With the network and influence ford by the global promotion of K Therapy, large-scale sample collection is underway worldwide.
Tumor Cell samples from major dostic Hospitals are quickly sent to the Sanbo Research Institute. Through the active operation of Griffin, Robert, John Ansen, August, Manstein, Takahashi, and others, low-temperature transport boxes with special biohazard labels and encrypted barcodes are converging to the Sanbo Research Institute from abroad, like a pilgrimage, from the Anderson Cancer Center to the European Molecular Biology Laboratory, from the Japan National Cancer Center to remote Institutes in Australia.
They brought invasion frontier tissues of glioblastoma, circulating Tumor Cell clusters of triple-negative breast cancer, tastatic lymph nodes of esophageal squamous cell carcinoma, rare biopsy specins of undifferentiated thyroid cancer, and even so challenging Tumor samples that are difficult to categorize even by the original units. Each sample cos with as detailed clinical pathological information and preliminary molecular typing data as possible.
Yang Ping stands in the Laboratory, with Song Zimo reporting the latest progress beside him.
"As of eight this morning, the number of solid tumor samples stored and completed primary quality control has reached 4876, covering 92% of the main types of solid tumors in the World Health Organization classification and more than 300 rare subtypes. The high-throughput surface proteomics analysis platform is running at full speed, and the preliminary antigen profiles of the first batch of 1200 samples have been generated. Over there, Lu Xiaolu’s side, the schedule for cryo-electron microscopy has been pushed back to six months later, and they are optimizing automated sample preparation and pre-screening processes, with throughput tripled."
Yang Ping nods slightly: "Samples are not numbers; they are keyholes. Every unique Tumor uses its surface molecular combination to show us the specific expression form of the TIM superfamily in this individual and environnt. What we are looking for is not commonality, but the grammar of commonality."
As the number of samples increases, Yang Ping also becos busier, spending almost all day in the Laboratory, returning ho late.
During the day, he moves between various platforms, discussing a sarcoma sample’s abnormal TIM structure low-resolution contour with Lu Xiaolu, debating clustering algorithm parater settings with Tang Shun, and personally checking the data quality of surface protein fluorescence labeling.
At night, he is imrsed in the office, where millions of protein structure prediction diagrams, interaction networks, and evolutionary tree models flow across the intelligent screen.
Jiang Jitong is occasionally called in to help organize data or operate visualization software. He is amazed at Yang Ping’s ability to process multidinsional information. Yang Ping can simultaneously view the TIM candidate structure comparisons of over a dozen Tumor types, point out systemic differences in a loop area angle that may be related to embryonic origin layers; instantly identify a certain non-coding RNA possibly regulating a group of TIM mbers’ expression within chaotic gene co-expression networks; even reverse deduce from clinical prognosis data that a TIM conformational variant might confer special resistance to the hypoxic microenvironnt.
More than 80% of solid tumor samples detected surface protein complexes with that characteristic core folding pattern. They are like different style buildings built with the sa basic component within a vast architectural complex. However, how are these components selected by cancer cells? What is the intrinsic link between them? Is it rely structural similarity, or do they share a deeper regulatory logic or functional hub?
What keeps Yang Ping sleepless is the thought about the "key" lineage.
If TIM is a lock, the K Factor is a key, then what exactly is the operating principle of this key? The earliest K Factor was found entirely by chance, and then the K Factor, once injected into the human body, can automatically find its corresponding identity lock. This suggests that under certain conditions, Tumor cells can either self-secrete or participate in the construction of the K Factor.
Could it be that the K Factor is not just a marker or an interrupter? Could it trigger an internal termination program within cancer cells that originally existed but was deeply suppressed or bypassed?
This thought sends a chill down Yang Ping’s spine. If cancer cells inherently carry a self-destruction switch, only shielded by the identity phantom and abnormal signals maintained by the TIM system, then the essence of treatnt might be awakening from within, not attacking from without.
In this sense, the process of K Factor treatnt for Osteosarcoma is actually a process of awakening, not extermination; it rely awakens the Tumor Cell’s self-destruction program.
This discovery enlightens Yang Ping’s thoughts, focusing his excitent on three cases.
A rare pediatric soft tissue sarcoma sample from Northern Europe. For this highly invasive and almost untreatable Tumor, the K Factor showed nearly miraculous effects in vitro experints, with over 70% of Tumor Cells undergoing typical apoptotic morphological changes within 48 hours. Further analysis, however, found that this apoptosis does not rely on the classic caspase pathway but is accompanied by dramatic fluctuations in mitochondrial mbrane potential and atypical chromatin condensation.
Another late-stage lanoma sample with acquired resistance to immune checkpoint inhibitors displays decreased standard K Factor binding affinity. Yet, when using a targeted improved K Factor fine-tuned according to its TIM variant, not only is binding restored, but tumor cell sensitivity to the original immunotherapy is unexpectedly resensitized. It seems K Factor binding changes the immune visibility of tumor cells.
There’s also a pancreatic cancer organoid provided subsequently by Catherine’s team, showing early resistance to PAC-FUS1-targeted K Factor. The TIM structure of resistant cells has not disappeared, but the shielding protein network around it has beco more complex. However, when using an enhanced K Factor variant designed with a transmbrane domain that can partially penetrate the cell mbrane, an abnormal localization and aggregation of the PAC-FUS1 fusion protein inside the cell was observed, ultimately cleared by autophagy pathways.
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