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"Spatial interactions modulate tumor growth and immune infiltration" Our latest preprint: Sadegh Marzban in collab w/ Amelio Lab! We apply methods from artificial life, Bert Chan's #Lenia, as a model of tumor-immune: - spatial growth dynamics - cell-cell competition & - cell migration Application to head & neck squamous... show more

Jeffrey West

9,158 subscribers

12,314 views • 2 years ago •via X (Twitter)

Health & Wellness Science & Technology #Lenia

Anya Rossi• Live Now

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Sadegh Marzban2 years ago

@AmelioLab @BertChakovsky Lenia as cancer model 🔬🤖 (A) Exploring Lenia's artificial life virtual creatures (Credits to @BertChakovsky for the reproduction) in our paper! #Lenia #ArtificialLife #Research #CancerResearch

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Ali Max Erturk

14,750 views • 2 months ago

We are thrilled to share that our first paper from my new lab, Spateo ( for spatiotemporal modeling of molecular holograms, is now online in Cell: Spateo is a comprehensive analytical framework for 3D whole-embryo spatiotemporal modeling. Its advanced features include: • 3D alignment and reconstruction at the whole-mouse-embryo scale (see the animation). • 3D spatial domain digitization and cell-cell communication analysis to understand spatial gene expression gradients and both inter- and intracellular communication. • 3D morphometric and volumetric analyses along with 3D morphogenesis vector field modeling to quantify dynamics such as surface area, volume, and cell density across organs, and to dissect the interplay between morphogenesis factors and cell migration. • A “Google Earth”-like browser, Spateo-viewer ( and for interactive and intuitive exploration of 3D spatial data. • Additional features, such as RNA signal-based single-cell segmentation. We are also honored that Nature “News and Views” has highlighted this work as well: This is really an amazing outcome after two years' heroic revision process that rewrite the entire paper using a new data ( for whole mouse embryos.

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evo-devo

58,343 views • 1 year ago

HUNDREDS of studies link 5G wireless radiation to DNA damage, oxidative stress, neurological injury, and cancer. Documented adverse biological effects of 5G span: • DNA damage (genotoxicity) • Tumor growth • Brain/neuronal injury • Fertility impairment • Endocrine disruption • Developmental abnormalities • Immune dysfunction • Memory impairment • Learning impairment • Cell death (apoptosis) • Oxidative stress • Gene expression changes • Cell membrane disruption • Cell proliferation changes • Neurotransmitter alterations • Electrophysiological effects • Behavioral changes • Hematological effects • Liver (hepatic) effects • Metabolic/enzyme dysfunction • Biochemical changes The multitrillion-dollar cellular industry does NOT care about your safety — only speed and surveillance.

HUNDREDS of studies link 5G wireless radiation to DNA damage, oxidative stress, neurological injury, and cancer. Documented adverse biological effects of 5G span: • DNA damage (genotoxicity) • Tumor growth • Brain/neuronal injury • Fertility impairment • Endocrine disruption • Developmental abnormalities • Immune dysfunction • Memory impairment • Learning impairment • Cell death (apoptosis) • Oxidative stress • Gene expression changes • Cell membrane disruption • Cell proliferation changes • Neurotransmitter alterations • Electrophysiological effects • Behavioral changes • Hematological effects • Liver (hepatic) effects • Metabolic/enzyme dysfunction • Biochemical changes The multitrillion-dollar cellular industry does NOT care about your safety — only speed and surveillance.

Nicolas Hulscher, MPH

27,905 views • 9 days ago

PantheonOS allows any biologist to perform complex data analyses of emerging single cell, multi-omics and spatial transcriptomics datasets end to end through AI agent and human collaboration. We are releasing six replays of use cases trajectories. Each "trajectory" is a complete end-to-end run, from prompt to analysis, to figures, and finally to report, and in fully inspectable and reproducible manner. See the six user cases in our PantheonOS Gallery: 1. 3D mouse embryo analysis: Tangram deconvolution and PyVista-based 3D visualization of E6 mouse embryo spatial transcriptomics data 2. 3D human fetal heart analysis: Spatial mapping of heart disease gene patterns using MERFISH data 3. Multi-omics spatial integration: Single cell multi-omics-to-spatial mapping with MOSCOT optimal transport 4. Gene panel design: 1000-plex immune-oncology MERFISH gene panel optimization 5. Cell segmentation benchmarking: Comparative evaluation of Cellpose-SAM, InstanSeg, StarDist, and other tools 6. Spatial disease biology: Ligand–receptor analysis of disease-associated tissue microenvironments We would love to hear how you can use PantheonOS for your research! Got an interesting agent run of your own and want to share? In the Pantheon UI, click Export Bundle (top-right of any chat) to package the full trajectory — chat history, code, figures, report — then submit it here:

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evo-devo

13,151 views • 2 months ago

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Bo Wang

59,008 views • 1 year ago

IVERMECTIN and LACTOFERRIN TESTIMONIAL - Oscar Nacu (Philippines, Aug.2022) IVERMECTIN and LACTOFERRIN Synergy Both compounds exhibit anticancer properties through overlapping pathways, such as inducing apoptosis (programmed cell death), modulating immune responses, and disrupting cancer cell metabolism and proliferation Lactoferrin can enhance Ivermectin’s effects by amplifying immune activation and oxidative stress, which may make cancer cells more vulnerable to IVM’s metabolic disruptions and apoptotic induction 1. Enhanced Apoptosis and Cell Death Pathways Individual Mechanisms: Lactoferrin induces apoptosis in cancer cells by damaging the cytoskeleton, activating caspases (e.g., caspase-3), upregulating pro-apoptotic proteins like BAX/BAK, and causing cell cycle arrest (e.g., G1/S or G2/M phases). It also reduces cell migration and invasion by reversing epithelial-mesenchymal transition (EMT), downregulating proteins like vimentin, SNAIL, and TWIST. Ivermectin promotes apoptosis via mitochondrial dysfunction, increasing reactive oxygen species (ROS), elevating the Bax/Bcl-2 ratio, and activating caspases 9/3. It also inhibits proliferation through cell cycle arrest and targets cancer stem cells. How They Work Together: Lactoferrin’s ability to induce oxidative stress and DNA damage complements Ivermectin’s ROS elevation and mitochondrial inhibition. This dual assault on cellular energy and redox balance could lower the threshold for apoptosis, making cancer cells more susceptible to Ivermectin’s effects 2. Immune Modulation and Tumor Microenvironment Remodeling Individual Mechanisms: Lactoferrin stimulates the adaptive immune response, reshapes the tumor microenvironment by downregulating pro-inflammatory cytokines (e.g., IL-6), and inhibits cancer progression through immunostimulatory effects. It also protects against iron disorders, depriving iron-dependent cancer cells while modulating immunity. Ivermectin has immunomodulatory properties, converting “cold” tumors (immune-deserted) to “hot” ones (immune-infiltrated) by inducing immunogenic cell death (ICD), releasing ATP and HMGB1, depleting immunosuppressive cells (e.g., MDSCs and Tregs), and enhancing CD8+ T-cell infiltration. How They Work Together: Lactoferrin’s cytokine downregulation and immune stimulation could amplify Ivermectin’s ICD and T-cell recruitment, creating a more hostile environment for cancer cells. For example, Ivermectin’s ability to boost Teff/Treg ratios pairs well with Lactoferrin’s anti-inflammatory effects, potentially enhancing overall antitumor immunity. 3. Disruption of Cancer Cell Metabolism and Proliferation Individual Mechanisms: Lactoferrin inhibits oncogenic pathways like PI3K/AKT/mTOR and Wnt, reducing proliferation and angiogenesis (e.g., downregulating VEGFR2). Ivermectin interferes with metabolic pathways, downregulating TCA cycle enzymes (e.g., IDH2, DLST), inhibiting glycolysis/oxidative phosphorylation, and limiting glutamine-derived intermediates for biosynthesis. How They Work Together: Lactoferrin’s iron sequestration starves cancer cells of essential metals for metabolic enzymes, synergizing with Ivermectin’s TCA cycle disruption to exacerbate energy shortages and biosynthetic limitations. This is particularly relevant in “glutamine-addicted” cancers like ovarian or prostate, where combined metabolic stress promotes apoptosis. (Podcast: Dr.Allan Landrito, Dr.Mahin Khatami, Dr.Shankara Chetty" === I have the world's largest Ivermectin Cancer Clientele, 7900 strong! Joseph A. Ladapo, MD, PhD

IVERMECTIN and LACTOFERRIN TESTIMONIAL - Oscar Nacu (Philippines, Aug.2022) IVERMECTIN and LACTOFERRIN Synergy Both compounds exhibit anticancer properties through overlapping pathways, such as inducing apoptosis (programmed cell death), modulating immune responses, and disrupting cancer cell metabolism and proliferation Lactoferrin can enhance Ivermectin’s effects by amplifying immune activation and oxidative stress, which may make cancer cells more vulnerable to IVM’s metabolic disruptions and apoptotic induction 1. Enhanced Apoptosis and Cell Death Pathways Individual Mechanisms: Lactoferrin induces apoptosis in cancer cells by damaging the cytoskeleton, activating caspases (e.g., caspase-3), upregulating pro-apoptotic proteins like BAX/BAK, and causing cell cycle arrest (e.g., G1/S or G2/M phases). It also reduces cell migration and invasion by reversing epithelial-mesenchymal transition (EMT), downregulating proteins like vimentin, SNAIL, and TWIST. Ivermectin promotes apoptosis via mitochondrial dysfunction, increasing reactive oxygen species (ROS), elevating the Bax/Bcl-2 ratio, and activating caspases 9/3. It also inhibits proliferation through cell cycle arrest and targets cancer stem cells. How They Work Together: Lactoferrin’s ability to induce oxidative stress and DNA damage complements Ivermectin’s ROS elevation and mitochondrial inhibition. This dual assault on cellular energy and redox balance could lower the threshold for apoptosis, making cancer cells more susceptible to Ivermectin’s effects 2. Immune Modulation and Tumor Microenvironment Remodeling Individual Mechanisms: Lactoferrin stimulates the adaptive immune response, reshapes the tumor microenvironment by downregulating pro-inflammatory cytokines (e.g., IL-6), and inhibits cancer progression through immunostimulatory effects. It also protects against iron disorders, depriving iron-dependent cancer cells while modulating immunity. Ivermectin has immunomodulatory properties, converting “cold” tumors (immune-deserted) to “hot” ones (immune-infiltrated) by inducing immunogenic cell death (ICD), releasing ATP and HMGB1, depleting immunosuppressive cells (e.g., MDSCs and Tregs), and enhancing CD8+ T-cell infiltration. How They Work Together: Lactoferrin’s cytokine downregulation and immune stimulation could amplify Ivermectin’s ICD and T-cell recruitment, creating a more hostile environment for cancer cells. For example, Ivermectin’s ability to boost Teff/Treg ratios pairs well with Lactoferrin’s anti-inflammatory effects, potentially enhancing overall antitumor immunity. 3. Disruption of Cancer Cell Metabolism and Proliferation Individual Mechanisms: Lactoferrin inhibits oncogenic pathways like PI3K/AKT/mTOR and Wnt, reducing proliferation and angiogenesis (e.g., downregulating VEGFR2). Ivermectin interferes with metabolic pathways, downregulating TCA cycle enzymes (e.g., IDH2, DLST), inhibiting glycolysis/oxidative phosphorylation, and limiting glutamine-derived intermediates for biosynthesis. How They Work Together: Lactoferrin’s iron sequestration starves cancer cells of essential metals for metabolic enzymes, synergizing with Ivermectin’s TCA cycle disruption to exacerbate energy shortages and biosynthetic limitations. This is particularly relevant in “glutamine-addicted” cancers like ovarian or prostate, where combined metabolic stress promotes apoptosis. (Podcast: Dr.Allan Landrito, Dr.Mahin Khatami, Dr.Shankara Chetty" === I have the world's largest Ivermectin Cancer Clientele, 7900 strong! Joseph A. Ladapo, MD, PhD

Dr. William Makis MD

48,226 views • 6 months ago

Exciting results in lung cancer today. It is my belief that treating lymphopenia in patients with low NK and T cell count, is as essential as treating anemia (low red blood cells count) or neutropenia (low neutrophil count) which occurs as a consequence of chemotherapy, independent of tumor types. This will herald in the paradigm change of treating the immune system itself and allow the immune system to cure the cancer, regardless of its anatomical location. The long-term survival in patients with bladder cancer and now in lung cancer provide evidence of the potential validity of this hypothesis, with ANKTVIA as the foundation of the Bioshield platform.

Exciting results in lung cancer today. It is my belief that treating lymphopenia in patients with low NK and T cell count, is as essential as treating anemia (low red blood cells count) or neutropenia (low neutrophil count) which occurs as a consequence of chemotherapy, independent of tumor types. This will herald in the paradigm change of treating the immune system itself and allow the immune system to cure the cancer, regardless of its anatomical location. The long-term survival in patients with bladder cancer and now in lung cancer provide evidence of the potential validity of this hypothesis, with ANKTVIA as the foundation of the Bioshield platform.

Dr. Pat Soon-Shiong

43,436 views • 10 months ago

How does an embryo reliably "compute" its form - "cell by cell" - using only local interactions and mechanics, yet produce a precise global body plan? I’m excited to share our Nature Methods paper "MultiCell: geometric learning in multicellular development", presenting #AIxBiology research led by Haiqian Yang and the result of a great collaboration with Ming Guo, George Roy, Tomer Stern, Anh Nguyen and Dapeng Bi. A long-standing challenge in developmental biology is to predict how thousands of cells collectively self-organize as tissues fold, divide, and rearrange. In MultiCell, we represent a developing embryo as a dual graph that unifies two complementary views of tissue mechanics with single-cell resolution: cells as moving points (granular) and cells as a connected foam (junction network). This lets the model learn dynamics from both geometry and cell–cell connectivity. On whole-embryo 4D light-sheet movies of Drosophila gastrulation (~5,000 cells), our model predicts key cell behaviors and the timing of events, including junction loss, rearrangements, and divisions with high accuracy, at single-cell resolution. Beyond prediction, the same representation supports robust time alignment across embryos and offers interpretable activation maps that highlight the morphogenetic "drivers" of development. The broader goal is a foundation for cell-by-cell forecasting in more complex tissues, and eventually for detecting subtle dynamical signatures of disease. Kudos to the team for this inspiring collaboration with brilliant researchers to push the boundary of AI for biology! Citation: Yang, H., Roy, G., Nguyen, A.Q., Buehler, M.J., et al. MultiCell: geometric learning in multicellular development. Nature Methods (2025), DOI: 10.1038/s41592-025-02983-x Code/data links are in the manuscript.

How does an embryo reliably "compute" its form - "cell by cell" - using only local interactions and mechanics, yet produce a precise global body plan? I’m excited to share our Nature Methods paper "MultiCell: geometric learning in multicellular development", presenting #AIxBiology research led by Haiqian Yang and the result of a great collaboration with Ming Guo, George Roy, Tomer Stern, Anh Nguyen and Dapeng Bi. A long-standing challenge in developmental biology is to predict how thousands of cells collectively self-organize as tissues fold, divide, and rearrange. In MultiCell, we represent a developing embryo as a dual graph that unifies two complementary views of tissue mechanics with single-cell resolution: cells as moving points (granular) and cells as a connected foam (junction network). This lets the model learn dynamics from both geometry and cell–cell connectivity. On whole-embryo 4D light-sheet movies of Drosophila gastrulation (~5,000 cells), our model predicts key cell behaviors and the timing of events, including junction loss, rearrangements, and divisions with high accuracy, at single-cell resolution. Beyond prediction, the same representation supports robust time alignment across embryos and offers interpretable activation maps that highlight the morphogenetic "drivers" of development. The broader goal is a foundation for cell-by-cell forecasting in more complex tissues, and eventually for detecting subtle dynamical signatures of disease. Kudos to the team for this inspiring collaboration with brilliant researchers to push the boundary of AI for biology! Citation: Yang, H., Roy, G., Nguyen, A.Q., Buehler, M.J., et al. MultiCell: geometric learning in multicellular development. Nature Methods (2025), DOI: 10.1038/s41592-025-02983-x Code/data links are in the manuscript.

Markus J. Buehler

387,913 views • 6 months ago

Dr. Patrick Soon-Shiong on the Cancer-Fighting Immune Breakthrough: Awakening the 450 Million-Year-Old Natural Killer Cell After decades of pioneering work since discovering the natural killer cell in the 1990s—a remarkable immune cell created by God and preserved through 450 million years—Dr. Patrick Soon-Shiong reveals an extraordinary breakthrough. This cell, unknown to many until the 1970s, serves as the body's first line of defense, designed to destroy cancer cells, infections like COVID, sepsis, bacteria, and fungus. Dr. Soon-Shiong emphasizes that this is not an invention, but an enlightenment: activating the body’s own natural killer cells to combat disease naturally, shifting away from toxic chemotherapy and radiation. With a single jab, they have unlocked the secret to empowering this primal cellular protector. This is evolution’s own weapon against illness, a game-changer that taps into ancient biology to revolutionize modern medicine. This insight reframes how we think about health and cancer treatment by harnessing the immune system's innate power, moving beyond harsh treatments, and embracing nature’s original disease-fighter from within. The discovery is a call to awaken the body’s own god-given defense system for a future of empowered healing.

Dr. Patrick Soon-Shiong on the Cancer-Fighting Immune Breakthrough: Awakening the 450 Million-Year-Old Natural Killer Cell After decades of pioneering work since discovering the natural killer cell in the 1990s—a remarkable immune cell created by God and preserved through 450 million years—Dr. Patrick Soon-Shiong reveals an extraordinary breakthrough. This cell, unknown to many until the 1970s, serves as the body's first line of defense, designed to destroy cancer cells, infections like COVID, sepsis, bacteria, and fungus. Dr. Soon-Shiong emphasizes that this is not an invention, but an enlightenment: activating the body’s own natural killer cells to combat disease naturally, shifting away from toxic chemotherapy and radiation. With a single jab, they have unlocked the secret to empowering this primal cellular protector. This is evolution’s own weapon against illness, a game-changer that taps into ancient biology to revolutionize modern medicine. This insight reframes how we think about health and cancer treatment by harnessing the immune system's innate power, moving beyond harsh treatments, and embracing nature’s original disease-fighter from within. The discovery is a call to awaken the body’s own god-given defense system for a future of empowered healing.

Camus

33,407 views • 8 months ago

A paradigm shift is urgently needed in oncology. Conventional wisdom views radiation as a localized tool, but emerging evidence reveals its profound capacity to systemically PROMOTE cancer metastasis. In a powerful summary, Dr. Nathan Goodyear outlines the mechanisms by which radiation can inadvertently fuel the spread of cancer: - Increases Circulating Tumor Cells (CTCs): Radiation can dislodge cells from the primary tumor, releasing them into circulation as seeds for future, distant tumors. - Damages the Tumor Microenvironment: Through the "bystander effect," radiation damages healthy cells, alters epigenetics, disrupts the extracellular matrix, and modifies the local immune landscape. - Enhances Invasion & Angiogenesis: It upregulates the cancer's ability to invade surrounding tissues and stimulates angiogenesis—building the very blood vessel "highways" that facilitate spread. - Subverts the Immune System: Radiation can polarize macrophages toward the pro-tumor M2 phenotype, creating a state of chronic inflammation that allows cancer cells to evade immune detection. - Activates Dormant Sites: Via the "concomitant theory," radiation can activate distant, dormant micro-metastases, awakening sleeping giants. - Forces Mutations & Stem Cell Transformation: The genomic instability caused by radiation forces phenotypic shifts, promotes cancer stem cell transformation, and drives oncogenic metabolic shifts like the Warburg Effect. This is not to dismiss radiation's role, but to demand a more sophisticated understanding of its systemic consequences. Treatment must consider these pro-metastatic risks to truly advance patient outcomes.

A paradigm shift is urgently needed in oncology. Conventional wisdom views radiation as a localized tool, but emerging evidence reveals its profound capacity to systemically PROMOTE cancer metastasis. In a powerful summary, Dr. Nathan Goodyear outlines the mechanisms by which radiation can inadvertently fuel the spread of cancer: - Increases Circulating Tumor Cells (CTCs): Radiation can dislodge cells from the primary tumor, releasing them into circulation as seeds for future, distant tumors. - Damages the Tumor Microenvironment: Through the "bystander effect," radiation damages healthy cells, alters epigenetics, disrupts the extracellular matrix, and modifies the local immune landscape. - Enhances Invasion & Angiogenesis: It upregulates the cancer's ability to invade surrounding tissues and stimulates angiogenesis—building the very blood vessel "highways" that facilitate spread. - Subverts the Immune System: Radiation can polarize macrophages toward the pro-tumor M2 phenotype, creating a state of chronic inflammation that allows cancer cells to evade immune detection. - Activates Dormant Sites: Via the "concomitant theory," radiation can activate distant, dormant micro-metastases, awakening sleeping giants. - Forces Mutations & Stem Cell Transformation: The genomic instability caused by radiation forces phenotypic shifts, promotes cancer stem cell transformation, and drives oncogenic metabolic shifts like the Warburg Effect. This is not to dismiss radiation's role, but to demand a more sophisticated understanding of its systemic consequences. Treatment must consider these pro-metastatic risks to truly advance patient outcomes.

Camus

22,773 views • 9 months ago

Dr. Soon-Shiong's Immune Trinity: Sleep, Red Light, and The Right Food. Everything Else is Noise. Dr. Patrick Soon-Shiong reframes human biology: we are a dynamic interplay of neutrons, photons, and electrons. A living, breathing battery. Central to this system is the natural killer (NK) cell, a guardian of our immune defense. Each cell is a intelligence network with 30,000 receptors. But this army doesn't run on willpower. It demands specific, natural inputs: Sleep: Non-negotiable. This is when your NK cell arsenal is rebuilt and restored. Without quality rest, your primary defense force is left depleted. Sunlight: Our most overlooked medicine. Specifically, the red wavelength is critical for stimulating these cells. It's not a supplement; it's a fundamental requirement for immune activation. This explains the stark seasonal patterns in human health. Why we get sicker in winter. The data from cloud-covered cities doesn't lie. Nature is about light. Plants fail without it, and so do we. Furthermore, we must fuel this "battery" correctly. Your gut biome can either activate your immune system or immunosuppress it. The formula for resilience is clear: Sleep to recharge. Sunlight to stimulate. Nourishing food to activate. It’s a return to the most fundamental elements of life. It’s time we started listening.

Dr. Soon-Shiong's Immune Trinity: Sleep, Red Light, and The Right Food. Everything Else is Noise. Dr. Patrick Soon-Shiong reframes human biology: we are a dynamic interplay of neutrons, photons, and electrons. A living, breathing battery. Central to this system is the natural killer (NK) cell, a guardian of our immune defense. Each cell is a intelligence network with 30,000 receptors. But this army doesn't run on willpower. It demands specific, natural inputs: Sleep: Non-negotiable. This is when your NK cell arsenal is rebuilt and restored. Without quality rest, your primary defense force is left depleted. Sunlight: Our most overlooked medicine. Specifically, the red wavelength is critical for stimulating these cells. It's not a supplement; it's a fundamental requirement for immune activation. This explains the stark seasonal patterns in human health. Why we get sicker in winter. The data from cloud-covered cities doesn't lie. Nature is about light. Plants fail without it, and so do we. Furthermore, we must fuel this "battery" correctly. Your gut biome can either activate your immune system or immunosuppress it. The formula for resilience is clear: Sleep to recharge. Sunlight to stimulate. Nourishing food to activate. It’s a return to the most fundamental elements of life. It’s time we started listening.

Camus

115,228 views • 9 months ago

NEW: Population wide immune pressure from "exposure to various countermeasures" We all know what Robert Malone is talking about here. As Professor Robert Clancy pointed out: "We're now creating a population of people who are on the cusp of getting more severe and more continuous covid infection" We've heard about IgG4 class switching, "T cell Exhaustion" and what Geert Vanden Bossche describes as "immune refocusing" because of mass mRNA vaccination. No wonder we're having record levels of Flu

NEW: Population wide immune pressure from "exposure to various countermeasures" We all know what Robert Malone is talking about here. As Professor Robert Clancy pointed out: "We're now creating a population of people who are on the cusp of getting more severe and more continuous covid infection" We've heard about IgG4 class switching, "T cell Exhaustion" and what Geert Vanden Bossche describes as "immune refocusing" because of mass mRNA vaccination. No wonder we're having record levels of Flu

Humanspective

42,948 views • 1 year ago

Excited to share our new work on building a multimodal atlas of human skin in health and inflammatory disease — a project I’m especially proud of, bringing together AI, high-throughput genomics, and clinical science to accelerate discovery. Over the past decade, single-cell genomics has transformed how we map cells in human tissues. But a major challenge remains: can we systematically decode how cells organize into functional niches in situ — including those invisible to standard histopathology? To address this, we integrated large-scale scRNA-seq, spatial transcriptomics, histopathology, and AI-driven modeling frameworks to build an in situ atlas of human skin across health and disease. Led by Lloyd Steele, an MD/PhD student working between Haniffa Lab and my lab at Wellcome Sanger Institute and Cambridge University . Another amazing collaboration with Muzz Haniffa, the mastermind behind the work as part of Human Cell Atlas. A key part of this study is that we didn’t build everything from scratch — we leveraged and combined AI methods that actually work! and showed how they can be used together to extract biological insight at scale. We used: • scArches to build and map into a reference scRNA-seq atlas of human skin: • NicheCompass to identify and characterize spatial niches: • MINT-Flow to extract microenvironment-induced cell states and gene programs: Together, these enabled an end-to-end workflow from atlas construction to spatial mapping, niche discovery, and cell state decoding. At scale, we integrated ~5 million cells and 100+ spatial sections, enabling a systematic view of tissue organization. Using this framework, we identified 26 niches in skin, including known histopathologic structures as well as hidden disease-associated niches not visible on H&E. Among the most striking findings were a resident memory T cell-rich sebaceous gland niche and a plasma cell-rich sweat gland niche, suggesting that appendageal structures act as active immunological microenvironments and may contribute to inflammatory memory and disease persistence. Importantly, this atlas is not just descriptive — it is usable. It can support mapping of new datasets, resolve finer cell types and niches, extract microenvironment-driven programs, and enable predictive analyses at scale. More broadly, this work shows what becomes possible when AI, spatial genomics, and atlas-scale data are integrated end-to-end: not just mapping tissues, but systematically decoding them. This was a massive collaboration, and I’m very grateful to the amazing scientists April Foster, Kenny Roberts, and Chloe Admane. Lloyd is an amazing scientist, and I’m especially excited for the community to see more of his work soon — stay tuned. The data and pre-trained models will be released soon. Preprint:

Excited to share our new work on building a multimodal atlas of human skin in health and inflammatory disease — a project I’m especially proud of, bringing together AI, high-throughput genomics, and clinical science to accelerate discovery. Over the past decade, single-cell genomics has transformed how we map cells in human tissues. But a major challenge remains: can we systematically decode how cells organize into functional niches in situ — including those invisible to standard histopathology? To address this, we integrated large-scale scRNA-seq, spatial transcriptomics, histopathology, and AI-driven modeling frameworks to build an in situ atlas of human skin across health and disease. Led by Lloyd Steele, an MD/PhD student working between Haniffa Lab and my lab at Wellcome Sanger Institute and Cambridge University . Another amazing collaboration with Muzz Haniffa, the mastermind behind the work as part of Human Cell Atlas. A key part of this study is that we didn’t build everything from scratch — we leveraged and combined AI methods that actually work! and showed how they can be used together to extract biological insight at scale. We used: • scArches to build and map into a reference scRNA-seq atlas of human skin: • NicheCompass to identify and characterize spatial niches: • MINT-Flow to extract microenvironment-induced cell states and gene programs: Together, these enabled an end-to-end workflow from atlas construction to spatial mapping, niche discovery, and cell state decoding. At scale, we integrated ~5 million cells and 100+ spatial sections, enabling a systematic view of tissue organization. Using this framework, we identified 26 niches in skin, including known histopathologic structures as well as hidden disease-associated niches not visible on H&E. Among the most striking findings were a resident memory T cell-rich sebaceous gland niche and a plasma cell-rich sweat gland niche, suggesting that appendageal structures act as active immunological microenvironments and may contribute to inflammatory memory and disease persistence. Importantly, this atlas is not just descriptive — it is usable. It can support mapping of new datasets, resolve finer cell types and niches, extract microenvironment-driven programs, and enable predictive analyses at scale. More broadly, this work shows what becomes possible when AI, spatial genomics, and atlas-scale data are integrated end-to-end: not just mapping tissues, but systematically decoding them. This was a massive collaboration, and I’m very grateful to the amazing scientists April Foster, Kenny Roberts, and Chloe Admane. Lloyd is an amazing scientist, and I’m especially excited for the community to see more of his work soon — stay tuned. The data and pre-trained models will be released soon. Preprint:

Mo Lotfollahi

11,759 views • 3 months ago

The Chemotherapy Paradox – A "Cure" That Preserves the Root of Cancer? You've been told chemotherapy is a cornerstone of cancer care. But what if the standard of care is fundamentally flawed, suppressing the very system designed to heal you while protecting the engine that drives the disease? In a stunning exposition, Dr. Paul Marik pulls back the curtain on oncology's biggest dilemma. Here's the shocking truth: - Chemotherapy annihilates your immune army. It wipes out your natural killer cells and T-cells—the very soldiers your body needs to fight cancer. You are immune-suppressed, allowing the tumor a clearer path to proliferate. - Chemotherapy preserves the cancer stem cell. This is the root of the tumor. While chemo kills rapidly dividing cells, it often leaves the stem cell—the queen bee—untouched. From this root, the cancer indefinitely divides, mutates, and regrows. - Some chemo drugs may even STIMULATE the stem cell. That's right. The very treatment intended to kill cancer can, in some cases, fuel its source. "So you can't cure the patient unless you get rid of the cancer stem cell," states Dr. Marik. "Interestingly, chemotherapy doesn't kill the stem cell." This explains why "remission" is not a "cure." The cancer can return 7, 8, or 10 years later because the root was never addressed. You are in remission, not cured. The conclusion? The high-dose, "burn-and-cut" approach of traditional oncology is not holistic. It weakens the host and empowers the enemy's most resilient forces. Dr. Marik confirms: The efficacy depends on the tumor type. Cancers with a low percentage of stem cells can see long-term remission. But for many, it's a ticking time bomb. This isn't an opinion; it's a biological reality. It’s time for a paradigm shift. Share this to spark a crucial conversation. The future of oncology depends on it.

The Chemotherapy Paradox – A "Cure" That Preserves the Root of Cancer? You've been told chemotherapy is a cornerstone of cancer care. But what if the standard of care is fundamentally flawed, suppressing the very system designed to heal you while protecting the engine that drives the disease? In a stunning exposition, Dr. Paul Marik pulls back the curtain on oncology's biggest dilemma. Here's the shocking truth: - Chemotherapy annihilates your immune army. It wipes out your natural killer cells and T-cells—the very soldiers your body needs to fight cancer. You are immune-suppressed, allowing the tumor a clearer path to proliferate. - Chemotherapy preserves the cancer stem cell. This is the root of the tumor. While chemo kills rapidly dividing cells, it often leaves the stem cell—the queen bee—untouched. From this root, the cancer indefinitely divides, mutates, and regrows. - Some chemo drugs may even STIMULATE the stem cell. That's right. The very treatment intended to kill cancer can, in some cases, fuel its source. "So you can't cure the patient unless you get rid of the cancer stem cell," states Dr. Marik. "Interestingly, chemotherapy doesn't kill the stem cell." This explains why "remission" is not a "cure." The cancer can return 7, 8, or 10 years later because the root was never addressed. You are in remission, not cured. The conclusion? The high-dose, "burn-and-cut" approach of traditional oncology is not holistic. It weakens the host and empowers the enemy's most resilient forces. Dr. Marik confirms: The efficacy depends on the tumor type. Cancers with a low percentage of stem cells can see long-term remission. But for many, it's a ticking time bomb. This isn't an opinion; it's a biological reality. It’s time for a paradigm shift. Share this to spark a crucial conversation. The future of oncology depends on it.

Camus

69,487 views • 8 months ago

Single-cell technologies now let us profile entire transcriptomes in individual cells. But how do we make sense of this complexity in a biologically meaningful way? Many methods summarise cells into a single embedding, but this often comes at the cost of interpretability, especially when multiple gene programs are active at once. We developed Tripso, a self-supervised transformer model that represents cells through multiple gene program-specific embeddings, while also uncovering new programs directly from the data. Instead of collapsing biology into a single vector, Tripso decomposes cell state into multiple representations, each reflecting a different gene program. We explored this across multiple systems. In human hematopoiesis, spanning development to aging, Tripso identified distinct age-associated program activity, including stronger JAK-STAT signalling in early life and dynamic IKZF1-related changes during B cell maturation. By comparing in vitro culture conditions with in vivo hematopoietic stem cell states, Tripso suggested that targeting the SEC61 translocon could enhance stem cell maintenance ex vivo, a prediction that we subsequently validated experimentally. In parallel, we identified a previously uncharacterised tissue-resident memory T-cell program associated with atopic dermatitis and mapped it to distinct spatial immune niches Together, these results show how modelling cells through gene programs can lead to interpretable and experimentally testable insights. More broadly, this work points toward a more interpretable and biologically grounded models of cell state. As single-cell datasets continue to grow, we hope approaches like Tripso will help bridge the gap between data-driven representations and biological insight. This work wouldn’t have been possible without the contributions of an amazing team. Thank you to co-first authors Marie, Tomoya Isobe, Amirhosein Vahidi, Carlo Leonardi, and everyone from roser's Lab, Haniffa Lab, Nicola Wilson and Bertie Gottgens's Lab, bringing together expertise across Cambridge Stem Cell Institute, Open Targets, Wellcome Sanger Institute and Cambridge University. Marie is one of the very best PhD students I have ever supervised. She is truly a force of nature, exceptionally resourceful, deeply innovative, and one of the most impressive scientists I have worked with. I am immensely proud of her and all that she has accomplished. As she begins her internship at Genentech , I have no doubt she will do amazing work there and continue to make her mark. paper: code:

Mo Lotfollahi

22,402 views • 3 months ago

Long COVID: The Immune & Lymphatic System Long COVID is associated with persistent immune dysregulation. Studies document chronic inflammation, abnormal immune activation, altered T- and B-cell signaling, and the presence of autoantibodies. This immune dysregulation can create a state of vulnerability in the body, which can increase susceptibility to infections, reactivation of latent-viruses as seen with EBV, CMV, HSV... and contribute to the emergence or unmasking of secondary conditions, including autoimmune diseases such as Lupus, neurologic disorders such as multiple sclerosis (MS), and even certain can also impact how your body responds to other infections and illnesses, impact vaccine efficacy and antibody response, and more. Long COVID can reflect a destabilized immune system with systemic consequences that vary by person, severity, and time since infection. We are all #OneInfectionAway Learn more about #LongCOVID and visit our #LongCOVIDAwareness Month page to take action, get involved, and spread the word! Access the video here:

Long COVID: The Immune & Lymphatic System Long COVID is associated with persistent immune dysregulation. Studies document chronic inflammation, abnormal immune activation, altered T- and B-cell signaling, and the presence of autoantibodies. This immune dysregulation can create a state of vulnerability in the body, which can increase susceptibility to infections, reactivation of latent-viruses as seen with EBV, CMV, HSV... and contribute to the emergence or unmasking of secondary conditions, including autoimmune diseases such as Lupus, neurologic disorders such as multiple sclerosis (MS), and even certain can also impact how your body responds to other infections and illnesses, impact vaccine efficacy and antibody response, and more. Long COVID can reflect a destabilized immune system with systemic consequences that vary by person, severity, and time since infection. We are all #OneInfectionAway Learn more about #LongCOVID and visit our #LongCOVIDAwareness Month page to take action, get involved, and spread the word! Access the video here:

COVID-19 Longhauler Advocacy Project

10,571 views • 4 months ago

Microsoft's AI can now detect cancer from a $10 tissue sample. For context, every time tumor cells are tested, doctors create a basic microscope slide to study tissue up close. These slides show cell shapes and structures, but they can't reveal which immune cells are actually fighting the cancer. That deeper picture is critical for knowing if a patient will respond to immunotherapy... But the advanced imaging needed costs THOUSANDS. So Microsoft built GigaTIME -- an AI system that generates advanced imaging from the cheap slides hospitals already collect. The system was trained on 40 million cancer cells, then applied to over 14,000 patients across 51 hospitals spanning 24 cancer types. The AI found over 1,200 hidden connections between immune cell behavior and tumor growth that researchers couldn't find before... because the data simply didn't exist at this scale. When validated against 10,000 additional patients from a completely separate database, the results held up. The model is now open source, so any hospital worldwide can use it on samples they already have. I think this is one of the most impactful AI papers I've seen this year!

Microsoft's AI can now detect cancer from a $10 tissue sample. For context, every time tumor cells are tested, doctors create a basic microscope slide to study tissue up close. These slides show cell shapes and structures, but they can't reveal which immune cells are actually fighting the cancer. That deeper picture is critical for knowing if a patient will respond to immunotherapy... But the advanced imaging needed costs THOUSANDS. So Microsoft built GigaTIME -- an AI system that generates advanced imaging from the cheap slides hospitals already collect. The system was trained on 40 million cancer cells, then applied to over 14,000 patients across 51 hospitals spanning 24 cancer types. The AI found over 1,200 hidden connections between immune cell behavior and tumor growth that researchers couldn't find before... because the data simply didn't exist at this scale. When validated against 10,000 additional patients from a completely separate database, the results held up. The model is now open source, so any hospital worldwide can use it on samples they already have. I think this is one of the most impactful AI papers I've seen this year!

Rowan Cheung

43,245 views • 3 months ago

⚔️ BLOCKING GLUTAMINE NATURALLY When cancer cells can’t get glucose, they often switch to glutamine, a key amino acid involved in cell growth and repair. 🍄 Mistletoe—immune-regulating and disrupts glutamine-dependent cancer growth 🌿 Curcumin—shown to interfere with glutamine metabolism in aggressive tumors 🍵 Green tea (EGCG)—again, powerful here as well 🌿 Berberine—reduces expression of glutamine transporters 🧠 Honokiol (from magnolia bark)—neuroprotective and suppresses glutamine usage 🍄 Turkey tail mushroom—modulates immune response and may slow glutamine-driven cell replication 🥬 Fermented vegetables—rich in butyrate, which opposes glutamine-fueled inflammation 🥥 Coconut oil—encourages ketone metabolism over glutamine ✅ Suggested Stack: • AM: Honokiol + green tea • PM: Curcumin + mistletoe extract (consult with a practitioner) • Daily: Coconut oil for brain fuel + fermented foods for terrain healing 🧬 Avoid excess animal protein during active treatment—glutamine is abundant in meat. ✅ STUDIES: • Cell Metabolism (2013): Glutamine metabolism is essential for tumor growth in low-glucose environments. • Molecules (2020): Curcumin inhibits glutaminase, the enzyme that converts glutamine to fuel in cancer cells. • Frontiers in Oncology (2022): Mistletoe extract shown to downregulate glutamine pathways in colorectal cancer cells. • Oncotarget (2015): Honokiol targets mitochondrial glutamine metabolism in glioma models. 🔥Cancer adapts fast. But so can you. Block the second fuel… And give your body the upper hand it was designed to have. -Dr Pete Sulack

⚔️ BLOCKING GLUTAMINE NATURALLY When cancer cells can’t get glucose, they often switch to glutamine, a key amino acid involved in cell growth and repair. 🍄 Mistletoe—immune-regulating and disrupts glutamine-dependent cancer growth 🌿 Curcumin—shown to interfere with glutamine metabolism in aggressive tumors 🍵 Green tea (EGCG)—again, powerful here as well 🌿 Berberine—reduces expression of glutamine transporters 🧠 Honokiol (from magnolia bark)—neuroprotective and suppresses glutamine usage 🍄 Turkey tail mushroom—modulates immune response and may slow glutamine-driven cell replication 🥬 Fermented vegetables—rich in butyrate, which opposes glutamine-fueled inflammation 🥥 Coconut oil—encourages ketone metabolism over glutamine ✅ Suggested Stack: • AM: Honokiol + green tea • PM: Curcumin + mistletoe extract (consult with a practitioner) • Daily: Coconut oil for brain fuel + fermented foods for terrain healing 🧬 Avoid excess animal protein during active treatment—glutamine is abundant in meat. ✅ STUDIES: • Cell Metabolism (2013): Glutamine metabolism is essential for tumor growth in low-glucose environments. • Molecules (2020): Curcumin inhibits glutaminase, the enzyme that converts glutamine to fuel in cancer cells. • Frontiers in Oncology (2022): Mistletoe extract shown to downregulate glutamine pathways in colorectal cancer cells. • Oncotarget (2015): Honokiol targets mitochondrial glutamine metabolism in glioma models. 🔥Cancer adapts fast. But so can you. Block the second fuel… And give your body the upper hand it was designed to have. -Dr Pete Sulack

Cleanse Parasites .com 🧹🪱 Herbal Cleanse Co.

137,614 views • 11 months ago

🔴Ivermectin and mebendazole attack cancer cells in many different ways. Chemotherapy usually attacks only one.... Cancer has to be attacked through multiple mechanisms simultaneously... Ivermectin and mebendazole together do exactly that: they block cell division, cut off glucose metabolism, target cancer stem cells, and much more... Dr. Peter McCullough. IVERMECTIN – 12 Known Anti-Cancer Actions: 1. Inhibits the WNT/β-catenin pathway: stops the proliferation of cancer cells. 2. Induces apoptosis: triggers programmed death of cancer cells. 3. Blocks importin α/β transporter proteins, preventing replication of cancer cells. 4. Inhibits the PAK1 enzyme: reduces inflammation and tumor progression. 5. Antiangiogenic: stops the formation of new blood vessels in tumors. 6. Immune system modulator: improves recognition of cancer cells. 7. Autophagy disruptor: interferes with cancer cells' survival strategies. 8. Targets glioblastoma stem cells: effective in brain cancers. 9. Inhibits mitochondrial respiration: cuts off energy supply to tumors. 10. Disrupts mTOR signaling, slowing cell growth. 11. Overcomes chemotherapy resistance: makes chemotherapy more effective. 12. Antiviral properties: potentially useful for virus-related cancers (like HPV). MEBENDAZOLE – 12 Known Anti-Cancer Action: 1. Microtubule destabilization: similar to fenbendazole 2. Inhibits angiogenesis and blocks the growth of new blood vessels. 3. Triggers apoptosis: causes the death of cancer cells. 4. Inhibits VEGF signaling: blocks blood supply signals to the tumor. 5. Crosses the blood-brain barrier: useful for brain cancers. 6. Activates caspase-3/7 enzymes, involved in programmed cell death. 7. Reduces expression of the MYC oncogene, slowing tumor growth. 8. Inhibits the Bcl-2 protein, reducing cancer cell survival. 9. Anti-metastatic: reduces cancer spread. 10. Alters mitochondrial function: impairs energy production in tumor cells. 11. Improves chemotherapy sensitivity: helps standard treatments work better. 12. Low toxicity + long safety history: used in humans for decades. Follow me for more Bombshell.

🔴Ivermectin and mebendazole attack cancer cells in many different ways. Chemotherapy usually attacks only one.... Cancer has to be attacked through multiple mechanisms simultaneously... Ivermectin and mebendazole together do exactly that: they block cell division, cut off glucose metabolism, target cancer stem cells, and much more... Dr. Peter McCullough. IVERMECTIN – 12 Known Anti-Cancer Actions: 1. Inhibits the WNT/β-catenin pathway: stops the proliferation of cancer cells. 2. Induces apoptosis: triggers programmed death of cancer cells. 3. Blocks importin α/β transporter proteins, preventing replication of cancer cells. 4. Inhibits the PAK1 enzyme: reduces inflammation and tumor progression. 5. Antiangiogenic: stops the formation of new blood vessels in tumors. 6. Immune system modulator: improves recognition of cancer cells. 7. Autophagy disruptor: interferes with cancer cells' survival strategies. 8. Targets glioblastoma stem cells: effective in brain cancers. 9. Inhibits mitochondrial respiration: cuts off energy supply to tumors. 10. Disrupts mTOR signaling, slowing cell growth. 11. Overcomes chemotherapy resistance: makes chemotherapy more effective. 12. Antiviral properties: potentially useful for virus-related cancers (like HPV). MEBENDAZOLE – 12 Known Anti-Cancer Action: 1. Microtubule destabilization: similar to fenbendazole 2. Inhibits angiogenesis and blocks the growth of new blood vessels. 3. Triggers apoptosis: causes the death of cancer cells. 4. Inhibits VEGF signaling: blocks blood supply signals to the tumor. 5. Crosses the blood-brain barrier: useful for brain cancers. 6. Activates caspase-3/7 enzymes, involved in programmed cell death. 7. Reduces expression of the MYC oncogene, slowing tumor growth. 8. Inhibits the Bcl-2 protein, reducing cancer cell survival. 9. Anti-metastatic: reduces cancer spread. 10. Alters mitochondrial function: impairs energy production in tumor cells. 11. Improves chemotherapy sensitivity: helps standard treatments work better. 12. Low toxicity + long safety history: used in humans for decades. Follow me for more Bombshell.

Commentary | Global Ivermectin Research Hub

24,921 views • 24 days ago