Latest news with #Basel
Yahoo
8 hours ago
- Business
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New data show Roche's Itovebi significantly extended survival in a certain type of HR-positive advanced breast cancer
The ItovebiTM (inavolisib)-based regimen reduced the risk of death by more than 30% in people with -mutated HR-positive, HER2-negative advanced breast cancer, compared with palbociclib and fulvestrant alone1 The mutation is found in approximately 40% of HR-positive advanced breast cancers and is associated with a poor prognosis2,3 New data are being presented in an oral session at the 2025 American Society of Clinical Oncology (ASCO) Annual Meeting and published in the 1 Basel, 31 May 2025 - Roche (SIX: RO, ROG; OTCQX: RHHBY) announced today positive final results from the overall survival (OS) analysis of the phase III INAVO120 study. These data showed ItovebiTM (inavolisib), in combination with palbociclib (Ibrance®) and fulvestrant, reduced the risk of death by more than 30% compared with palbociclib and fulvestrant alone. This represents a statistically significant and clinically meaningful improvement in overall survival for people with PIK3CA-mutated, hormone receptor (HR)-positive, human epidermal growth factor receptor 2 (HER2)-negative, endocrine-resistant, locally advanced or metastatic breast cancer.1 The results are being presented in an oral session at the 2025 American Society of Clinical Oncology (ASCO) Annual Meeting and simultaneously published in the New England Journal of Medicine (NEJM).1 "For the first time, a PI3K pathway-targeted drug has shown it can help people with this breast cancer subtype live longer," said Levi Garraway, M.D., Ph.D., Roche's Chief Medical Officer and Head of Global Product Development. "Itovebi exemplifies our continued commitment to improve survival rates for people with this common PIK3CA mutation, for whom more effective treatment options are needed.' 'The landmark data for the inavolisib-based regimen showed not only a doubling in progression-free survival, but importantly that it extended lives and gave people more time without chemotherapy,' said Professor Nicholas Turner, Lead Study Author and Professor of Molecular Oncology at The Institute of Cancer Research, and Consultant Medical Oncologist at The Royal Marsden NHS Foundation Trust, London, United Kingdom. 'These results give us confidence that this regimen could become the new standard of care in the first-line setting, having demonstrated a substantial benefit on patient outcomes and quality of life.' The Itovebi-based regimen demonstrated a meaningful OS benefit compared with palbociclib and fulvestrant alone.1 The median OS was 34.0 months (95% CI: 28.4–44.8) for people in the Itovebi arm, compared with 27.0 months (95% CI: 22.8–38.7) in the palbociclib and fulvestrant arm (stratified hazard ratio [HR]=0.67; 95% CI: 0.48–0.94, p-value=0.0190 [boundary=0.0469]).1 The benefit seen in delaying cancer progression was maintained in the updated analysis, with the Itovebi-based regimen showing a consistent improvement in median progression free survival of 17.2 months versus 7.3 months (stratified HR=0.42; 95% CI: 0.32-0.55) in the comparator arm.1 The Itovebi-based regimen also led to a statistically significant improvement in objective response rate (the percentage of patients whose signs of cancer completely disappear or their tumours shrink significantly after treatment) and ad-hoc exploratory analyses showed it substantially delayed time to chemotherapy by approximately two years (stratified HR=0.43; 95% CI: 0.30-0.60).1 No new safety signals were observed at the time of the final OS analysis, with a low discontinuation due to adverse events supporting good tolerability.1 The Itovebi-based regimen is approved in the United States, Switzerland, Canada, Australia, United Arab Emirates and China. In May, it received a positive opinion from the European Medicines Agency's Committee for Medicinal Products for Human Use (CHMP), with a final decision regarding the approval expected from the European Commission in the near future. Data from the INAVO120 study are currently under review with other global health authorities. Beyond INAVO120, Itovebi is currently being investigated in three company-sponsored phase III studies (INAVO121, INAVO122, INAVO123), all in PIK3CA-mutated, locally advanced or metastatic breast cancer in various combinations.4-7 We are exploring additional studies in breast cancer and other tumour types with the hope of providing the benefit of this targeted therapy to more people with PIK3CA mutations. About Itovebi TM (inavolisib)Itovebi is an oral, targeted treatment that has been shown to provide well-tolerated and durable disease control in people with PIK3CA-mutated, hormone receptor-positive, human epidermal growth factor receptor 2-negative, advanced breast cancer, who often have a poor prognosis and are in urgent need of new treatment options.2,3,8 Itovebi has been designed to help minimise the overall burden and toxicity of treatment and is differentiated from other PI3K inhibitors due to its high potency and specificity for the PI3K alpha isoform versus other isoforms, and unique mechanism of action that facilitates the degradation of mutated PI3K alpha.9,10 About the INAVO120 studyThe INAVO120 study [NCT04191499] is a phase III, randomised, double-blind, placebo-controlled study evaluating the efficacy and safety of Itovebi™ (inavolisib) in combination with palbociclib and fulvestrant versus placebo plus palbociclib and fulvestrant in people with PIK3CA-mutated, hormone receptor (HR)-positive, human epidermal growth factor receptor 2 (HER2)-negative, locally advanced or metastatic breast cancer whose disease progressed during treatment or within 12 months of completing adjuvant endocrine therapy and who have not received prior systemic therapy for metastatic disease.4 The study included 325 patients, who were randomly assigned to either the investigational or control treatment arm.4 The primary endpoint is progression-free survival, as assessed by investigators, defined as the time from randomisation in the clinical trial to the time when the disease progresses, or a patient dies from any cause.4 Secondary endpoints include overall survival, objective response rate, and clinical benefit rate.4 Beyond INAVO120, Itovebi is currently being investigated in three additional company-sponsored phase III clinical studies in PIK3CA-mutated locally advanced or metastatic breast cancer in various combinations:5-7 in combination with fulvestrant versus alpelisib plus fulvestrant in HR-positive/HER2-negative breast cancer post cyclin-dependent kinase 4/6 (CDK4/6) inhibitor and endocrine combination therapy (INAVO121; NCT05646862). in combination with pertuzumab plus trastuzumab for subcutaneous injection (SC) versus pertuzumab plus trastuzumab for SC and optional physician's choice of endocrine therapy as a maintenance treatment in HER2-positive disease (INAVO122; NCT05894239). in combination with CDK4/6 inhibitor and letrozole versus placebo plus a CDK4/6 inhibitor and letrozole in the first-line setting in PIK3CA-mutated HR-positive/HER2-negative, endocrine-sensitive breast cancer (INAVO123; NCT06790693). About hormone receptor (HR)-positive breast cancerHR-positive breast cancer is the most prevalent type of all breast cancers, accounting for approximately 70% of cases.11,12 A defining feature of HR-positive breast cancer is that its tumour cells have receptors that attach to one or both hormones – oestrogen or progesterone – which can contribute to tumour growth. People diagnosed with HR-positive metastatic breast cancer often face the risk of disease progression and treatment side effects, creating a need for additional treatment options.12-14 The PI3K signalling pathway is commonly dysregulated in HR-positive breast cancer, often due to activating PIK3CA mutations, which have been identified as a potential mechanism of intrinsic resistance to standard of care endocrine therapy in combination with cyclin-dependent kinase 4/6 inhibitors.3 About Roche in breast cancerRoche has been advancing breast cancer research for more than 30 years with the goal of helping as many people with the disease as possible. Our medicines, along with companion diagnostic tests, have contributed to bringing breakthrough outcomes in human epidermal growth factor 2-positive and triple-negative breast cancers. As our understanding of breast cancer biology rapidly improves, we are working to identify new biomarkers and approaches to treatment for other subtypes of the disease, including oestrogen receptor-positive breast cancer, which is a form of hormone receptor-positive breast cancer, the most prevalent type of all breast cancers.11,12About Roche Founded in 1896 in Basel, Switzerland, as one of the first industrial manufacturers of branded medicines, Roche has grown into the world's largest biotechnology company and the global leader in in-vitro diagnostics. The company pursues scientific excellence to discover and develop medicines and diagnostics for improving and saving the lives of people around the world. We are a pioneer in personalised healthcare and want to further transform how healthcare is delivered to have an even greater impact. To provide the best care for each person we partner with many stakeholders and combine our strengths in Diagnostics and Pharma with data insights from the clinical practice. For over 125 years, sustainability has been an integral part of Roche's business. As a science-driven company, our greatest contribution to society is developing innovative medicines and diagnostics that help people live healthier lives. Roche is committed to the Science Based Targets initiative and the Sustainable Markets Initiative to achieve net zero by 2045. Genentech, in the United States, is a wholly owned member of the Roche Group. Roche is the majority shareholder in Chugai Pharmaceutical, Japan. For more information, please visit All trademarks used or mentioned in this release are protected by Turner NC, et al. INAVO120 Phase III trial final overall survival (OS) analysis of first-line inavolisib (INAVO)/placebo (PBO) + palbociclib (PALBO) + fulvestrant (FULV) in patients (pts) with PIK3CA-mutated, hormone receptor-positive (HR+), HER2-negative (HER2–), endocrine-resistant advanced breast cancer (aBC). Presented at the American Society of Clinical Oncology (ASCO) Annual Meeting, 2025 May 30-June 03; Chicago, USA. Abstract #1003.[2] Fillbrunn M, et al. PIK3CA mutation status, progression and survival in advanced HR+/HER2- breast cancer: a meta-analysis of published clinical trials. BMC Cancer. 2022;22(1):1002.[3] Anderson E, et al. A Systematic Review of the Prevalence and Diagnostic Workup of PIK3CA Mutations in HR+/HER2– Metastatic Breast Cancer. Int J Breast Cancer. 2020;2020:3759179.[4] A Study Evaluating the Efficacy and Safety of Inavolisib + Palbociclib + Fulvestrant vs Placebo + Palbociclib + Fulvestrant in Patients With PIK3CA-Mutant, Hormone Receptor-Positive, Her2-Negative, Locally Advanced or Metastatic Breast Cancer (INAVO120) [Internet; cited 2025 May]. Available from: [5] A Study Evaluating the Efficacy and Safety of Inavolisib Plus Fulvestrant Compared With Alpelisib Plus Fulvestrant in Participants With HR-Positive, HER2-Negative, PIK3CA Mutated, Locally Advanced or Metastatic Breast Cancer Post CDK4/6i and Endocrine Combination Therapy (INAVO121) [Internet; cited 2025 May]. Available from: [6] A Study to Evaluate the Efficacy and Safety of Inavolisib in Combination With Phesgo Versus Placebo in Combination With Phesgo in Participants With PIK3CA-Mutated HER2-Positive Locally Advanced or Metastatic Breast Cancer (INAVO122) [Internet; cited 2025 May]. Available from: [7] A Study Evaluating the Efficacy and Safety of Inavolisib Plus CDK4/6 Inhibitor and Letrozole vs Placebo + CDK4/6i and Letrozole in Participants With Endocrine-Sensitive PIK3CA-Mutated, Hormone Receptor-Positive, HER2-Negative Advanced Breast Cancer (INAVO123) [Internet; cited 2025 May]. Available from: Turner NC, et al. Inavolisib-Based Therapy in PIK3CA-Mutated Advanced Breast Cancer. NEJM. 2024;391(17):1584-96.[9] Juric D, et al. A phase I/Ib study of inavolisib (GDC-0077) in combination with fulvestrant in patients (pts) with PIK3CA-mutated hormone receptor-positive/HER2-negative (HR+/HER2–) metastatic breast cancer. Presented at San Antonio Breast Cancer Symposium, 2020 December 7-10; San Antonio, USA. Abstract #P5-17-05.[10] Hong R, et al. GDC-0077 is a selective PI3K alpha inhibitor that demonstrates robust efficacy in PIK3CA mutant breast cancer models as a single agent and in combination with standard of care therapies. Cancer Res. 2018;78(4):4-14.[11] National Cancer Institute: Surveillance, Epidemiology and Ends Result Program. Cancer Stat Facts: Female Breast Cancer Subtypes [Internet; cited 2025 May]. Available from: [12] Lim E, et al. The natural history of hormone receptor-positive breast cancer. Oncology (Williston Park). 2012;26(8):688-94,696.[13] Tomas R and Barrios CH. Optimal management of hormone receptor positive metastatic breast cancer in 2016. Ther Adv Med Oncol. 2015;7(6):304-20.[14] Galipeau N, et al. Understanding key symptoms, side effects, and impacts of HR+/HER- advanced breast cancer: qualitative study findings. J Patient-Rep Outcomes. 2019;3(1):10. Roche Global Media RelationsPhone: +41 61 688 8888 / e-mail: Hans Trees, PhDPhone: +41 79 407 72 58 Sileia UrechPhone: +41 79 935 81 48 Nathalie AltermattPhone: +41 79 771 05 25 Lorena CorfasPhone: +41 79 568 24 95 Simon GoldsboroughPhone: +44 797 32 72 915 Karsten KleinePhone: +41 79 461 86 83 Nina MählitzPhone: +41 79 327 54 74 Kirti PandeyPhone: +49 172 6367262 Yvette PetillonPhone: +41 79 961 92 50 Dr Rebekka SchnellPhone: +41 79 205 27 03 Roche Investor Relations Dr Bruno EschliPhone: +41 61 68-75284e-mail: Dr Sabine BorngräberPhone: +41 61 68-88027e-mail: Dr Birgit MasjostPhone: +41 61 68-84814e-mail: Investor Relations North America Loren KalmPhone: +1 650 225 3217e-mail: Attachment 31052025_INAVO120 study Itovebi_enError in retrieving data Sign in to access your portfolio Error in retrieving data Error in retrieving data Error in retrieving data Error in retrieving data
Yahoo
2 days ago
- Business
- Yahoo
Roche's fenebrutinib maintains near-complete suppression of disease activity and disability progression for up to two years in people with relapsing multiple sclerosis
Patients on fenebrutinib had low relapse rates with data showing no active brain lesions or disability progression after nearly two years of treatment Phase III studies for fenebrutinib in relapsing and primary progressive multiple sclerosis are expected to start reading out at year end Basel, 30 May 2025 - Roche (SIX: RO, ROG; OTCQX: RHHBY) announced today new, 96-week data for fenebrutinib demonstrating that patients with relapsing multiple sclerosis (RMS) maintained no disability progression and low levels of disease activity for up to two years. The latest results for this investigational Bruton's tyrosine kinase (BTK) inhibitor from the Phase II FENopta open-label extension (OLE) study were presented at the Consortium of Multiple Sclerosis Centers (CMSC) Annual Meeting in Phoenix, Arizona. 'These data show that patients treated with fenebrutinib experienced an annualised relapse rate equal to one relapse every 17 years and no observed disability progression up to two years,'' said Levi Garraway, M.D., Ph.D., Roche's Chief Medical Officer and Head of Global Product Development. 'Fenebrutinib is potent, highly selective and the only reversible BTK inhibitor currently in Phase III trials for multiple sclerosis, and we look forward to seeing the first of those results later this year.' Ninety-nine patients entered the OLE and 93 remained in the OLE after 96 weeks. During the OLE period, patients treated with fenebrutinib for up to 96 weeks had a low annualised relapse rate (ARR) of 0.06, and during this time there was no disability progression, as measured by the Expanded Disability Status Scale (EDSS). MRI scans showed that fenebrutinib treatment suppressed disease activity in the brain. At 96 weeks zero new T1 gadolinium-enhancing (T1-Gd+) lesions, which are markers of active inflammation, were detected. In the treatment group that switched from placebo to fenebrutinib in the OLE, the annualised rate of new or enlarging T2 lesions, which represent chronic disease burden, decreased from 6.72 at the end of the 12 week double-blind period to 0.34 by 96 weeks. The safety profile of fenebrutinib in the OLE was consistent with previously reported data, with no new safety concerns identified at 96 weeks. The most common adverse events (AEs) in ≥5% of patients were COVID-19 (10%), urinary tract infection (10%), pharyngitis (6%) and respiratory tract infection (5%). Serious AEs occurred in two patients (2%). During the OLE, one patient experienced asymptomatic alanine aminotransferase elevation at OLE week 4, after 16 weeks on treatment, which resolved with treatment discontinuation. Three Phase III clinical trials are ongoing, including the FENhance 1 and 2 trials in RMS and the FENtrepid trial in primary progressive multiple sclerosis (PPMS). The first data from these studies, which will characterise the effects of fenebrutinib on disease progression across the multiple sclerosis spectrum, are expected at the end of 2025. About fenebrutinibFenebrutinib is an investigational oral, reversible and non-covalent Bruton's tyrosine kinase (BTK) inhibitor that blocks the function of BTK. BTK, also known as tyrosine-protein kinase BTK, is an enzyme that regulates B-cell development and activation and is also involved in the activation of innate immune system myeloid lineage cells, such as macrophages and microglia. Preclinical data have shown fenebrutinib to be potent and highly selective, and it is the only reversible BTK inhibitor currently in Phase III trials for multiple sclerosis. Fenebrutinib has been shown to be 130 times more selective for BTK vs. other kinases. Fenebrutinib is a dual inhibitor of both B-cell and microglia activation. This dual inhibition may be able to reduce both multiple sclerosis disease activity and disability progression, thereby potentially addressing the key unmet medical need of disability progression in people living with multiple sclerosis. The fenebrutinib Phase III programme includes two identical trials in relapsing multiple sclerosis (RMS) (FENhance 1 & 2) with active comparator teriflunomide and the only trial in primary progressive multiple sclerosis (PPMS) (FENtrepid) in which a BTK inhibitor is being evaluated against OCREVUS. To date, more than 2,700 patients and healthy volunteers have been treated with fenebrutinib in Phase I, II and III clinical programmes across multiple diseases, including multiple sclerosis and other autoimmune disorders. About the FENopta studyThe FENopta study was a global Phase II, randomised, double-blind, placebo-controlled 12-week study to investigate the efficacy, safety and pharmacokinetics of fenebrutinib in 109 adults aged 18-55 years with relapsing multiple sclerosis (RMS). The primary endpoint was the total number of new T1 gadolinium-enhancing (T1-Gd+) lesions as measured by MRI scans of the brain at 4, 8 and 12 weeks. Secondary endpoints included the number of new or enlarging T2-weighted lesions as measured by MRI scans of the brain at 4, 8 and 12 weeks, and the proportion of patients free from any new T1-Gd+ lesions and new or enlarging T2-weighted lesions as measured by MRI scans of the brain at 4, 8 and 12 weeks. The goal of the FENopta study was to characterise the effect of fenebrutinib on MRI and soluble biomarkers of disease activity and progression, and it included an optional substudy to measure cerebrospinal fluid fenebrutinib levels and biomarkers of neuronal injury. Data from the 12-week study showed that fenebrutinib is central nervous system (CNS) penetrant (crosses the blood-brain barrier) and has the potential to impact mechanisms underlying chronic progressive disease biology in multiple sclerosis patients. Fenebrutinib significantly reduced new T1-Gd+ lesions and new/enlarging T2 lesions compared to placebo. The safety profile of fenebrutinib was consistent with previous and ongoing fenebrutinib clinical trials and there were no new safety concerns identified. Patients who completed the FENopta study were given the option to take part in an open-label extension (OLE) study, in which all patients receive fenebrutinib up to 192 weeks. About multiple sclerosisMultiple sclerosis is a chronic disease that affects more than 2.9 million people worldwide. Multiple sclerosis occurs when the immune system abnormally attacks the insulation and support around nerve cells (myelin sheath) in the central nervous system (brain, spinal cord and optic nerves), causing inflammation and consequent damage. This damage can cause a wide range of symptoms, including weakness, fatigue and difficulty seeing, and may eventually lead to disability. Most people with multiple sclerosis experience their first symptom between 20 and 40 years of age, making the disease the leading cause of non-traumatic disability in younger adults. People with all forms of multiple sclerosis experience disease progression from the beginning of their disease. Therefore, delays in diagnosis and treatment can negatively impact people with multiple sclerosis, in terms of their physical and mental health, and contribute to the negative financial impact on the individual and society. An important goal of treating multiple sclerosis is to slow, stop and ideally prevent progression as early as possible. Approximately 85% of people with multiple sclerosis have a relapsing form of the disease (RMS) characterised by relapses and also worsening disability over time. Primary progressive multiple sclerosis (PPMS) is a debilitating form of the disease marked by steadily worsening symptoms but typically without distinct relapses or periods of remission. Approximately 15% of people with multiple sclerosis are diagnosed with the primary progressive form of the disease. Until the FDA approval of OCREVUS, there had been no FDA-approved treatments for PPMS and OCREVUS is still the only approved treatment for PPMS. About Roche in NeuroscienceNeuroscience is a major focus of research and development at Roche. Our goal is to pursue groundbreaking science to develop new treatments that help improve the lives of people with chronic and potentially devastating diseases. Roche is investigating more than a dozen medicines for neurological disorders, including multiple sclerosis, spinal muscular atrophy, neuromyelitis optica spectrum disorder, Alzheimer's disease, Huntington's disease, Parkinson's disease and Duchenne muscular dystrophy. Together with our partners, we are committed to pushing the boundaries of scientific understanding to solve some of the most difficult challenges in neuroscience today. About Roche Founded in 1896 in Basel, Switzerland, as one of the first industrial manufacturers of branded medicines, Roche has grown into the world's largest biotechnology company and the global leader in in-vitro diagnostics. The company pursues scientific excellence to discover and develop medicines and diagnostics for improving and saving the lives of people around the world. We are a pioneer in personalised healthcare and want to further transform how healthcare is delivered to have an even greater impact. To provide the best care for each person we partner with many stakeholders and combine our strengths in Diagnostics and Pharma with data insights from the clinical practice. For over 125 years, sustainability has been an integral part of Roche's business. As a science-driven company, our greatest contribution to society is developing innovative medicines and diagnostics that help people live healthier lives. Roche is committed to the Science Based Targets initiative and the Sustainable Markets Initiative to achieve net zero by 2045. Genentech, in the United States, is a wholly owned member of the Roche Group. Roche is the majority shareholder in Chugai Pharmaceutical, Japan. For more information, please visit All trademarks used or mentioned in this release are protected by law. Roche Global Media RelationsPhone: +41 61 688 8888 / e-mail: Hans Trees, PhDPhone: +41 79 407 72 58 Sileia UrechPhone: +41 79 935 81 48 Nathalie AltermattPhone: +41 79 771 05 25 Lorena CorfasPhone: +41 79 568 24 95 Simon GoldsboroughPhone: +44 797 32 72 915 Karsten KleinePhone: +41 79 461 86 83 Nina MählitzPhone: +41 79 327 54 74 Kirti PandeyPhone: +49 172 6367262 Yvette PetillonPhone: +41 79 961 92 50 Dr Rebekka SchnellPhone: +41 79 205 27 03 Roche Investor Relations Dr Bruno EschliPhone: +41 61 68-75284e-mail: Dr Sabine BorngräberPhone: +41 61 68-88027e-mail: Dr Birgit MasjostPhone: +41 61 68-84814e-mail: Investor Relations North America Loren KalmPhone: +1 650 225 3217e-mail: Attachment 30052025_96-week data for fenebrutinib_enError while retrieving data Sign in to access your portfolio Error while retrieving data Error while retrieving data Error while retrieving data Error while retrieving data
Malay Mail
3 days ago
- Entertainment
- Malay Mail
Eurovision 2025 in Basel draws 166 million viewers in 37 countries, voting received from 146 states
GENEVA, May 29 — The Eurovision Song Contest confirmed its place as the world's biggest live televised music event, with 166 million viewers in 37 countries watching the 2025 competition, organisers said yesterday. This year's 69th edition in Basel, Switzerland, attracted three million more viewers than last year's contest in Malmo, Sweden, said the European Broadcasting Union. The EBU said Eurovision had seen significant increases in youth engagement with a record 60 percent of viewers aged 15-24 tuning in. The May 17 final was won by 24-year-old Austrian JJ, whose real name is Johannes Pietsch, singing 'Wasted Love', which blended techno beats with operatic vocals. 'This year's Eurovision Song Contest has once again demonstrated its extraordinary power to unite millions across continents through the joy of music and shared celebration,' said Eurovision director Martin Green. After the nail-biting drama as the votes from national juries and the public were revealed, Austria finished with 436 points, ahead of Israel — whose participation drew protests — on 357 and Estonia on 356. Votes were cast from 146 states, with viewers in the United States and Canada voting the most outside Europe, ahead of Mexico, the United Arab Emirates and South Africa. The final commanded viewing shares above 50 percent in 19 of the 37 European markets, led by Iceland (98 percent), Finland (91 percent), Sweden (90 percent), Norway (85 percent), and Denmark (75 percent). The viewing shares in Finland, and in France (40 percent), were the highest ever for Eurovision. The highest average audience was in Germany, with 9.1 million viewers — the best figures since 2016, said the EBU. Meanwhile there were 969 million views on Instagram and 748.5 million on TikTok. Following JJ's win, next year's event will be hosted in Austria. — AFP
Express Tribune
3 days ago
- General
- Express Tribune
Strangers to home
As a convoy moves in to raze brick houses to the ground, a community of villagers cries out. That's the limit to the brave front they can put up, as long as it doesn't upset their armed oppressors enough to open fire. These uniformed individuals then cite impassive demolition papers to justify bearing down on homes made of love and labour in Masafer Yatta in Palestine. A woman watches her quarters, her belongings, every corner of memory in her precious home being crushed to dust. Not subdued by aloof demands of relocation, she protests, "Where do we go? We have no other land. That's why we suffer for it." This picture might be familiar to you if you're on social media and have scrolled through countless pleas and tears entreating justice, all emerging from one Palestine torn apart by Israel's genocide. In that spirit, Palestinian activist Basel Adra picked up a camera to film his documentary, No Other Land, the moment he believed that the beginning of the end had become unavoidable. It's harrowing enough to watch social media to spell out the atrocities for you within a minute or two. But as I sat for over two hours at the screening for No Other Land organised by The Second Floor (T2F), I was compelled to face the spine-chilling reality with an intimacy that was difficult to evade. And that's exactly the point. Following a non-linear structure, the story of Masafer Yatta through Basel's eyes begins in 2019. In addition, Basel's own memories from 1999 slip into the narrative time and again to put into perspective that Israel's brutality following the October 7, 2023 attack wasn't merely a response but one aided by a veneered pretext. Letting it sink in Be it class debates or close-knit settings discussing the Palestinian struggle, I sit quietly and listen as intently as my twitchy mind allows me to. But when it comes to contributing to the conversation, I often find myself struggling to string together pointers that haven't already been said. Unsurprisingly, the same happened as No Other Land unfolded before my eyes. I was rendered speechless, as the cousin accompanying me would say. Basel's sturdy sense of hope along with the smiles that his people sport as defense are as heart-rending as they are warm, and just as soul-crushing as when Basel himself admits to Yuval that he's losing energy. It felt futile - speaking from a distance, watching from a distance. Then I saw Harun Abu Aram. Mirrored fragments The documentary shows Harun, an unarmed resident of Al-Tuwanah (a village to the south of Hebron), resisting as Israeli troops seize his electric generator. Moments into the heated escalation, the troops shoot Harun, cruelly subjecting him to lifelong paralysis. As time prolongs his suffering, Harun's mother hopes for one of two miracles: for God to take her life and restore her son to full health in exchange, or for death to relieve her son once and for all. Her second prayer is answered. Watching Harun and his family struck me with heart-sinking unease and thoughts that aren't easy to confront or pen down. Even after the screen faded to black, their plight stayed with me, haunted me to some capacity. It followed me back home to my bedridden aunt. For months, I have been struggling to put into words how I feel. When you're informed from the distance of a phone call that a loved one - a particularly lively one — has bled from the inside, the first companion to comfort you is denial. There are no tears, no adrenaline rush, no grief — just restless pacing and sleepless midnights that fade to tomorrows. Over and over again. When you see her again, you can barely recognise her. She looks the same, smooth-skinned and relaxed as she always has. But she's no longer fishing for compliments over an outfit she carefully picked or dissolving flimsy debates with a harmless joke. She just rests. That's all she prefers doing these days. The denial tricks you into thinking it's gone. But then you revisit old texts and send new ones for no real reason. Some days, you surprise yourself at your eagerness to initiate drawn-out conversations despite knowing that she can't respond. Every now and then, you recall a vivid memory because at least in your mind, her verve is eternal. Regularly, you squeeze her hand, fix her scarf, help her move, and cling onto hope. But now, you sit with the reminder that hope is a luxury in a war-torn world — and your smaller world is safely tucked away from it. Denial is not a helpful instrument for Harun's loved ones, who wait with bated breath for both good and bad news. Where they possess a wealth of love, they are robbed of resources. There is no comfort zone for them to retreat to. All they have is hope. And hope can be deceptive. It hurts differently when you watch Harun's family reserve the warmest blankets for him; it hurts close to home, even. But it can never hurt quite the same because no one can snatch those blankets from you or ruthlessly bury them under rubble. Because many of us didn't grow up surrounded by echoes of the same desperate question: "Why is it only illegal for us?" From the river to the sea At the time of writing this, a video has been circulating on social media: a silhouette of a girl moving hurriedly as she flees a line of flames rising well over her height. Israeli forces bombed her school, Fahmi al-Jargawi School, in Gaza while she was still inside. Earlier, the BBC reported that an Israeli airstrike targeted the home of a doctor in Gaza. While on duty at al-Tahrir hospital, she received the news that nine of 10 children had been killed. The eldest was 12 years old. In 2024, heavy rain poured down on over hundreds of tents of displaced Palestinians in Khan Younis, as per Al Jazeera. Israel still blocked aid to the civilians. In 2023, medics evacuated premature babies from Gaza's al-Shifa Hospital after the Israeli army raided it over claims that Hamas was secretly operating from there. In 2020, Israeli authorities shot down 27 Palestinians, including seven minors, across occupied territories. And the scroll keeps on rolling. Individuals become stories, stories form headlines, and headlines are buried under statistics. It is as Basel said as he accepted the Oscar for his documentary, "No Other Land reflects the harsh reality that we have been enduring for decades and still we resist and call on the world to take serious action to stop this injustice." Against the shelling and gunfire, Palestinian resistance — as No Other Land depicts — births a throng fuelled by hope, chants with the ease of an anthem, and marches on. And resistance is the weight they all shoulder. It looks like mothers humouring their children out of despair, fathers stirring up spirits, and children standing up against armed soldiers as their schools are demolished. It exists in one shared sentiment: "They'll never make Palestinians leave this land."
Yahoo
4 days ago
- Entertainment
- Yahoo
What is the furthest a footballer has been offside when scoring a goal?
'Leyton Orient's Charlie Kelman was four yards offside ' begins Jessica Hibbert. 'What's the furthest a player has been indisputably offside before going on to score?' In the spirit of Annie Hall, let's get Jeff Astle out the way so that we can relax and digest our offside goals better. His infamous tap-in at Elland Road in April 1971 isn't relevant here because Jessica asked specifically about goal scorers who were offside. In that case the controversy – 'And Leeds will go mad! And they've every right to go mad!' – was about the position of Colin Suggett and whether he was interfering with play. Scoring a goal is possibly the ultimate interference with play, and there are plenty of goal scorers who look bang to rights through modern eyes. Let's start with a couple from the World Cup. Roberto Baggio (Italy 2-1 England, 1990, although he probably should have had a penalty seconds earlier, and don't get us started on Nicola Berti's disallowed goal in the same game) Carlos Tevez (Argentina 3-1 Mexico, 2010) From the World Cup to League One, where Steven Fletcher's winner for Wrexham at Huddersfield this season had not so much a whiff of offside as a stench. Hearts' stirring Uefa Cup run in 1988-89 included a hard-fought 1-0 aggregate win over Austria Vienna, with Mike Galloway scoring the decisive goal in the away leg. We can't be certain because of the camera angles, but both Galloway and the creator, Walter Kidd, look so far offside that they could have done with their passports just in case. While Hearts lost to Bayern Munich in the quarter-finals, Longford Town went all the way in the FAI Cup of 2003, beating St Patrick's Athletic 2-0 in the final to win their first major trophy. They would have won anyway, as the second goal from was the last action of the game, but it did not entirely satisfy the requirements of Law 11.1. Thanks to Mike Slattery for explaining the context behind this. The St Pat's keeper Chris Adamson had gone up for a corner, meaning Barrett was six or seven yards offside when he received the ball. 'I can't find a reference to any controversy about the goal,' writes Mike, 'meaning that nobody (including the match officials, apparently) realised there was anything wrong.' Barrett is clearest offside in terms of distance beyond the last defender, but our favourite – sent in by Pete Tomlin and others – is 's goal for Schalke against Basel in the 2013-14 Champions League. Basel's offside trap worked perfectly – or it would have done had the assistant registered that four Schalke players were offside. Schalke 04 indeed. One of them was Matip, who had time to go through the alphabet backwards before putting the ball into the net. Or, as the Uefa website said at the time, 'The Basel defence mistimed their offside trap as the forward's right-wing free-kick swung over, allowing Matip all the time and space he needed to chest down and plant past the stranded Sommer.' Thank goodness we've got VAR now. 'Last week you listed the worst European finals based on league position,' says Richie Farquhar. 'What are the best? How many times have two champions of their country met in the final?' Thanks to the netbusting adventures of Scott McTominay and Romelu Lukaku, Saturday's Champions League final between Internazionale and Paris Saint-Germain will involve only the champions of France. Nothing new there: only 13 out of 70 European Cup and Champions League finals have been between teams who both won their domestic title the same season. 1964-65 Inter 1-0 Benfica 1972-73 Ajax 1-0 Juventus 1976-77 Liverpool 3-1 Borussia Mönchengladbach 1990-91 Red Star Belgrade 0-0 Marseille (5-3 pens) 1992-93 Marseille* 1-0 Milan 1993-94 Milan 4-0 Barcelona 1998-99 Man Utd 2-1 Bayern Munich 2008-09 Barcelona 2-0 Man Utd 2009-10 Inter 2-0 Bayern Munich 2010-11 Barcelona 3-1 Man Utd 2014-15 Barcelona 3-1 Juventus 2016-17 Real Madrid 4-1 Juventus 2019-20 Bayern Munich 1-0 Paris Saint-Germain * Marseille were subsequently stripped of their French title but not the Champions League. 'My son is a goalkeeper and he wondered if there has ever been a professional goalkeeper in top-tier football who has worn No 10?' asks Dave Sturges. A number of you mentioned the bald maverick Cristiano Lupatelli, who wore No 10 when he played in Serie A with Chievo from 2001 to 2003. The shirt was vacant after Raffaele Cerbone left the club, which gave Lupatelli an idea. 'According to an interview with Italian goalkeeping website Il Numero 1 he said that it came about because of a bet with friends,' writes Pete Tomlin. 'He said: 'It all started as a joke, and it became a reality. I think it is a funny and nice thing.'' Jim Hearson tells us that, when Lupatelli rejoined Roma in the summer of 2003, he took the No 3 shirt. The No 10 wasn't available, alas, due to some clingy killjoy called Francesco Totti. 'Ignacio 'Nacho' Gonzáles did it for Argentina in the 1997 Copa América,' writes Pablo Zadunaisky. And here's the proof. 'Spurs finished 17th in the Premier League,' notes Paul Savage. 'Has a team ever finished lower while winning a European trophy in the same season?' The short answer is: nope. There have been finalists who finished lower than 17th – see last week's Knowledge – but, excluding the Intertoto Cup for obvious reasons, Spurs are the lowest of the low in this particular sphere. We think only eight teams have won a European trophy while finishing outside the top 10 of their domestic league. And here they are: 17 Tottenham Hotspur (Europa League, 2024-25)14 West Ham (Conference League, 2022-23)13 Internazionale (Uefa Cup, 1993-94)12 Arsenal (Fairs Cup 1969-70), Schalke (Uefa Cup, 1996-97), Sevilla (Europa League 2022-23)11 Aston Villa (European Cup 1981-82), Eintracht Frankfurt (Europa League 2021-22) 'Luis Suárez picked up a championship winner's medal for Ajax while playing for Liverpool against Spurs,' wrote Nick Young in 2011 and yes we did pluck this from the archive because of Khvicha Kvaratskhelia winning the title with Paris Saint-Germain and Napoli. 'Has a player ever won two championship winner's medals in the same season by playing for two different clubs in two different countries?' 'When Suárez was transferred from Ajax to Liverpool last winter, Urby Emanuelson also left Ajax for Milan. Unlike Liverpool, Milan did grab the title, so Urby won two championship titles this season,' writes Stephan Wijnen, who is clearly prepared to overlook the fact that Emanuelson has made only eight appearances for Milan, which wouldn't qualify him for a medal under Premier League rules. 'Wolves striker Kevin Doyle won a League of Ireland medal in November 2005, when my beloved Cork City clinched the title on the final day,' suggests Colin Owens. 'Doyler had left for Reading the previous June for a measly €117,000, where he would go on the fire the Royals into the Premier League, pocketing a Championship medal in the process.' Richard Bald would like to nominate Crawley Town's Scottish midfielder Willie Gibson as another player that fits the bill. 'He picked up winners' medals for Dunfermline in the Scottish First Division and for Crawley Town in the Conference,' he writes, but fails to mention which of the two titles Willie considers more prestigious. 'Sheffield United have lost their last eight games at Wembley,' weeps Darren White. 'Does anyone have a worse streak on that ground?' 'Billy Gilmour, who almost gave Napoli the lead in their title-winning victory on Friday night, has made 146 club appearances in his career without scoring a goal. Are there are any other midfielders with a similarly long drought?' wonders Rob McCluskey. 'The success of Scott McTominay, Billy Gilmour, Harry Kane and Eric Dier means that British players have won three of the big five leagues this season. Has that happened before? And have any countries managed five out of five?' wonders Philipp Lohan. 'Royal Union Saint-Gilloise have just won the title in Belgium – 90 years after their last championship in 1935. Are there any longer gaps between two national titles for any team?' asks Holger Seiffert. with your questions and answers
