Baseline characteristics

A total of 52 adult patients with R/R DLBCL were identified and enrolled. The median age at diagnosis was 45years (range, 1763), with marginal male predominance (n=30, 57.7%). 36 patients (69.2%) were identified as having an advanced-stage disease (Ann Arbor stage IIIIV), whereas 15 (28.8%) suffered from B symptoms. Thirteen patients (25.0%) had BM involvement of DLBCL at the time of diagnosis, and 8 of 13 (61.5%) had complex karyotypes. All enrolled patients were classified as low (n=15, 28.8%), low-intermediate (n=13, 25.0%), high-intermediate (n=14, 26.9%), and high (n=10, 19.2%) risks based on international prognostic index (IPI) risk classification. Four patients had a double-hit mutation (7.7%), and according to Hans criteria, 32 and 13 patients were categorized as ABC type (61.5%) and GCB type (25.0%), respectively. The baseline characteristics at the time of diagnosis are summarized in Table 1.

Notably, most enrolled patients had previously undergone intensive treatments, and the median number of chemotherapy lines before allo-HSCT was 4 (range, 26). Sixteen patients (30.8%) had previously undergone auto-HSCT, and the median time from diagnosis and auto-HSCT to allo-HSCT was 27.1months (range, 6.2117.7months) and 18.5months (range, 6.544.8months), respectively. The disease status at the time of transplantation was CR (n=14, 26.9%), PR (n=16, 30.8%), and active disease (n=22, 42.3%). Donor types included matched sibling (n=18, 34.6%), haploidentical (n=18, 34.6%), matched unrelated (n=11, 21.2%), and unrelated donors with one allele mismatch (n=5, 9.6%). The conditioning regimen comprised MAC (n=2, 3.9%) and RIC (n=50, 96.1%). Half of the enrolled patients were ABO-type matched (n=26, 50.0%), 27 (51.9%) were in donor-to-recipient sex mismatch, and 44 (84.6%) were both donor and recipient cytomegalovirus (CMV) IgG seropositive. Table 2 presents the demographic information of the patients who underwent allo-HSCT.

Over a median follow-up period of 38.3months (range, 1.9112.0), the estimated 5-year OS and EFS were 38.4% (95% CI, 24.751.8) and 30.6% (95% CI, 18.843.3), respectively. The estimated 5-year CIR, NRM, and GRFS were 36.7% (95% CI, 23.649.8), 32.7% (95% CI, 20.345.6), and 15.1% (95% CI, 6.926.2), respectively. Figure1 shows the 1-year (100days outcomes in CIR and NRM) and 5-year survival outcomes. Compared to the active-disease group, the remission-achieved group showed a significantly superior rate of CR in the first 3months after allo-HSCT (76.7% vs. 36.4%, p=0.003) and at the last follow-up (50.0% vs. 13.6%, p=0.006) (Fig.2). Moreover, except for NRM (26.7% vs. 40.9%, p=0.217), the clinical outcomes of OS (54.1% vs. 15.6%, p=0.001), EFS (46.4% vs. 9.1%, p<0.001), and GRFS (22.9% vs. 4.6%, p=0.002) were significantly superior in the remission-achieved group with lower CIR (26.9% vs. 50.0%, p=0.047). In detail (Fig.3), among patients in the remission-achieved group before allo-HSCT (n=30), 23 achieved CR, one achieved PR, four experienced disease relapse after allo-HSCT and died due to disease progression, and three died after engraftment (two from bacterial septic shock and one from veno-occlusive disease [VOD]) without relapse. In contrast, among patients in the active-disease group before allo-HSCT (n=22), eight achieved CR. However, only two remained in CR, four experienced disease relapse, and two died due to septic shock during disease remission. All eight of the remaining patients who achieved PR eventually relapsed, and six died after engraftment either due to allo-HSCT-related complications (one with grade IV hemorrhagic cystitis combined with renal failure, one with VOD, and two with grade IV acute hepatic GVHD complicated with liver failure) or infection (two with CMV pneumonia).

Survival outcomes of patients with relapsed/refractory diffuse large B-cell lymphoma after undergoing allogeneic hematopoietic stem-cell transplantation. The estimated 1- and 5-year (A) OS is 45.0% (95% CI, 30.758.3) and 38.4% (95% CI, 24.751.8). The estimated 1- and 5-year (B) EFS is 32.7% (95% CI, 20.545.4%) and 30.6% (95% CI, 18.843.3). The CIR and NRM at day 100 after allo-HSCT is (C) 15.4% (95% CI, 7.126.5) and (D) 17.3% (95% CI, 8.528.8). Furthermore, the estimated 5-year CIR and NRM are 36.7% (95% CI, 23.649.8) and 32.7% (95% CI, 20.345.6), respectively. The estimated 1- and 5-year (E) GRFS is 17.3% (95% CI, 8.528.6) and 15.1% (95% CI, 7.026.2). CI, confidence interval; CIR, cumulative incidence of relapse; EFS, event-free survival; GRFS, graft-versus-host disease-free, relapse-free survival; HSCT, hematopoietic stem-cell transplantation; NRM, non-relapsed mortality; OS, overall survival; R/R DLBCL, relapsed/refractory diffuse large B-cell lymphoma.

Response rate and clinical course of patients with diffuse relapsed/refractory large B-cell lymphoma after undergoing allogenic hematopoietic stem-cell transplantation. (A) Remission-achieved group: Among 30 patients in the remission-achieved group, the overall response rate (23 CR and 1 PR) was 80.0% (n=24) at 3months after allo-HSCT. At the last follow-up, 15 patients remained CR (including 1 PR patient who achieved CR after donor leukocyte infusion), but three died after engraftment without relapse, and six experienced DLBCL relapse. (B) Active-disease group: Among 22 active-disease group patients, the overall response rate (8 CR and 8 PR) was 72.7% (n=16) at 3months after allo-HSCT. However, at the last follow-up, only two patients remained CR, two died after engraftment without relapse, and 12 (4 CR and 6 PR) experienced DLBCL relapse. CMV, cytomegalovirus; CR, complete remission; GVHD, graft-versus-host disease; HSCT, hematopoietic stem-cell transplantation; NRM, non-relapsed mortality; PD, progression of disease; PR, partial remission.

Comparison of survival outcomes between the remission-achieved and active-disease groups in patients with diffuse large B-cell lymphoma who underwent allogeneic hematopoietic stem-cell transplantation. The clinical outcomes of (A) OS (54.1% vs. 15.6%, p=0.001), (B) EFS (46.4% vs. 9.1%, p<0.001), and (E) GRFS (22.9% vs. 4.6%, p=0.002) were significantly superior in the remission-achieved group with (C) lower CIR (26.9% vs. 50.0%, p=0.047), except for (D) NRM (26.7% vs. 40.9%, p=0.217). CI, confidence interval; CIR, cumulative incidence of relapse; EFS, event-free survival; GRFS, graft-versus-host disease-free, relapse-free survival; HSCT, hematopoietic stem-cell transplantation; NRM, non-relapsed mortality; OS, overall survival; R/R DLBCL, relapsed/refractory diffuse large B-cell lymphoma.

The overall cumulative incidence of grade 3 to 4 acute GVHD and moderate-to-severe chronic GVHD that required steroid pulse therapy was 17.3% (95% CI, 8.528.8%) and 29.1% (95% CI, 17.242.0%), respectively. The active-disease group had a significantly higher incidence of grade 34 acute GVHD than the remission-achieved group before allo-HSCT (6.7% vs. 31.8%, p=0.023). However, no significant differences in moderate-to-severe chronic GVHD incidence (37.1% vs. 18.2%, p=0.172) were observed between the two groups. The allo-HSCT-related complication incidence, response rate, and survival outcomes in the remission-achieved and active-disease groups before allo-HSCT are presented in Table 3.

The results of the univariate analysis for OS, EFS, CIR, NRM, and GFRS are presented in Supplementary Tables 1 and 2. In the multivariate analysis, a shorter interval from diagnosis to allo-HSCT (median of<27.1months), which reflects relatively rapid disease progression, showed significantly poor OS (hazard ratio [HR], 3.92; 95% CI, 1.838.43; p<0.001) and EFS (HR, 2.65; 95% CI, 1.285.46; p=0.008). Complex karyotypes in BM involving DLBCL were also associated with poor OS (HR, 1.42; 95% CI, 1.061.90; p=0.018) and NRM (HR, 1.41; 95% CI, 1.021.94; p=0.040). Active disease before allo-HSCT was associated with significantly lower EFS (HR. 2.50; 95% CI, 1.215.17; p=0.014), GFRS (HR, 2.54; 95% CI, 1.374.72; p=0.003), and higher CIR (HR, 3.03; 95% CI, 1.148.02; p=0.026). The MAC regimen for allo-HSCT was associated with significantly higher CIR (HR, 11.3; 95% CI, 3.3338.1; p<0.001), and patients with previous autologous stem-cell transplantation (ASCT) had significantly better GRFS (HR, 0.50; 95% CI, 0.260.98; p=0.043). The results of the multivariate analysis are presented in Fig.4.

Multivariable analysis of survival outcomes related to allogeneic hematopoietic stem-cell transplantation in patients with relapsed/refractory diffuse large B-cell lymphoma. (A) The multivariable analysis for each survival outcome shows that a shorter interval of the median of<27.1months from diagnosis to allo-HSCT (HR, 3.92; 95% CI, 1.838.43; p<0.001) and complex karyotype presenting bone marrow (HR, 1.42; 95% CI, 1.061.90; p=0.018) are significantly related to poor OS. In the case of EFS, a shorter interval compared to the median of<27.1months from diagnosis to allo-HSCT (HR, 2.65; 95% CI, 1.285.46; p=0.008) and active disease before allo-HSCT (HR, 2.50; 95% CI, 1.215.17; p=0.014) are significantly related to poor EFS. Previous ASCT are significantly related to better GRFS (HR, 0.50; 95% CI, 0.260.98; p=0.043), but active disease before allo-HSCT are significantly related to poor GRFS (HR, 2.54; 95% CI, 1.374.72; p=0.003). (B) Active disease before allo-HSCT (HR, 3.03; 95% CI, 1.148.02; p=0.026) is also significantly related to higher CIR with MAC conditioning (HR, 11.3; 95% CI, 3.3338.1; p<0.01). Complex karyotype presenting bone marrow is also related to higher NRM (HR, 1.41; 95% CI, 1.021.94; p=0.040). CI, confidence interval; ASCT, autologous stem-cell transplantation; CIR, cumulative incidence of relapse; EFS, event-free survival; GRFS, graft-versus-host disease free, relapse-free survival; HR, hazard ratio; HSCT, hematopoietic stem-cell transplantation; MAC, myeloablative conditioning; NRM, non-relapsed mortality; OS, overall survival; R/R DLBCL, relapsed/refractory diffuse large B-cell lymphoma.

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The salvage role of allogeneic hematopoietic stem-cell ... - Nature.com

A new interim analysis of an open label trial presented at the 2023 MSMilan, the 9th Joint ECTRIMS-ACTRIMS meeting, held October 1113, in Milan, Italy, revealed significant beneficial effects on cognition and on objective biomarkers of neuroinflammation and neurodegeneration, among patients with progressive multiple sclerosis (MS) treated with repeated intrathecal (IT) injections of autologous mesenchymal stem cells (MSC).1

In 15 tested patients treated by at least 2 injections of MSC, 9 such patients improved between 5% and 18% in 25 feet walking. In addition, the average standard score of 4 cognitive tests taken by patients improved from 0.11 at baseline to 0.33 following 3 MSC injections over a year. Among 22 patients who received at least 1 MSC treatment, 13 of them showed improvement in the Symbol Digit Modalities Test (SDMT) scores, one of the cognitive tests. Notably, 6 of 17 treated patients improved by more than 4 degrees in SDMT in 3 consecutive tests over a year.

In this analysis, lead author, Petrou Panayiota, MD, senior neurologist, Unit of Neuroimmunology and Multiple Sclerosis Center and The Agnes-Ginges Center for Neurogenetics at Hadassah University Hospital in Jerusalem, Israel, and colleagues primarily evaluated the effect of repeated MSC transplantations on cognition in patients with progressive MS. Additionally, the researchers investigated objective serum biomarkers of neuroinflammation and neurodegeneration, specifically neurofilaments light chain (NfL) and glial fibrillary acidic protein (GFAP) with the therapy.

The open-label extension enrolled 48 patients with either secondary progressive MS or primary progressive MS who participated in the previous double-blind trial (NCT02166021) with MSC injections. The researchers used 4 cognitive tests including the SDMT, California Verbal Learning Test, Brief Visuospatial Memory Test, and Controlled Oral Word Association Test to assess patients at baseline before treatment, and at 4-5 time points following the first MSC-injection. At the same time, researchers also tested for serum NfL and GFAP levels using Quanterix technology (SIMOA).

READ MORE: Satralizumab Continues to Show Long-Term Efficacy in AQP4-IgG-Seropositive NMOSD

Among available data, 17 patients were treated with at least 2 intrathecal injections of MSC between 3 and 6 months apart, and 12 patients received 3 MSC injections. For treated patients, NfL levels reduced from a mean of 15.7 pmol/ml at baseline to 12.8 pmol/ml during the post-treatment year while GFAP levels also reduced from 191.4 pmol/ml at baseline to 155.4 pmol/ml.

In the previous double-blind randomized study conducted by Petrou and colleagues, IT injection of autologous bone marrow derived MSC showed robust clinical and radiological effects in patients with active and progressive MS.2 Enrolled patients had evidence of either clinical worsening or activity during the previous year between 2015 and 2018 andwere randomized into 3 groups: IT or intravenous (IV) autologous MSCs (1 106/kg) or sham injections.

After 6 months, half of the patients from the MSC-IT and MSC-IV groups were retreated with MSCs, and the other half with sham injections. Patients initially assigned to sham treatment were divided into 2 subgroups and treated with either MSC-IT or MSC-IV. After 14 months of the study, instigators did not observe any serious treatment-related safety adverse events. Significantly fewer patients experienced treatment failure in the MSC-IT and MSC-IV groups compared with those in the sham-treated group (6.7%, 9.7%, and 41.9%, respectively, P = .0003 and P = .0008).

During the 1-year follow-up, 58.6% and 40.6% of patients treated with MSC-IT and MSC-IV, respectively, had no evidence of disease activity compared with 9.7% in the sham-treated group (P <.0001 and P <.0048, respectively). In addition, the MSC-IT transplantation induced additional benefits on the relapse rate, on the monthly changes of the T2 lesion load on MRI, and on the timed 25-foot walking test, 9-hole peg test, optical coherence tomography, functional MRI and cognitive tests. Overall, treatment with MSCs was well-tolerated and induced short-term beneficial effects, especially in the patients with active disease. Notably, the IT administration was more efficacious than the intravenous in several parameters of the disease.

Click here for more coverage of MSMilan 2023.

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Mesenchymal Stem Cell Therapy Shows Cognitive and Biomarker ... - Neurology Live

Every Wednesday at 8:30we're joined by John Perreault, Executive Director of theBerkshire Humane Societyto discuss all the happenings at their Barker Road facility, plus talk about their Pet of the Week.

This week's Pet of the Week is a beautiful brindle-coated girl named Tilly. Tilly is an approximately 2-year-old American Pit Bull terrier mix who arrived at Berkshire Humane Society as an unclaimed stray.

An energetic girl, who is equally sweet,Tilly issure to keep you on an exercise regimen and will provide you with endless entertainment. She has been doing wonderfully keeping her kennel clean, so Berkshire Humanestaff believe she was mostly housetrained in her previous living situation.

Tilly can be a little weary and become stressed with excessive handling, mostly with the veterinarian, so an adopter who is willing to watch and understand her body language and signals would be ideal for Tilly. She loves to hang out with her people and receive pets and love, but she also likes her own personal time.

Tilly does not prefer the company of other female dogs or rambunctious male dogs, but she could possibly live with a calm and mellow male dog. She can be a bit reactive to other dogs while outside, but the kennel staff have been working with her on this and she has been making great progress! Tilly could potentially live with kids aged 10 years or older, but not small animals please as she does have a high prey drive.

If you are interested in more information on Tilly, please reach out to the Berkshire Humane kennel staff at (413)-447-7878 ext. 126 to learn more!

To prepare yourself for a potential incident, always keep your vet's phone number handy, along with an after-hours clinic you can call in an emergency. The ASPCA Animal Poison Control Center also has a hotline you can call at (888) 426-4435 for advice.

Even with all of these resources, however, the best cure for food poisoning is preventing it in the first place. To give you an idea of what human foods can be dangerous, Stacker has put together a slideshow of 30 common foods to avoid. Take a look to see if there are any that surprise you.

Gallery Credit: Rachel Cavanaugh

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Berkshire Humane Society Pet of the Week: Meet Tilly - Live 95.9

In the fiscal year 2023, the Global Parkinsons Disease Industryis poised to achieve an estimated worth of US$ 5.41 Billion, reflecting a notable increase from the US$ 4.82 Billion recorded in the fiscal year 2022. The projected growth trajectory for this decade, spanning from 2023 to 2033, anticipates a consistent annual growth rate of 12.2%, leading to a projected market value of US$ 17.12 Billion by the conclusion of 2033.

Parkinsons disease, a complex brain disorder characterized by the degeneration of nerve cells in a specific brain region, manifests in a myriad of ways, encompassing symptoms such as rigidity, emotional fluctuations, cognitive impairments, coordination and balance challenges, fluctuations in blood pressure, and cognitive functions. While Parkinsons disease remains incurable, it is crucial to recognize the availability of various treatment modalities, including surgical interventions, pharmaceutical therapies, and other advanced medical approaches.

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When a patients medications are not functioning effectively, it can lead to an increase in Parkinsons disease (PD) symptoms including tremor and walking problems, which is known as an off episode. In the US, NOURIANZ (istradefylline), an antagonist of the adenosine A2A receptor, is used for Parkinsons disease. The medication offers patients with Parkinsons disease a brand-new non-dopaminergic once-daily oral treatment alternative. Such developments are expected to spur global growth in the Parkinsons disease market from 2023-2033.

Key Takeaways from the Market Study

The market is anticipated to expand as more drugs are approved for the treatment of Parkinsons disease and as there is a robust pipeline of novel medications being developed for the condition. comments a Future Market Insights analyst.

Discovering the assumptions behind the study. Ask an Analyst https://www.futuremarketinsights.com/ask-question/rep-gb-16241

Competitive Landscape

Some of the top players in the global Parkisons disease market are:

Some of the recent developments in this domain are:

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More Valuable Insights Available

Future Market Insights, in its new offering, presents an unbiased analysis of the Parkinsons disease Industry, presenting historical demand data (2018-2022) and forecast statistics from 2023 to 2033.

The study divulges essential insights on the market based on the Parkinsons disease industry by type (juvenile parkinson disease, young-onset parkinsons disease, idiopathic parkinson disease), by age (adult and pediatric), by diagnosis (CT Scan, MRI Scan, DaTSCAN-SPECT scan, PET Scan), by drug class (carbidopa-levodopa, carbidopa-levodopa infusion, dopamine agonists, monoamine oxidase b inhibitors, catechol o-methyltransferase inhibitors, anticholinergics, amantadine) and regions.

Key Segments Profiled in the Amyotrophic Lateral Sclerosis Industry Survey

Treatment:

Distribution Channel:

Region:

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Future Market Insights, Inc. (ESOMAR certified, recipient of the Stevie Award, and a member of the Greater New York Chamber of Commerce) offers profound insights into the driving factors that are boosting demand in the market. FMI stands as the leading global provider of market intelligence, advisory services, consulting, and events for the Packaging, Food and Beverage, Consumer Technology, Healthcare, Industrial, and Chemicals markets. With a vast team of over 5,000 analysts worldwide, FMI provides global, regional, and local expertise on diverse domains and industry trends across more than 110 countries.

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Global Parkinson's Disease Industry Set for US$17.12 Billion ... - PharmiWeb.com

A study reveals that the delayed mental health benefits of SSRI antidepressants may be due to physical brain changes leading to enhanced brain plasticity during the first weeks of SSRI consumption. Using PET scans on volunteers, the researchers found a noticeable increase in synapse density in the brains of those taking SSRIs compared to those on a placebo.

Researchers have uncovered that the weeks-long delay in SSRI antidepressant benefits may stem from increased brain plasticity and synapse density over initial weeks of intake, offering new insights into the drugs workings and onset timing.

SSRI antidepressants normally take a few weeks before any showing mental health benefits, but how come it takes so long? Now a study from a group of clinicians and scientists provides the first human evidence that this is due to physical changes in the brain leading to greater brain plasticity developing over the first few weeks of SSRI intake. This may also begin to explain one of the mechanisms of how antidepressants work.

This work was presented at the ECNP conference in Barcelona on October 9th. This work is also due to be published (has been accepted) in a peer-reviewed journal.

Selective Serotonin Reuptake Inhibitors (SSRIs) are a class of drugs commonly prescribed for depression and other mood disorders. Here are some common SSRIs:

Doctors have been puzzled as to why Selective Serotonin Reuptake Inhibitors (SSRIs) take time before having an effect. Researchers in Copenhagen, Innsbruck, and University of Cambridge have undertaken a randomized, double-blind placebo-controlled study in a group of healthy volunteers which shows a gradual difference in how many nerve cell connections (synapses) the brain cells have between those taking the antidepressants and a control group, depending on how long the treatment lasts.

17 volunteers were given a 20mg daily dose of the SSRI escitalopram, with 15 volunteers given a placebo. Between 3 and 5 weeks after starting the trial, their brains were scanned with a PET (Positron Emission Tomography) scanner, which showed the amount of synaptic vesicle glycoprotein 2A in the brain: this is an indicator of the presence of synapses, so the more of the protein is found in an area, the more synapses are present in that area (i.e., greater synaptic density). These scans showed significant between-group differences in how the synapse density evolved over time.

Location of the neocortex and hippocampus. Credit: Marc Dingman, Neuroscientifically Challenged

Researcher Professor Gitte Knudsen (of Copenhagen University Hospital) said: We found that with those taking the SSRI, over time there was a gradual increase in synapses in the neocortex and the hippocampus of the brain, compared to those taking placebo. We did not see any effect in those taking placebo.

The neocortex takes up around half of the brains volume; it is a complex brain structure that deals with higher functions, such as sensory perception, emotion, and cognition. The hippocampus, which is found deep in the brain, functions with memory and learning.

Professor Knudsen continued, This points towards two main conclusions. Firstly, it indicates that SSRIs increase synaptic density in the brain areas critically involved in depression. This would go some way to indicating that the synaptic density in the brain may be involved in how these antidepressants function, which would give us a target for developing novel drugs against depression. The second point is that our data suggest that synapses build up over a period of weeks, which would explain why the effects of these drugs take time to kick in.

Commenting, Professor David Nutt (Imperial College, London) said The delay in therapeutic action of antidepressants has been a puzzle to psychiatrists ever since they were first discerned over 50 years ago. So these new data in humans that uses cutting edge brain imaging to demonstrate an increase in brain connections developing over the period that the depression lifts are very exciting. Also, they provide more evidence enhancing serotonin function in the brain can have enduring health benefits.

This is an independent comment, Professor Nutt was not involved in this work.

The conference abstract, Escitalopram increases synaptic density in the human brain over weeks, (Johansen et al) can be seen at https://www.ecnp.eu/congress2023/ECNPcongress/programme/programme#!abstractdetails/0000552740

This work has also been accepted in a peer-reviewed journal. Unfortunately, it is still in the final stages of the publication process, so we are not yet allowed to give publication details.

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Brain Plasticity & SSRIs: Breakthrough on How Antidepressants ... - SciTechDaily

A linear dose-response association was observed between radiation doses to the large bowel and risk for developing colorectal cancer (CRC) that only worsens with the rising doses of procarbazine (Matulane) in Hodgkin lymphoma survivors, according to findings from a nested case-control study published in JAMA Oncology.

"Although [Hodgkin lymphoma] treatments have evolved considerably during the recent decades, with fewer patients receiving subdiaphragmatic [radiotherapy] or high-dose procarbazine, these findings remain relevant and important for clinicians treating patients for [Hodgkin lymphoma] in the modern era," according to the study authors.

Investigators found that 62% of cases received subdiaphragmatic radiotherapy compared with 41% of controls (rate ratio [RR], 2.4; 95% CI, 1.4-4.1). The rates of relapse treatment in each respective group were 37% and 23% (RR, 2.1; 95% CI, 1.2-3.8). There was a 2.1 to 3.0-fold increase in CRC incidence for those who received 10 or more Gy to the whole large bowel compared with patients who received less than 1.0 Gy or no radiation at all.

Those who received a cumulative procarbazine dose of more than 8.4 g/m2 experienced a significantly higher incidence of CRC compared with those who did not receive procarbazine (RR, 2.5; 95% CI, 1.3-5.0). Additionally, patients receiving both 10 Gy or more of radiation plus more than 4.2 g/m2 of procarbazine had a 5.2-fold (95% CI, 2.2-12.3) increase in CRC rates compared with those who received less than 10 Gy plus 4.2 or less g/m2 of procarbazine.

Although [Hodgkin lymphoma] treatments have evolved considerably during the recent decades, with fewer patients receiving subdiaphragmatic [radiotherapy] or high-dose procarbazine, these findings remain relevant and important for clinicians treating patients for [Hodgkin lymphoma] in the modern era, the study authors stated.

This evidence enables individualized estimation of [CRC] risk and selection of the optimal treatment strategy for patients who are treated with subdiaphragmatic [radiotherapy] or with procarbazine. These findings also emphasize the need for clinicians to identify [Hodgkin lymphoma] survivors previously treated with subdiaphragmatic [radiotherapy] and procarbazine for whom [CRC] screening should be considered.

Investigators of the nested case-control study examined data from 5-year Hodgkin lymphoma survivors treated at 5 hospital centers in the Netherlands. Estimations of mean radiation doses to the large bowel involved reconstructing individual radiotherapy treatments on representative CT datasets. Investigators also estimated cumulative procarbazine doses using typical doses per cycle for each chemotherapy regimen.

In terms of outcomes, calculations of CRC odds ratios and CIs involved using conditional logistic regression to compare the exposure history of patients with those of matched controls. Investigators modeled excess rate ratios (ERRs) to assess the excess risk related to each 1-Gy increase in radiation dose.

Patients 15 to 50 years old at time of first treatment for Hodgkin lymphoma who were diagnosed from 1964 to 2000 were included in the analysis. For each patient who developed CRC, investigators selected up to 5 controls individually matched based on sex, age at Hodgkin lymphoma diagnosis, and date of diagnosis.

The study population included a total of 316 Hodgkin lymphoma survivors, 78 of whom had developed CRC and 238 of whom were control patients. The mean age at Hodgkin lymphoma diagnosis was 33.0 years (standard deviation, 9.8), and 69.9% of patients were male. Additionally, the mean interval between Hodgkin lymphoma and CRC diagnosis was 25.7 years (interquartile range [IQR], 18.2-31.6), and the median age at CRC diagnosis was 59.1 years (IQR, 51.9-63.3).

Overall, 72% of patients had colon cancer and 28% had rectal cancer. Additionally, 69% of patients died due to CRC; the 5-year CRC-specific survival rate was 66%.

The ERR/Gy was 3.5% (95% CI, 0.4%-12.6%) for those who received radiation doses to the whole large bowel without procarbazine; the ERR/Gy increased 1.19-fold (95% CI, 1.06-1.33) for each g/m2 increase in procarbazine dose, with an ERR/Gy of 15.0% for those receiving 8.4 g/m2 of procarbazine.

Sex, age at Hodgkin lymphoma diagnosis, time since first treatment for Hodgkin lymphoma, and receipt of anthracyclines did not alter the dose-response association for radiation doses to the whole large bowel. The dose-response association for radiation dose administered to the affected segment needed to be modified based on sex; investigators noted an ERR/Gy of 39.1% for female patients compared with 3.5% for male patients.

Geurts YM, Shakir R, Ntentas G, et al. Association of radiation and procarbazine dose with risk of colorectal cancer among survivors of Hodgkin lymphoma. JAMA Oncol. 2023;9(4):481-489. doi:10.1001/jamaoncol.2022.7153

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Possible Association Between Radiation/CRC Risk in Hodgkin ... - Cancer Network

The River Road Veterinary Clinic has outlined four popular types of dog toy that are actually dangerous and could cause serious harm to your pet

A vet has outlined the four popular dog toys you should not give to your pets, branding them dangerous.

The River Road Veterinary Clinic has stated that these toys could cause serious injury, including teeth and tongue damage and, in some cases, leaving them needing surgery.

The first item on the list to watch out for are marrow bones, which are often given to pets that like to chew on things.

However, the clinic warned owners of the risk of pancreatitis that dogs can suffer after eating marrow from the bone.

They said: "Unfortunately, marrow bones do not come without risk.

"The fatty marrow found in the centre of the bones can cause pancreatitis in sensitive dogs so it is best to scoop most of the centre out before giving it to your pet."

There is also a risk of splintering if the bone is cooked, which can ultimately lead to surgery. Owners are advised to give their pets raw marrow bones only.

Another popular toy that can cause issues for dogs are rubber balls, which can lead to tissue damage.

In some instances, balls with holes have become suctioned onto a dogs tongue, leading to blocked blood flow.

The vet clinic has recommended balls with no holes or multiple holes, to avoid this from happening.

Similar to marrow bones are rawhide bones, which can easily cause damage dogs due to potential splintering.

The clinic said: "They are often swallowed and they absorb water and swell within the stomach, growing in size and rendering them unable to pass through the intestines.

"Foreign body surgery to remove the large chunk of rawhide is then the only way to solve the problem."

The clinic suggested rawhide chews as an alternative, which dissolve in your dogs stomach, allowing them to still enjoy the flavour.

The final toys the vets have outlined are ones that are small. Small, stuffed toys can be dangerous for dogs because they are easy to tear apart and swallow.

The clinic advised: " Another common culprit are pieces of larger toys that have been torn apart and are then eaten. Swallowing these things can result in an intestinal blockage that requires emergency surgery to correct."

Excerpt from:
Vet's warning over four toys you must never give to your dogs - as they could kill - The Mirror

A Ballymoney football team has put out an appeal to help find a stem cell donor for one of its biggest fans.

Glebe Rangers Football Club put out the appeal on social media, asking followers to share it far and wide, in a bid to help 20-year-old Ballymoney man Kofi Blair.

In their post on Facebook, Glebe wrote: Football Fans - We Need Your Help. One of our Glebe family, young Kofi Blair, needs a blood stem cell transplant to recover from Hodgkin's Lymphoma.

"Are you the match he's looking for? Let's share this campaign far and wide and get Kofi a matching donor. #letsbeatcancertogether #glebefamily

In September 2021, Kofi was diagnosed with Hodgkin's lymphoma. Several months before his diagnosis, Kofi had begun to suffer from really bad sweating and fatigue, symptoms which lasted for a few months until a lump appeared on the left side of his neck.

After undergoing blood tests, CT scans, a biopsy and a PET scan, his diagnosis was confirmed and Kofi began treatment, including immunotherapy and radiotherapy. Kofi's doctors have now advised that a stem cell transplant is the next step for him, once his current course of treatment is finished.

A search for a stem cell match has been carried out within Kofi's family. His three older sisters have all been tested but are not compatible.

Now an international charity called DKMS which is dedicated to the fight against blood cancer and blood disorders is beginning a search for an unrelated donor who may possibly save Kofi's life.

The charity said: Previously unaware, Kofi's family discovered the work of DKMS, and the importance of stem cell donors, through their awareness of the #DoitforDaniel campaign which reached across Northern Ireland searching for potential donors to help Daniel and others. Daniel found his match and has undergone a successful transplant.

"Now Kofi's family are hoping and appealing for a similarly successful outcome for Kofi. Every 14 minutes, someone in the UK is diagnosed with a blood cancer or disorder. You could be their lifesaver if youre aged 17-55 and in generally good health. Please consider helping Kofi and others like him by joining the register.

Here is the link to request a swab pack

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Ballymoney football club Glebe Rangers appeals on social media ... - NorthernIrelandWorld

PRESS RELEASE

Published April 27, 2023

Newark, New Castle, USA Growth Plus Reports most recent study examines the global Preclinical Imaging Market production, prospective uses, demand, key companies, and SWOT analysis.

The Preclinical Imaging Market Report will help you determine the best distribution strategies for specific products and identify potential markets. In addition, the report examines the purchasing and supply patterns that impact the market. The Preclinical Imaging market research report provides insights into the limitations, market trends, prospects, drivers, and competition in the Preclinical Imaging sector.

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Growth Plus Reports studies the key trends in each category and sub-segment of the Preclinical Imaging market, along with global and regional projections from 2023 to 2031. Our research splits the market into product type and application segments.

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GLOBAL PRECLINICAL IMAGING MARKET ANALYSIS & FORECAST, BY TYPE

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Companies may utilize Preclinical Imaging market report to get insights on market variables and any restraints that may affect the manufacturing of their product. Companies that are expanding abroad require thorough global market research that includes real market data to assist with their marketing strategy. This global market Preclinical Imaging industry study analyzes important market dynamics and provides in-depth information and statistics to help companies flourish. This research report on the Preclinical Imaging market takes advantage of advanced and professional approaches such as SWOT analysis and GRG Healths unique GrowthMIX strategy.

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Market segment by Region/Country including: -

-North America (United States, Canada and Mexico)-Europe (Germany, UK, France, Italy, Russia and Spain etc.)-Asia-Pacific (China, Japan, Korea, India, Australia and Southeast Asia etc.)-South America (Brazil, Argentina and Colombia etc.)-Middle East and Africa (South Africa, UAE and Saudi Arabia etc.)

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See more here:
Preclinical Imaging Market to grow at a CAGR of over 3.8% from ... - Digital Journal

By Damayanti Datta : (NOTE: The article was published in the INDIA TODAY edition dated June 26, 2017)

He was a ruggedly handsome man in life: shirt unbuttoned, muscles rippling, cigarette dangling rakishly from his lips. He was unrecognisable in death: pinched, pale, almost skeletal. For those who knew him onscreen, there was shock and despair at the final terror of his illness. Vinod Khanna, one of the last screen titans of a generation, battled a lethal form of bladder cancer, resistant to chemotherapy, for six long years and finally succumbed on April 27. That very week, however, the world of science celebrated a "huge breakthrough": the discovery of a new drug based on malaria proteins that can dramatically reduce hard-to-treat bladder cancers.

Read More

Another breakthrough, another life. "It's finally here. A new ray of hope in the field of cancer. 'Nivolumab' for aggressive Hodgkin's lymphoma. Spread the word." Mamta Mohandas, 32, calls herself 'Actor. Singer. Survivor' on Twitter and posts messages of hope to her 495K followers. Her rising career graph in Malayalam and Telugu cinema, despite her seven-year-long fight against an aggressive lymph cancer, Diffuse Large B-Cell Lymphoma, is legend. Ever since she joined a clinical trial for an experimental drug in Los Angeles, USA, the southern beauty has been upbeat. "It's working for me," she informs her fans. "Brave girl", "love u", "jaldi aaja", they respond.

It is the best of times, it is the worst of times, on the cancer front. Scientists continue to be baffled by the complexity and smartness of cancer cells: that they find ways to dodge even the most powerful therapies, that 'cancer' encompasses not one but hundreds of distinct diseases, that each individual cancer behaves differently, that two people with the same cancer, at the same stage, receiving the same treatment, can experience radically different outcomes. As US-based oncologist and Pulitzer-winning writer Dr Siddhartha Mukherjee says, "All cancers are alike, but they are alike in a unique way." With all that, cancer is catching up with heart disease as the leading cause of deaths globally, reports the World Health Organization. In India, the latest study based on the National Cancer Registry shows that there are 1.45 million new cases every year, a prevalence of over 3 million at any point of time, over 680,000 deaths a year. Although early detection saves lives, just 12.5 per cent Indians call on a doctor in the early stages.

But it's also a time of exceptional breakthroughs and innovations. No, there is no single death-defying magic bullet, but new generations of life-saving and life-extending 'smart drugs' are currently being developed and tested. At the root of all this is the idea that the cure for cancer is inside the patient. And the mantra in labs around the world is 'precision medicine'. That is, a line of treatment that is personalised to a patient's genetic make-up or molecular changes within one's tumour. Up until now, therapies have all been geared to treat cancer based on where it is located, say, in the breast, bladder or lung. Now, the shift is increasingly evident in finding precision medicine targeted at genetic glitches. On May 23, in a first, a cancer drug has won approval from the US Food and Drug Administration (USFDA) that can be given to anyone who harbours specific genetic abnormalities found in as many as 15 different types of cancers, all in patients for whom traditional treatment, like chemotherapy, has failed.

There has not been so much excitement as there is now since 2001, when one of the first cancer therapies to show the potential for targeted action, Imatinib, was approved. Thousands of clinical trials are humming with promising drug pipelines, many of which are being used by doctors to benefit patients. "It's an exciting time," says Dr Anil Suri, director of the National Institute of Immunology in Delhi and the man who discovered SPAG9, the cancer antigen to be used in India's first anti-cancer vaccine, now under phase II clinical trial in cervical cancer patients. "Cancer research is at the tipping point of major breakthroughs. Advances in molecular biology, next-generation gene sequencing, big data and innovative diagnostics are opening up a whole new world of possibilities."

The war on cancer is now looking within, at the patient's own arsenal of weapons: genes, molecules and the immune system. The conventional regimen of surgery-radiotherapy-chemotherapy is slowly but surely giving way to targeted, personalised treatments and more intricate diagnostic tools. Combination therapies to keep cancers in check are being worked upon. The emerging field of cancer immunotherapy, or using the body's own immune system to help fight off the disease, is especially promising. Of the 30 new drugs for more than a dozen different types of cancers approved by the USFDA in the past one year, almost all are in immunotherapy. Indian scientists, too, are engaged in the battle to unlock the answers on how to prevent, detect and treat patients, in the best example of 'Make in India'.

A paradigm shift is taking place, with the approach moving toward a regimen where cancer may not have to be cured, but controlled, say, like diabetes or heart disease, explains Dr Mammen Chandy, director of Tata Medical Centre, Kolkata, and chair of the Human Genome Task Force of the department of biotechnology (DBT), Union ministry for science and technology. "With greater knowledge of the molecular genetics of cancer, we can study genetic mutations in a patient and target these with specific drugs," he says. A whole range of new drugs today can shrink and kill cancer cells without collateral damage. "We can precisely quantify the extent of the disease at diagnosis with better imaging techniques." The precision and accuracy of radiation technology make it possible to hit tumours with minimal damage to surrounding normal cells. "In several cancers, a patient can now pop a pill a day and live a normal life for many years. We are, thus, converting cancer into a chronic disease that one can live with."

ATCG. ATCG. AGGCCTT. Oops, a typographical error. A tiny mistake can change the meaning of a sentence. What if there's a typo in your genes? Imagine a social network humming in each of your 37.2 trillion cells, with up to 100,000 genes talking to each other in a chemical code of four letters, A, T, C and G-to post, copy, tweak, repeat, adapt, modify messages and instructions constantly-for you to function. The proofreading tools inside cells correct some typos, junk many, but some get overlooked. And they fester. Like fake news on social media, they spread lies, sending wrong signals to other cells giving rise to a series of mistakes, sometimes profoundly altering the biology of cells. If 10 million cells repeat the same error, a tumour forms, as big as the head of a pin, and starts shedding bits of its genes into the bloodstream, like a trail of bread crumbs.

Francis S. Collins, geneticist and head of the National Institutes of Health, US, wrote in his book Language of God: A Scientist Presents Evidence for Belief: "Science reveals that the universe, our own planet and life itself are engaged in an evolutionary process. The consequences of that can include the unpredictability of the weather, the slippage of a tectonic plate, or the misspelling of a cancer gene in the normal process of cell division." With the Human Genome Project (HGP), a massive international effort to unlock the secrets of our genetic script, taking off in 1991, cancer research got a massive leg up. Genes could be isolated from cells in pure form, analysed in full detail, multiplied manifold in the lab, changed at will. They could also be used to discover defects in the blueprint of one's body and to take proactive measures to stem the consequences, most significantly, the processes that give rise to cancers. The 2015 Nobel Prize in Chemistry was awarded to three scientists for explaining precisely how cells make mistakes, repair those and predispose people to cancer when repair mechanisms fail.

Now cancer researchers from Johns Hopkins University and Harvard Medical School have published a new study on the biology of cancer cells (Science, March 2017) that has kicked up a new debate. Based on the mathematical modelling of 32 types of cancers from 69 countries, they argue that about 66 per cent of cancers occur due to random mistakes during cell division, with only 29 per cent due to environmental factors (say, smoking or sun exposure) and 5 per cent to inherited genetic traits. These percentages, however, vary from cancer to cancer. In some lung tumours, environmental factors account for 65 per cent, while in prostate, brain and bone cancers, more than 95 per cent are due to random errors in cells. The study, despite the fears that its conclusions would undercut prevention efforts, has evoked the need for a new strategy, one that would emphasise early detection and treatment, in addition to prevention.

The problem with early detection is that when tumours form, they do not shed enough of a "bread crumbs trail" that can be picked up by CT-MRI-PET scans or by needle biopsies for possible malignancy. But what if cancer can be detected at such an early stage? The idea of a simple blood test as an alternative has come up recently. In India, Bengaluru-based genetic diagnostics company, Strand Life Sciences, has started offering the first phase of liquid biopsies: a simple, non-invasive diagnostic test using circulating tumour genes in a patient's blood, the first such test in India. "In the case of cancer patients, such blood tests can provide early information about tumour presence, relapse after therapy and response to therapy," explains Dr Vijay Chandru, CEO of Strand, who launched the test in April in association with the Mazumdar Shaw Centre for Translational Research, also in Bengaluru.

But what about therapies? Ever since former US president Jimmy Carter announced in 2015 that he was free of a deadly form of skin cancer after receiving surgery, radiation and "a new kind of treatment", he became a poster boy for the exciting new field: immunotherapy. Dr Suri explains that normal cells of the body die when they are not needed, are damaged, or are infected with virus, bacteria, parasites or fungi. "The immune system, the body's first line of defence, keeps track and as soon as it detects anything abnormal or unknown, it attacks and kills it," he says. But cancer cells trick the immune system into not recognising them as a threat. "This allows the tumours to grow and spread," he says. In immunotherapy, the immune system is enlisted to attack and force cancer cells to kill themselves.

Where does India stand in all this? Indian cancer patients have been the key partners in discovery of cancer antigen SPAG9, which is being used for personalised intervention by modulating the immune response, says Dr Suri. "Most new technologies are available in the country," says Dr Thangarajan Rajkumar, head of molecular oncology, Cancer Institute (WIA), Adyar, Chennai. "It is the cost of the newer therapies that is the major impediment. But that's true not only for India. Even some developed countries are finding it difficult to provide cancer care to people because of the prohibitive costs." The institute is conducting clinical trials of India's first therapeutic anti-cancer vaccine, SPAG9, in collaboration with Dr Suri and funded by the department of biotechnology and department of science and technology, Government of India. "Rather than directly attacking cancer cells, this therapy involves priming a patient's own immune cells to fight the cancer," he says. "Our immune system prevents most of us from developing cancer, but once cancer develops, the immune system becomes very subdued. The newer immunotherapies are addressing precisely this area, with great results."

With cervical cancer rising dramatically among Indian women-nearly 23 per cent of all cancers in women and over 100,000 deaths a year-it might just be a game-changer. One of the patients included in phase I of the clinical trials at the Cancer Institute, whose persistent cervical cancer had spread to the lungs even after radiotherapy, has been disease-free now for over nine years. The vaccine is being manufactured at a world-class industrial facility, owned by Biocon. Researchers at the institute have also developed a simple kit for cervical cancer screening, a biomarker panel for early diagnosis of ovarian cancer and a therapy to inhibit an aggressive bone cancer, Ewing's sarcoma-all awaiting further verification.

"There are major institutions across the country working on basic, translational and clinical research as applied to cancer," says Dr Rajkumar. New and potentially therapeutic molecules have been identified at the Indian Institute of Science, Bangalore, he points out. A multi-centre study under Professor Partha Majumdar of the National Institute of Biomedical Genomics at Kalyani, West Bengal, and Dr Rajiv Sarin of Tata Memorial Centre's ACTREC (Advanced Centre for Treatment, Research and Education in Cancer) in Mumbai, are doing promising work in cancer genomics. Truly cutting edge research may be taking place only at a few centres, but at hospitals and laboratories across the country, innovative molecular genetic tests, technology and techniques are being used. From next generation sequencing (NGS) technology to detecting genetic change driving a cancer, molecular diagnosis and monitoring, best-in-class radiotherapy equipment, new small molecules to specifically target the tumour cells, stem cell transplantation, hormone therapy to cellular therapy, it's all happening.

In December 2015, when Jimmy Carter called a press conference to announce that he had been cured of his cancer, the 'breakthrough' immunotherapy drug, Pembrolizumab, sold by pharma giant Merck as Keytruda, got a new moniker, "the president's drug". Keytruda, along with Bristol-Myers Squibb's Opdivo (Nivolumab), is one of a growing number of 'immuno-onco' drugs that unleash the body's immune system to fight malignant cells. Keytruda and Opdivo, effective against some forms of lung, skin, kidney and other cancers, are set to launch in the Indian market soon. Prohibitively expensive, above Rs 1 crore for an entire treatment, the drugs may not be for the general public. But they are shaping up to be the biggest blockbusters for the global pharma industry.

Most patented medicines are unaffordable to the average patient in India, even if priced lower than their western counterparts. But Indian companies, with their track record in generic drugs, are emerging as strong global players in the biosimilar (or exact copies of biological medicines that are already approved) segment of molecularly targeted cancer drugs. From Biocon, Cipla, Aurobindo Pharma, Dr Reddy's Laboratories, Intas Pharmaceuticals to Hetero Drugs, they are all expanding their biosimilar portfolios. Roche has teamed up with Emcure Pharmaceuticals to manufacture and sell its breast cancer drug, Herceptin, at a reduced price in India. "Biosimilars have made cancer treatment affordable to the middle class, and most companies have compassionate usage programmes," says Dr Chandy.

Immunotherapy is emerging as a 'sweet spot' among smaller research companies as well as investors. Biotech company Aurigene Discovery Technologies of Bengaluru has got into off-licence deals with global pharma companies like Curis, Orion and Pierre Fabre for its novel immunotherapy molecules. Delhi-based Curadev, a drug discovery company, has entered into collaboration with Roche. Ratan Tata, chairman emeritus of Tata Sons, has invested an undisclosed amount in biopharmaceutical firm Invictus Oncology, Delhi, to develop a cancer technology platform.

Jugnu Jain, molecular geneticist, cell biologist and inventor with three patents, returned to India from the US in 2011 and realised, surprisingly, that India did not have a human biobank. Globally, there are over 350. "Leftover tissues from surgery or diagnostic procedures, say, cancer tissue, blood or urine, are precious," she says, "highly sought after worldwide by researchers, diagnostics, biotech and pharma companies" to validate their drug candidates in target patient population samples, prior to launching clinical trials. They spur research into diseases: from identifying risk factors to diagnosing early, screening family members at risk to customising a patient's treatment to improve outcomes. Results from such studies can boost, sometimes even replace, the need to test new drugs. Ultimately, the war against cancer depends on cancer research.

Jain co-founded a health science firm, Saarum Innovations, and finally set up India's first commercial biobank and personalised medicine company, Sapien Biosciences, a joint venture with Apollo Hospitals, in Hyderabad in 2013. The work is in full flow. Imagine live cancer cells growing in the lab. Study those to understand the complexity of a tumour, screen new drug candidates, use cultured cancer cells as models to investigate the changes that may have caused cancer, or its spread, or its resistance to a therapy. There are many other applications of fresh samples in a biobank, she says. "Several companies in China have built thousands of cancer models in biobanks, which are being used by pharma companies to screen drug molecules. We can too."

With excitement building around the innovative research in the cancer space, it's hard not to think of a cure. "But to conquer a complicated, costly and devastating disease such as cancer, many more major scientific breakthroughs are needed," says Mukherjee. Medicine still needs to catch up. The battle still relies largely on three brute-force weapons: surgery, radiation and chemotherapy. Cancer cells are subtle and smart. So the treatment needs to be more sophisticated. And bringing in the latest and the best are gene therapies. He points to an important development that took place in 2013: a unique technology, the CRISPR-Cas9 system, currently the most versatile method of genetic manipulation. It's somewhat like conducting a molecular surgery on genes: remove abnormal sequences, replace them with normal ones, pull out genes that give an advantage to cancer cells. The idea comes from some types of bacteria that have a built-in gene editing system against invaders, say, a virus. "Your genome has three billion letters, ATCGs. If it were to be written down, it would be 66 full sets of Encyclopaedia Britannica," he explains. "What if you can take out a letter, one that predisposes you to cancer, erase or tweak it to your advantage?"

Can that be the future of cancer? Or, perhaps, our future without cancer?

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From the India Today archives (2017) | A future without cancer? - India Today