHEA

CONTRAINDICATIONS

WARNINGS AND PRECAUTIONS

Neutropenia: Severe, life-threatening, or fatal neutropenia can occur and may require dose modification. Neutropenia occurred in 61% of patients treated with Trodelvy. Grade 3-4 neutropenia occurred in 47% of patients. Febrile neutropenia occurred in 7%. Withhold Trodelvy for absolute neutrophil count below 1500/mm3 on Day 1 of any cycle or neutrophil count below 1000/mm3 on Day 8 of any cycle. Withhold Trodelvy for neutropenic fever.

Diarrhea: Diarrhea occurred in 65% of all patients treated with Trodelvy. Grade 3-4 diarrhea occurred in 12% of patients. One patient had intestinal perforation following diarrhea. Neutropenic colitis occurred in 0.5% of patients. Withhold Trodelvy for Grade 3-4 diarrhea and resume when resolved to Grade 1. At onset, evaluate for infectious causes and if negative, promptly initiate loperamide, 4 mg initially followed by 2 mg with every episode of diarrhea for a maximum of 16 mg daily. Discontinue loperamide 12 hours after diarrhea resolves. Additional supportive measures (e.g., fluid and electrolyte substitution) may also be employed as clinically indicated. Patients who exhibit an excessive cholinergic response to treatment can receive appropriate premedication (e.g., atropine) for subsequent treatments.

Hypersensitivity and Infusion-Related Reactions: Serious hypersensitivity reactions including life-threatening anaphylactic reactions have occurred with Trodelvy. Severe signs and symptoms included cardiac arrest, hypotension, wheezing, angioedema, swelling, pneumonitis, and skin reactions. Hypersensitivity reactions within 24 hours of dosing occurred in 37% of patients. Grade 3-4 hypersensitivity occurred in 2% of patients. The incidence of hypersensitivity reactions leading to permanent discontinuation of Trodelvy was 0.3%. The incidence of anaphylactic reactions was 0.3%. Pre-infusion medication is recommended. Observe patients closely for hypersensitivity and infusion-related reactions during each infusion and for at least 30 minutes after completion of each infusion. Medication to treat such reactions, as well as emergency equipment, should be available for immediate use. Permanently discontinue Trodelvy for Grade 4 infusion-related reactions.

Nausea and Vomiting: Nausea occurred in 66% of all patients treated with Trodelvy and Grade 3 nausea occurred in 4% of these patients. Vomiting occurred in 39% of patients and Grade 3-4 vomiting occurred in 3% of these patients. Premedicate with a two or three drug combination regimen (e.g., dexamethasone with either a 5-HT3 receptor antagonist or an NK1 receptor antagonist as well as other drugs as indicated) for prevention of chemotherapy-induced nausea and vomiting (CINV). Withhold Trodelvy doses for Grade 3 nausea or Grade 3-4 vomiting and resume with additional supportive measures when resolved to Grade 1. Additional antiemetics and other supportive measures may also be employed as clinically indicated. All patients should be given take-home medications with clear instructions for prevention and treatment of nausea and vomiting.

Increased Risk of Adverse Reactions in Patients with Reduced UGT1A1 Activity: Patients homozygous for the uridine diphosphate-glucuronosyl transferase 1A1 (UGT1A1)*28 allele are at increased risk for neutropenia, febrile neutropenia, and anemia and may be at increased risk for other adverse reactions with Trodelvy. The incidence of Grade 3-4 neutropenia was 67% in patients homozygous for the UGT1A1*28, 46% in patients heterozygous for the UGT1A1*28 allele and 46% in patients homozygous for the wild-type allele. The incidence of Grade 3-4 anemia was 25% in patients homozygous for the UGT1A1*28 allele, 10% in patients heterozygous for the UGT1A1*28 allele, and 11% in patients homozygous for the wild-type allele. Closely monitor patients with known reduced UGT1A1 activity for adverse reactions. Withhold or permanently discontinue Trodelvy based on clinical assessment of the onset, duration and severity of the observed adverse reactions in patients with evidence of acute early-onset or unusually severe adverse reactions, which may indicate reduced UGT1A1 function.

Embryo-Fetal Toxicity: Based on its mechanism of action, Trodelvy can cause teratogenicity and/or embryo-fetal lethality when administered to a pregnant woman. Trodelvy contains a genotoxic component, SN-38, and targets rapidly dividing cells. Advise pregnant women and females of reproductive potential of the potential risk to a fetus. Advise females of reproductive potential to use effective contraception during treatment with Trodelvy and for 6 months after the last dose. Advise male patients with female partners of reproductive potential to use effective contraception during treatment with Trodelvy and for 3 months after the last dose.

ADVERSE REACTIONS

In the ASCENT study (IMMU-132-05), the most common adverse reactions (incidence 25%) were fatigue, neutropenia, diarrhea, nausea, alopecia, anemia, constipation, vomiting, abdominal pain, and decreased appetite. The most frequent serious adverse reactions (SAR) (>1%) were neutropenia (7%), diarrhea (4%), and pneumonia (3%). SAR were reported in 27% of patients, and 5% discontinued therapy due to adverse reactions. The most common Grade 3-4 lab abnormalities (incidence 25%) in the ASCENT study were reduced neutrophils, leukocytes, and lymphocytes.

In the TROPHY study (IMMU-132-06), the most common adverse reactions (incidence 25%) were diarrhea, fatigue, neutropenia, nausea, any infection, alopecia, anemia, decreased appetite, constipation, vomiting, abdominal pain, and rash. The most frequent serious adverse reactions (SAR) (5%) were infection (18%), neutropenia (12%, including febrile neutropenia in 10%), acute kidney injury (6%), urinary tract infection (6%), and sepsis or bacteremia (5%). SAR were reported in 44% of patients, and 10% discontinued due to adverse reactions. The most common Grade 3-4 lab abnormalities (incidence 25%) in the TROPHY study were reduced neutrophils, leukocytes, and lymphocytes.

DRUG INTERACTIONS

UGT1A1 Inhibitors: Concomitant administration of Trodelvy with inhibitors of UGT1A1 may increase the incidence of adverse reactions due to potential increase in systemic exposure to SN-38. Avoid administering UGT1A1 inhibitors with Trodelvy.

UGT1A1 Inducers: Exposure to SN-38 may be substantially reduced in patients concomitantly receiving UGT1A1 enzyme inducers. Avoid administering UGT1A1 inducers with Trodelvy.

Please see full Prescribing Information , including BOXED WARNING.

About Gilead Sciences

Gilead Sciences, Inc. is a biopharmaceutical company that has pursued and achieved breakthroughs in medicine for more than three decades, with the goal of creating a healthier world for all people. The company is committed to advancing innovative medicines to prevent and treat life-threatening diseases, including HIV, viral hepatitis and cancer. Gilead operates in more than 35 countries worldwide, with headquarters in Foster City, California.

Forward-Looking Statements

This press release includes forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 that are subject to risks, uncertainties and other factors, including Gileads ability to initiate, progress or complete clinical trials within currently anticipated timelines or at all, and the possibility of unfavorable results from ongoing or additional clinical trials, including those involving Trodelvy; uncertainties relating to regulatory applications for Trodelvy and related filing and approval timelines, including with respect to the pending sBLA for Trodelvy, and pending or potential applications for the treatment of metastatic TNBC, mUC, HR+/HER2- breast cancer, NSCLC, SCLC, head and neck cancer, and endometrial cancer, in the currently anticipated timelines or at all; Gileads ability to receive regulatory approvals for such indications in a timely manner or at all, and the risk that any such approvals may be subject to significant limitations on use; the possibility that Gilead may make a strategic decision to discontinue development of Trodelvy for such indications and as a result, Trodelvy may never be commercialized for these indications; and any assumptions underlying any of the foregoing. These and other risks, uncertainties and other factors are described in detail in Gileads Quarterly Report on Form 10-Q for the quarter ended June 30, 2022, as filed with the U.S. Securities and Exchange Commission. These risks, uncertainties and other factors could cause actual results to differ materially from those referred to in the forward-looking statements. All statements other than statements of historical fact are statements that could be deemed forward-looking statements. The reader is cautioned that any such forward-looking statements are not guarantees of future performance and involve risks and uncertainties, and is cautioned not to place undue reliance on these forward-looking statements. All forward-looking statements are based on information currently available to Gilead, and Gilead assumes no obligation and disclaims any intent to update any such forward-looking statements.

U.S. Prescribing Information for Trodelvy including BOXED WARNING, is available at http://www.gilead.com .

Trodelvy, Gilead and the Gilead logo are trademarks of Gilead Sciences, Inc., or its related companies.

For more information about Gilead, please visit the companys website at http://www.gilead.com , follow Gilead on Twitter (@GileadSciences) or call Gilead Public Affairs at 1-800-GILEAD-5 or 1-650-574-3000.

i Referenced with permission from the NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines) for Breast Cancer Version 4.2022. National Comprehensive Cancer Network, Inc. 2022. All rights reserved. Accessed August 2022. To view the most recent and complete version of the guideline, go online to NCCN.org. NCCN makes no warranties of any kind whatsoever regarding their content, use or application and disclaims any responsibility for their application or use in any way.

View source version on businesswire.com: https://www.businesswire.com/news/home/20220906006036/en/

Jacquie Ross, Investorsinvestor_relations@gilead.com

Nathan Kaiser, MediaNathan.kaiser@gilead.com

Source: Gilead Sciences, Inc.

The rest is here:
Trodelvy Significantly Improved Overall Survival in Pre-Treated HR+/HER2- Metastatic Breast Cancer Patients in TROPiCS-02 Study - Gilead Sciences

A team of Israeli researchers based at Tel Aviv University have recently published research showing that eliminating or inhibiting the ability of brain cells called astrocytes to provide energy to glioblastoma cells resulted in cancer cell death and tumor regression. The team developed a method to achieve these results after discovering two mechanisms in the brain that support tumor growth and survival. One protects cancer cells from the immune system, and the other supplies the energy required for rapid tumor growth. Both mechanisms are controlled by astrocytes and, in their absence, the tumor cells die and are eliminated.

Glioblastoma is an extremely aggressive and invasive brain cancer, for which there exists no known effective treatment, the researchers noted in their paper published in the journal Brain. The tumor cells are highly resistant to all known therapies, and, sadly, patient life expectancy has not increased significantly in the last 50 years. Our findings provide a promising basis for the development of effective medications for treating glioblastoma and other types of brain tumors.

The study was led by doctoral candidate Rita Perelroizen, under the supervision of Dr. Lior Mayo of the Shmunis School of Biomedicine and Cancer Research and the Sagol School of Neuroscience, in collaboration with Prof. Eytan Ruppin of the National Institutes of Health (NIH).

For their study, the researchers used an animal model that allowed them to eliminate active astrocyte around the tumor. Applying their method to eradicate the astrocytes, the investigators found that all the cancer disappeared in the animals within days and all the animals survived. Animals that had the presence of astrocytes near their tumor all died within five weeks.

Here, we tackled the challenge of glioblastoma from a new angle. Instead of focusing on the tumor, we focused on its supportive microenvironment, that is, the tissue that surrounds the tumor cells, Mayo said. Specifically, we studied astrocytesa major class of brain cells that support normal brain function. Over the past decade, research from us and others revealed additional astrocyte functions that either alleviate or aggravate various brain diseases.

In the absence of astrocytes, the tumor quickly disappeared, and in most cases, there was no relapseindicating that the astrocytes are essential to tumor progression and survival, Mayo continued. But why did the astrocytes behave this way, essentially changing from cells that support normal brain activity to ones that help foster tumor growth. To get to the bottom of this, the researchers compared the gene expression profiles of astrocytes from health brains with those from glioblastoma tumors.

The team found two significant differences. The first related to how the immune system responded to glioblastoma. The tumor mass includes up to 40% immune cells mostly macrophages recruited from the blood or from the brain itself. Furthermore, astrocytes can send signals that summon immune cells to places in the brain that need protection. In this study, we found that astrocytes continue to fulfill this role in the presence of glioblastoma tumors. However, once the summoned immune cells reach the tumor, the astrocytes persuade them to change sides and support the tumor instead of attacking it, Mayo said.

The second change noted was how the astrocytes helped modulate glioblastomas access to energy needed to thrive, via the production and transfer of cholesterol to tumor cells. The investigators hypothesized that since the tumor cells were reliant on the cholesterol produced by the astrocytes as their main source of energy, eliminating it would starve the tumor.

To test their theory, Mayo and team engineered astrocytes near the tumor to stop expressing the specific proteinABCA1that transports cholesterol, effective preventing it from supplying the tumor. This method also produced good results, with the glioblastoma tumor dying within days. The researchers achieved these results in both animal models and glioblastoma samples taken from human patients.

This work sheds new light on the role of the blood-brain barrier in treating brain diseases. The normal purpose of this barrier is to protect the brain by preventing the passage of substances from the blood to the brain. But in the event of a brain disease, this barrier makes it challenging to deliver medications to the brain and is considered an obstacle to treatment. Our findings suggest that, at least in the specific case of glioblastoma, the blood-brain barrier may be beneficial to future treatments, as it generates a unique vulnerabilitythe tumors dependence on brain-produced cholesterol. We think this weakness can translate into a unique therapeutic opportunity, Mayo concluded.

View post:
Manipulating Astrocytes in Tumor Environment Effective Against Glioblastoma - Inside Precision Medicine

This month Jane Fonda, the Oscar-winning actress, and activist, announced she has been diagnosed with non-Hodgkins lymphoma (NHL), a type of cancer.

Fonda, 84, shared the news in a post on her Instagram account.

So, my dear friends, I have something personal I want to share, she wrote. Ive been diagnosed with non-Hodgkins lymphoma and have started chemo treatments.

However, her outlook was positive. This is a very treatable cancer, she continued. 80% of people survive, so I feel very lucky.

According to the American Cancer Society, NHL is a common cancer in the US accounting for 4% of all cases. The group estimates that in 2022 around 80,500 adults and children will be diagnosed with the disease.

This isnt Fondas first experience with cancer. She has previously spoken of having skin cancers removed, along with a non-cancerous tumor in her breast (before having a mastectomy several years later).

NHL is a cancer of one of your immune cells, lymphocytes. Its one of your blood cells, and their normal function is to fight infection, Dr. Dima El-Sharkawi, consultant hematologist at The Royal Marsden NHS Foundation Trust in London, told Healthline.

However, theres not just one type of NHL.

When we say NHL, thats a pretty wide umbrella, Dr. Guillermo de Angulo, pediatric hematologist/oncologist at KIDZ Medical Services in Florida, explained to Healthline.

It could be anything from a B cell lymphoma or a T cell lymphoma to a Burkitts lymphoma or what we call anaplastic large cell, he continued.

El-Sharkawi added that most NHL cases are B cell lymphomas and broadly speaking, they can be high-grade or low-grade.

High-grade lymphomas, she shared, involve more rapid cell turnover. As such, patients typically present as more unwell and with a greater number of symptoms.

On the other hand, low-grade lymphomas grow at a slower rate and are sometimes not discovered until a patient has a scan or test for another reason.

It has not been disclosed which subtype of NHL Fonda has. But, due to the high cure rate she pointed to, both El-Sharkawi and de Angulo said it may be a high-grade B cell lymphoma.

When you talk about lymphomas, we divide them into two groups: Hodgkins lymphoma (HL) and NHL, de Angulo said.

HL has certain characteristics, and we look for certain proteins or markers that identify and confirm whether it is Hodgkins. If its [doesnt have these], we classify it as NHL.

According to de Angulo, the symptoms of NHL are similar to HL. One of the signs we often see, he said, is an enlarged lymph node or a palpable mass.

These typically occur in the neck, armpits, or groin area but, in rarer instances, can present in other areas of the body.

Patients can have lymphoma affecting their stomach or liver, and you can even get lymphoma affecting the brain, El-Sharkawi stated.

The location of the mass or enlarged node can lead to secondary symptoms. For example, if [it] is in an area where its compressing a structure or pressing a nerve, it can cause irritation or pain, shared de Angulo.

Aside from an enlarged node or mass, there are several other key signs, including:

The only way to definitively diagnose NHL is to biopsy the affected area, stated El-Sharkawi, because there are other reasons for swollen glands and enlarged lymph nodes.

In most cases, there are no known causes of NHL, Dallas Pounds, director of services at UK-based charity Lymphoma Action, told Healthline.

However, its thought there may be a few potential risk factors.

In terms of genetics, theres no particular gene linked to the development of NHL unlike some other types of cancer, like breast cancer.

That said, there does seem to be some familial predisposition, noted El-Sharkawi. If youve got a first-degree relative with NHL, then you are slightly more likely (over the general population) to get it [but] its still very rare.

Fondas age may be a factor in her diagnosis. Generally speaking, NHL is more common in the over-60s and 70s, El-Sharkawi said. However, she added, it can be in any age group children may develop NHL.

De Angulo explained that individuals with existing health conditions such as certain autoimmune diseases may also be at higher risk of NHL. People that have undergone certain forms of treatment, such as for ulcerative colitis or lupus, can [have] increased risk of lymphoma.

Furthermore, patients who have undergone solid organ transplants (such as liver or kidney) are also sometimes at greater risk, he said. This is because of the immunosuppressive medications they have to take after the operation.

When youve had a solid organ transplant, you want to suppress the immune system so you dont reject the organ thats been transplanted, he explained. But, that same immune system is the one that makes sure you dont get lymphoma.

Every person diagnosed with lymphoma will have an individual treatment plan depending on them as an individual and their presenting symptoms, said Pounds.

While low-grade lymphomas grow more slowly, they are only treatable but not curable with current therapies.

High-grade lymphomas, however, are potentially curable with chemotherapy, explained El-Sharkawi. Because [they] are more rapidly dividing, theyre more susceptible to the chemo, which essentially targets the ability of those cells to divide and proliferate.

Chemotherapy is generally used because, unlike targeted therapies, such as radiotherapy or surgery, the treatment can reach numerous areas. This is critical as blood is constantly moving around the body.

Additionally targeted antibody therapy is given in combination with chemotherapy, which can increase the chances of remission.

Fonda shared that she has started six months of chemotherapy treatments. These are primarily conducted on an outpatient basis, de Angulo said, and administered across six cycles.

Other treatments for lymphomas are available, although these tend to be in relapsed/refractory [high-grade patients] so when the disease has either come back after treatment or they didnt respond, noted El-Sharkawi.

These include smart drugs, stated de Angulo, which attack the cells that express a certain antigen.

Another option is called CAR-T therapy. [This] is an exciting new way of treating lymphoma, El-Sharkawi enthused. Essentially, the patients T cell lymphocytes are manipulated in a laboratory setting so that they know to target the B lymphocytes, before being put back into the body.

Its like a living medicine made from their own blood cells, she added.

NHL is a type of blood cancer that impacts the immune cells and is one of the most common cancers in the US. It can affect people of all ages but is more often seen in those over 60.

There are numerous NHL subtypes, but symptoms generally include an enlarged lymph node or mass, night sweats, tiredness, and weight loss.

Chemotherapy is the most popular treatment type, although new targeted therapies continue to emerge and be of benefit.

The outlook for an individual with non-Hodgkins lymphoma will depend on several factors, said Pounds. But many people will respond well to treatment and enter a time of remission or stability after it.

Link:
Jane Fonda Diagnosed with Non-Hodgkin's Lymphoma: What to Know - Healthline

Hatim Husain, MD, associate professor in the Department of Medicine at UC San Diego, discuses must-haves for successful biomarker testing in lung cancerin particular, nonsmall cell lung cancer (NSCLC)and how the field is adapting to the targeted treatment needs of its patients.

In this interview from the Quality Cancer Care Alliance Summer 2022 National Leadership Summit, Hatim Husain, MD, associate professor in the Department of Medicine at UC San Diego, discuses must-haves for successful biomarker testing in lung cancerin particular, nonsmall cell lung cancer (NSCLC)and how this field of clinical research is adapting to the targeted treatment needs of its patients.

Transcript

How do we improve biomarker testing in lung cancer?

Biomarker testing in lung cancer is truly a cornerstone for treatment selection in patients who have nonsmall cell lung cancer. Improving it really relies on a few principles. One is understanding the importance. Second is getting access to technologies that can obtain the results quickly and reliably. And third is waiting for the test results, when feasible, to inform the treatment decision.

The technologies have really expanded to include both tissue comprehensive testing, as well as plasma-, or blood-based, comprehensive testing. And there are important considerations around time to a test result, as well as comprehensiveness, that is important across each of those strategies. So its really important that we have these results early and up front, as now the number of targetable mutations within genes of interest are really expanding over time.

How has biomarker testing in lung cancer evolved over the last few years?

Over the last several years, theres been additions to our armamentarium of agents that can really target specific mutations that previously were not possible. These include some atypical EGFR mutations, such as the EGFR Exon 20 insertion, KRAS G12C, which is a different mutationwhich previously also had not had precision-oriented therapeutic strategiesas well as other genes, including MET and HER2, which also are on the horizon.

View original post here:
Dr Hatim Husain: Biomarker Testing Is a Treatment Cornerstone in NSCLC - AJMC.com Managed Markets Network

SUZHOU, China, Aug. 29, 2022 /PRNewswire/ -- On August 20, 2022, Porton Advanced Solutions (hereinafter referred to as "Porton Advanced") and Kun Tuo Medical Research and Development (Beijing) Co., Ltd. (hereinafter referred to as "Kun Tuo") established a strategic partnership in gene and cell therapy R&D, manufacturing and clinical services to accelerate the development and industrialization of innovative drugs.

Through this strategic cooperation, Porton Advanced and Kun Tuo will fully leverage their strengths, client resources and professional team capabilities to deepen cooperation in gene and cell therapy R&D, manufacturing and clinical research, providing one-stop CDMO and clinical research services for innovative drug companies and cooperating to establish a high-quality gene and cell therapy industry ecosystem.

Focusing on gene and cell therapy, Porton Advanced has built CDMO platforms for plasmids, cell therapy, gene therapy, oncolytic virus, nucleic acid therapy and microbial vector based gene therapy .In the process of gene and cell therapy drug development, Porton Advanced can provide CDMO services such as IND-CMC pharmacological research and clinical sample GMP production. Up to now, the cell therapy CDMO platform houses more than 22 cell therapy IND-CMC projects, covering various cell types such as CAR-T, UCAR-T, TCR-T, TIL, CAR-MSC, CAR-NK, NK and RBC.

As a clinical research organization (CRO) specially established by IQVIA for the Chinese market, Kun Tuo inherits its refined quality management system and standards, coupled with abundant clinical resources, offering high quality CRO services throughout IND to NDA. Since its establishment in 2011, Kun Tuo has provided over 1,000 clinical study services for multiple renowned pharmaceutical companies at home and abroad.

Dr. Wang Yangzhou, CEO of Porton Advanced, said, "We are very pleased to announce that we entered into a strategic partnership with Kun Tuo. Porton Advanced focuses on the field of gene and cell therapy and is committed to establishing a global, end-to-end CDMO service platform, while Kun Tuo delves into clinical research services and has very rich clinical resources as well as a highly professional clinical research & reporting team with strict quality standards. Through our in-depth cooperation and integration of resources and advantages, both parties will help to promote the construction of the gene and cell therapy industry ecosystem and empower more new drugs to scale new level based on an integrated drug service platform, thereby allowing enabling public's early access to good medicines."

Wang Ling, General Manager of Kun Tuo, said, "Cell and gene therapy is a new generation of breakthrough therapies after small molecule and large molecule targeted therapies, and it is also one of the most promising sectors of biopharmaceuticals at present. As a full-service CRO focusing on local clinical trials in China, Kun Tuo has built a dedicated team to conduct clinical trials of cell therapy-related products since 2018, and has been taking the lead in the field of cell and gene therapy. We also provide services from clinical development to commercialization strategy research for our clients with the commercialization team of our group company IQVIA, so that the products can serve patients faster and better. Porton Advanced is a well-known CDMO company d with professional and rich experience in drug development and manufacturing in the industry We hope that by joining hands with Porton Advanced, we can combine the expertise and strengths of both sides to provide domestic biopharmaceutical companies with a one-stop solution from drug R&D, clinical trials to commercialization."

About Porton Advanced SolutionsEstablished in Suzhou Industrial Park in December 2018, by its parent company Porton Pharma Solutions Ltd. (Stock Code: 300363), Porton Advanced has built a CDMO platform integrating plasmid, cell therapy, gene therapy, oncolytic virus, nucleic acid therapy and microbial vectors used for gene therapy (MVGTs), providing end-to-end services from cell banking, process development and analytical development, cGMP production to final Fill and Finish , investigator-initiated clinical trials (IIT), investigational new drugs (IND), clinical trials to commercial production. Porton Advanced is dedicated to support sponsors advance their GCT drug development and market launches.

Porton Advanced focuses solely on gene and cell therapy services. Built on the professional experience of its cohort of world-class professionals, as well as on the successes of its parent company, Porton Advanced insists on "Customer First" and the tenet of "Compliance, Expertise, Focus, Open Collaboration". With its key focus on protecting IP for its sponsors, through its comprehensive project management and quality systems, Porton Advanced strives to bring gene and cell therapy products to the clinic and the market through its quality CDMO services, and help bring the best medicine to the public sooner.

About KunTuoKunTuo, as a full-service Contract Research Organization (CRO) specially set up in China by IQVIA (a wholly owned subsidiary of IQVIA) and with a team of nearly 1000 employees, is dedicated to provide high-quality and reliable clinical research services for Pharmaceutical and Medical Device & Diagnostic (MDD) enterprises. Since its establishment in 2011, Kuntuo has provided more than 1000 clinical research services for many well-known pharmaceutical and device companies in China and abroad and now has accumulated rich clinical resources, including more than 10,000 departments' enrollment data and nearly 500 institutions'/departments' process information. Kuntuo inherits IQVIA's sound quality management system and quality standards, and provides biomedical enterprises with higher quality and more responsive service model from IND to NDA through the application and optimization of IQVIA's global operation experience and expertise.

SOURCE Porton Advanced Solutions

See the original post:
Porton Advanced and Kun Tuo Announce Strategic Partnership to Deepen Gene and Cell Therapy CDMO and Clinical Research Services - PR Newswire

There are many diagnostic, prognostic, and treatment challenges in managing patients with chronic obstructive pulmonary disease (COPD), as the pathogenesis of COPD is convoluted, and many knowledge gaps remain in the underlying cellular and molecular mechanisms. Blood eosinophil count is becoming increasingly recognized by the respiratory specialist community as a clinically relevant biomarker to help estimate effective management strategies, but its use is still widely debated.

Nathaniel Marchetti, DO, answers questions about the role of eosinophils as a biomarker to inform treatment decisions for patients with COPD. Dr Marchetti is a pulmonologist with Temple Lung Centerand a professor of clinical thoracic medicine and surgery at the Lewis Katz School of Medicine at Temple University.

Consultant360: What is the threshold for defining high and low eosinophil blood count?

Dr Nathaniel Marchetti: Most clinicians would consider a blood eosinophil count greater than 300 cells/L to be elevated.1 In in patients with COPD, there is not a low or high threshold for eosinophil counts. It can be thought of as a spectrum, with those having an eosinophil count less than 100 cells/L unlikely to respond to inhaled corticosteroids (ICS) and those with an eosinophil count greater than 300 cells/L more likely to respond.1 Most clinicians would agree that an eosinophil count greater than 300 cells/L would indicate a response to ICS. It is important to understand that this is not the only factor involved in deciding when to use ICS, and other factors, such as exacerbation frequency, need to be considered as well.

C360: Approximately what percentage of patients with COPD have evidence of eosinophilic inflammation?

NM: This question is difficult to answer.However, it appears as though individuals with COPD have more eosinophils in their blood compared with the rest of the population. Some studies estimate that 20.1% of patients with COPD will have an eosinophil count greater than 300 cell/L.2

C360: What role do eosinophils play in COPD during exacerbations and stable disease?

NM: It appears patients with higher blood eosinophil levels during stable disease have more frequent exacerbations and are likely to respond better to systemic corticosteroids.3

C360: What role might eosinophils play as a biomarker to inform treatment decisions for patients with COPD?

NM: Current Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines1 suggest that inhaled corticosteroids (ICS) should be used in those with an eosinophil count greater than 300 cells/L. However, this is not the only factor. If patients have more than 2 moderate exacerbations per year, they should be on an ICS regardless of eosinophil count. For those with blood eosinophils of 100 or greater, an inhaled corticosteroid can be considered.If the eosinophil count is less than 100/L, then ICS is not likely going to benefit patients.4

C360: What therapies targeting eosinophilic inflammation are available or in development?

NM: Inhaled corticosteroids are available and important in targeting eosinophilic inflammation in patients with COPD.

Biologic agents targeting eosinophilic inflammatory pathways have been studied with mixed results.These studies have targeted the ability of these medications to reduce exacerbations of COPD. Currently, it is not recommended to use these agents in COPD until better data are available. There are clinical trials ongoing with these medications to determine if they can help reduce exacerbations. Targeted pathways include IL-5, anti-TSLP, IL-33, IL-25.All of these are important in eosinophilic inflammation.4

C360: What gaps exist in the research of patients with COPD and eosinophilic inflammation? And what is next for research?

NM: Eosinophil counts vary over time.We do not entirely understand how they vary and the meaning of the variation. As mentioned, there are numerous inflammatory pathways that can be targeted to help with eosinophilic inflammation, and there are medications in development and clinical trials to find if they can help.4

References:

Read more:
The Role of Eosinophils as a Biomarker to Inform Treatment Decisions for Patients With COPD - Consultant360

Experiments from the UNC School of Medicine lab of Nobel Prize-winning scientist Aziz Sancar, MD, PhD, show how a common molecular tool for DNA labeling also has anticancer properties worthy of further investigation, especially for brain cancers.

CHAPEL HILL, NC Scientists at the UNC School of Medicine have made the surprising discovery that a molecule called EdU, which is commonly used in laboratory experiments to label DNA, is in fact recognized by human cells as DNA damage, triggering a runaway process of DNA repair that is eventually fatal to affected cells, including cancer cells.

The discovery, published in the Proceedings of the National Academy of Sciences, points to the possibility of using EdU as the basis for a cancer treatment, given its toxicity and its selectivity for cells that divide fast.

The unexpected properties of EdU suggest it would be worthwhile to conduct further studies of its potential, particularly against brain cancers, said study senior author Aziz Sancar, MD, PhD, the Sarah Graham Kenan Professor of Biochemistry and Biophysics at the UNC School of Medicine and member of the UNC Lineberger Comprehensive Cancer Center. We want to stress that this is a basic but important scientific discovery. The scientific community has much work ahead to figure out if EdU could actually become a weapon against cancer.

EdU (5-ethynyl-2-deoxyuridine) is essentially a popular scientific tool first synthesized in 2008 as an analog, or chemical mimic, of the DNA building block thymidine which represents the letter T in the DNA code of adenine (A), cytosine (C), guanine (G) and thymine (T). Scientists add EdU to cells in lab experiments to replace the thymidine in DNA. Unlike other thymidine analogs, it has a convenient chemical handle to which fluorescent probe molecules will bond tightly. It thus can be used relatively easily and efficiently to label and track DNA, for example in studies of the DNA replication process during cell division.

Since 2008, scientists have used EdU as a tool in this way, as published in thousands of studies. Sancar, who won the 2015 Nobel Prize for Chemistry for his seminal work on DNA repair, is one such scientist. When his lab began using EdU, his team unexpectedly observed that EdU-labeled DNA triggered a DNA repair response even when it wasnt exposed to DNA-damaging agents, such as ultraviolet light.

That was quite a shock, Sancar said. So we decided to explore it further.

Following up on the strange observation, the team discovered that EdU, for reasons that are still unclear, alters DNA in a way that provokes a repair response called nucleotide excision repair. This process involves the removal of a short stretch of damaged DNA and re-synthesis of a replacement strand. This is the mechanism that repairs most damage from ultraviolet light, cigarette smoke, and DNA-altering chemo drugs. The researchers mapped EdU-induced excision repair at high resolution and found that it occurs across the genome, and it apparently occurs again and again, since each new repair strand includes EdU and thus provokes the repair response anew.

It had been known that EdU is moderately toxic to cells, though the mechanism of its toxicity had been a mystery. The teams findings strongly suggest that EdU kills cells by inducing a runaway process of futile excision repair, which ultimately leads the cell to terminate itself through a programmed cell-death process called apoptosis.

That discovery was interesting in its own right, Sancar said, because it suggested that researchers using EdU to label DNA need to take into account its triggering of runaway excision repair.

As we speak, hundreds and maybe thousands of researchers use EdU to study DNA replication and cell proliferation in lab experiments without knowing that human cells detect it as DNA damage, Sancar said.

Sancar and colleagues also realized that EdUs properties might make it the basis for an effective brain cancer drug because EdU becomes incorporated into DNA only in cells that are actively dividing, whereas, in the brain, most healthy cells are non-dividing. Thus, in principle, EdU could kill fast-dividing cancerous brain cells while sparing non-dividing, healthy brain cells.

Sancar and his team hope to pursue follow-up collaborations with other researchers to investigate EdUs properties as an anticancer agent.

Prior studies have already found evidence that EdU kills cancer cells, including brain cancer cells, but strangely, no one has ever followed up on those results, Sancar said.

Nucleotide excision repair removes thymidine analog 5-ethynyl-2-deoxyuridine from the mammalian genome was co-authored by Li Wang, Xuemei Cao, Yanyan Yang, Cansu Kose, Hiroaki Kawara, Laura Lindsey-Boltz, Christopher Selby, and Aziz Sancar. Funding was provided by the National Institutes of Health (GM118102, ES02755).

Media contact: Mark Derewicz, UNC School of Medicine, 919-923-0959

Continued here:
Scientists Discover Surprise Anticancer Properties of Common Lab Molecule | Newsroom - UNC Health and UNC School of Medicine

1. There was no difference in median overall survival between minimal follow-up and CT-based follow-up groups.

2. Disease-free survival was not significantly different between minimal follow-up and CT-based follow-up groups.

Evidence Rating Level: 1 (Excellent)

Study Rundown: For patients with non-small-cell lung cancer (NSCLC) who meet the guidelines, the standard of care is to receive surgical resection of their tumour(s). Regardless, there is a high risk of recurrent disease and lung cancer is the primary cause of death in this population. This randomized controlled study aimed to compare the outcomes between CT-based surveillance and minimal follow-up measures post-surgical resection of NSCLC tumours. The primary outcome of interest was overall survival (OS) and secondary outcomes included disease-free survival. In the minimal follow-up group, 44.9% of patients died, compared to 42.0% of those in the CT-based group. There was no significant difference between the groups for median OS; 8.5 years for the minimal follow-up group and 10.3 years for the CT-based group. There was similarly no difference statistically between the groups for disease-free survival. There were 404 recurrences, second primary cancers, or deaths in the minimal follow-up group, compared to 440 in the CT-based group. Limitations to this study include the high proportion of patients who had stage I and I NSCLC that contributed to less OS events and reduced power of the study. Additionally, the study excluded patients who had received wedge resections, so applications of the results from this study should be considered cautiously in those patient groups. Overall, the results from this study provide evidence that the inclusion of CT scan for follow-up post surgical intervention for non-small-cell lung cancer does not improve overall survival as compared to minimal follow-up strategies that include chest x-ray.

Click to read the study in The Lancet Oncology

Relevant Reading: Let us not underestimate the long-term risk of SPLC after surgical resection of NSCLC

In-Depth [ randomized controlled trial]: This open-label, phase 3, randomized controlled trial was conducted out of 122 healthcare centres in France. The study enrolled 1,775 adult patients to receive one of two follow-up options; 888 were allocated to the minimal follow-up group, consisting of chest x-ray, and 887 were allocated to receive CT-based follow-up, which included chest x-rays, thoraco-abdominal contrast-enhanced CT scan, and fibre-optic bronchoscopy. Patients had received their surgical resections within the previous 8 weeks of enrollment. The median OS for patients in the minimal follow-up group was 8.5 years (95% confidence interval (CI), 7.4-9.6 years) compared to 10.3 years (95% CI, 8.1 not reached) for patients in the CT-based group (hazard ratio (HR) 0.95, 95% CI, 0.83-1.10). There were also no differences between 3- and 5-year OS rates between the groups. Three year OS for the minimal follow-up group was 77.2% (95% CI, 74.5-80) vs 76.1% (95% CI, 73.3-78.9) for the CT-based group. The median OS after 5 years for the minimal follow-up group was 66.8% (95% CI, 63.7-69.0) vs 65.8% (95% CI, 62.6-68.9) for the CT-based group. There was no significant difference between groups for disease-free survival; 4.9 years (95% CI, 4.3-not reached) in the CT-based group compared to median not reached (95% CI not reached-not reached) in the minimal follow-up group (adjusted HR 1.14; 95% CI, 0.99-1.30).

Image: PD

2022 2 Minute Medicine, Inc. All rights reserved. No works may be reproduced without expressed written consent from 2 Minute Medicine, Inc. Inquire about licensing here. No article should be construed as medical advice and is not intended as such by the authors or by 2 Minute Medicine, Inc.

See original here:
Overall survival is similar for patients receiving CT-based or minimal follow-up after surgical resection of non-small-cell lung cancer - 2 Minute...

Researchers at Oregon State Universitys Carlson College of Veterinary Medicine are moving forward with developing a specialized antibody treatment for dogs with cancer, thanks to a recent grant from the National Science Foundation.

The research team plans for this treatment to be a gentler, more targeted and effective option for addressing canine cancer, just as immunotherapeutics are used in human cancer patients.

Its not a drug like chemotherapy where its a toxin. Youre actually recruiting the bodys natural immune response for clearing out transformed cells for instance, a tumor and then it kills them, said Dan Mourich, senior OSU research associate and the molecular biologist on the research team.

Currently, veterinarians can use radiation, chemotherapy and surgery to tackle canine cancer, but these typically involve frequent trips to veterinary hospitals where the dog must be sedated, and can take a physical and emotional toll on both pets and owners, Mourich said.

In contrast, the OSU therapy will be administered daily in the home as a small subcutaneous injection, similar to how pet owners with diabetic animals inject them with insulin.

The research team includes Dr. Chris Cebra, camelid expert and the chair of the clinical sciences department in OSUs veterinary college; former OSU professor and clinical veterinary oncologist Dr. Shay Bracha, who recently joined the Ohio State University Veterinary Medical Center; and Carl Ruby, veterinary pharmacology instructor at OSU.

The treatment was developed with help from some unlikely collaborators: the llamas and alpacas that OSU owns, which are both members of the camelid family. Researchers injected them with a protein found in canine tumors, which provoked the alpacas immune system to respond by creating a specific antibody.

The researchers then screened a genetic library of the resultant antibodies to determine which were most effective at binding and blocking tumors from interacting with that protein on dogs cytotoxic killer T-cells, the cells responsible for fighting cancer.

Killer T-cells are essentially the smallest scalpel you can have, Mourich said. They identify the cancer cell, remove that cell and leave healthy tissue alone. Theyre so precise that you can utilize them to go and eliminate all the little pieces of tumor around the body.

Camelids can produce a specialized smaller type of antibodies referred to as nanobodies.

Their smaller structure allows nanobodies to penetrate tissues that arent accessible to larger antibodies, and also makes them easier to produce and store for long periods of time, which reduces the overall cost.

The $250,000 grant from the National Science Foundation Partnership for Innovation will allow the researchers to develop their clinical candidate and establish a production method for the treatment, after which they can hold a clinical trial to test its effectiveness.

The efficacy of immune-based therapeutics has already been tested in the human clinic for cancer and other diseases, but were not going to take human drugs and try to adapt them to the dog, Mourich said. Were going to make the dog drug that does the same thing.

Read this article:
NSF Grant to Aid OSU Researchers Developing Treatment for Canine Cancer - The Corvallis Advocate