Tanjina Kader 🎗️
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tanjinakader.bsky.social
Tanjina Kader 🎗️
@tanjinakader.bsky.social
71 followers 80 following 33 posts
Cancer research | Post doctoral Fellow, Harvard Medical School | previously Peter MacCallum Cancer Centre, Melbourne.
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tanjinakader.bsky.social
Tanjina Kader 🎗️ @tanjinakader.bsky.social · Jun 16
🚨🚨Paper out!! 🚨🚨
Excited to share our work (Pre-cancer Atlas of High Grade Serous Ovarian Cancer (HGSOC)), now published in
@CD_AACR
!
aacrjournals.org/cancerdiscov...

What if I told you HGSOC often starts in the Fallopian Tube and progresses through precancerous lesions? 1/n
🧵👇
tanjinakader.bsky.social
www.cell.com/cell-reports...
The tumor microenvironment of 14,837 breast cancers is associated with clinical outcome independently of genomic subtypes
Tu et al. present a systematic analysis of the tumor microenvironment across 14,837 breast cancers, identifying distinct cellular patterns that predict disease-specific survival independently of genom...
www.cell.com
November 13, 2025 at 12:16 PM
tanjinakader.bsky.social
Finally this paper is out (my most neglected kid). Huge thanks to co-first authors, collaborators & mentor @kylie-gorringe.bsky.social. This work was selected for AACR press conference presentation at the annual meeting in 2022, followed by media & press releases.
doi.org/10.1002/path...
Phylogenetic analysis of paired breast carcinomas identifies genetic events associated with clonal recurrence and invasive progression
Development of ipsilateral breast carcinoma following a diagnosis of breast ductal carcinoma in situ (DCIS) has been assumed to represent recurrence of the primary tumour. However, this may not alway....
doi.org
October 30, 2025 at 5:23 PM
tanjinakader.bsky.social
Thanks for having me @vumedi to talk about the significance of our recent findings on HGSOC development!
www.vumedi.com/video/immune...
Immune Suppression in Fallopian Tube Precursors: Relevance for High-Grade Serous Ovarian Cancer
A video from Tanjina Kader, posted on Oct 21, 2025.
www.vumedi.com
October 27, 2025 at 11:37 PM
tanjinakader.bsky.social
I can't thank Claude enough for teaching and fixing my errors in R in a daily basis! 🙏🏻 And it's very polite 🤭
October 26, 2025 at 6:24 PM
tanjinakader.bsky.social
dailyreporter.esmo.org/esmo-congres...
Survival benefits demonstrated with immunochemotherapy in platinum-resistant ovarian cancer
The ENGOT-ov65/KEYNOTE-B96 trial reported small but clinically relevant progression-free survival increments and significantly improved overall survival in platinum-resistant ovarian cancer
dailyreporter.esmo.org
October 18, 2025 at 10:09 PM
tanjinakader.bsky.social
Even cells are smiling! 😊
September 25, 2025 at 10:40 PM
tanjinakader.bsky.social
Truly honored to present my post doctoral work at the #AACRovca25 last weekend at the tumor initiation plenary session. Incredibly thankful to the organizing committee for inviting me and letting me share our multi-institutional Pre-cancer Atlas work, now published in @CD_AACR.
September 23, 2025 at 12:22 PM
Reposted by Tanjina Kader 🎗️
nature.com
Single-cell analysis reveals the extent of genome doubling in ovarian cancer, its variability and its role in enabling tumours to evade the immune system

go.nature.com/4kJLAjZ
Genome doubling fuels ovarian cancer evolution and immune dysregulation
Single-cell analysis reveals the extent of genome doubling in ovarian cancer, its variability and its role in enabling tumours to evade the immune system.
go.nature.com
July 17, 2025 at 8:14 AM
tanjinakader.bsky.social
🚨🚨Paper out!! 🚨🚨
Excited to share our work (Pre-cancer Atlas of High Grade Serous Ovarian Cancer (HGSOC)), now published in
@CD_AACR
!
aacrjournals.org/cancerdiscov...

What if I told you HGSOC often starts in the Fallopian Tube and progresses through precancerous lesions? 1/n
🧵👇
June 16, 2025 at 5:49 PM
Reposted by Tanjina Kader 🎗️
chorye.bsky.social
Everyone should watch and share. Thank you David. youtu.be/8YhJM6zxYDw
Breakthrough Prize-Winning Biochemist on the Deadly Cost of Funding Cuts | Amanpour and Company
YouTube video by Amanpour and Company
youtu.be
May 26, 2025 at 1:00 AM
tanjinakader.bsky.social
Multiplex tissue imaging 💪🏻
Why translational researchers are looking to spatial proteomics
Researchers have long used spatial proteomics, particularly immunofluorescence-based methods, to identify, quantify and map proteins within tumours and their microenvironments. Now, these tools are ed...
www.nature.com
May 13, 2025 at 12:07 PM
Reposted by Tanjina Kader 🎗️
rdrapkin8-penn.bsky.social
Surprising findings of BRCA mutations on the Fallopian tubes. Result of a tremendous team effort with @shenhui1986.bsky.social @vainstitute.bsky.social, Chuck Drescher @fredhutch.bsky.social, and Jarrod Marto @danafarber.bsky.social.
@pennmedcso.bsky.social
www.nature.com/articles/s41...
Impact of BRCA mutations, age, surgical indication, and hormone status on the molecular phenotype of the human Fallopian tube - Nature Communications
The human Fallopian tube (FT) is implicated as a site of origin for pelvic serous cancers. Here the authors conduct multi-omics analysis on over 100 FTs. The results challenge the assumption that BRCA...
www.nature.com
March 27, 2025 at 2:29 PM
tanjinakader.bsky.social
Very honoured to be an AACR Scholar in training awardee! Excited to talk about our pre-cancer atlas work in the plenary session of Cancer Evolution & Tumor microenvironment. @AACRJCA2025. Sunshine at Maui, Hawaii gives an incredible flavour to the meeting!
February 2, 2025 at 11:00 PM
Reposted by Tanjina Kader 🎗️
stephenturner.us
Simply Statistics: Biologists, stop putting UMAP plots in your papers https://simplystatistics.org/posts/2024-12-23-biologists-stop-including-umap-plots-in-your-papers/ from @rafalab.bsky.social 🧬🖥️🧪
December 31, 2024 at 9:00 PM
Reposted by Tanjina Kader 🎗️
rdrapkin8-penn.bsky.social
This paper is the result of an incredibly fun collaboration with Sandro Santagata and Peter Sorger. Led by an amazing postdoc @tanjinakader.bsky.social and JiaRen Lin, we provide a pre-cancer atlas of Fallopian tube precursors to High-Grade Serous Ovarian Cancer. The data is also on cbioportal!
elizsmckenna.bsky.social Elizabeth McKenna @elizsmckenna.bsky.social · Dec 20
Now online in Cancer Discovery: Multimodal Spatial Profiling Reveals Immune Suppression and Microenvironment Remodeling in Fallopian Tube Precursors to High-Grade Serous Ovarian Carcinoma - by Tanjina Kader, Jia-Ren Lin, Clemens Hug, Ronny Drapkin, Sandro Santagata, et al. doi.org/10.1158/2159...
Schematic representation of HGSCO progression, emphasizing the temporal development of hallmark cancer features and the dynamic interplay and interactions between immune cells and precancer/cancer cells. Cancer often starts with oncogenic changes (mutations, aneuploidy, and other cancer hallmarks), under selective pressure. These cells may remain latent for decades. Only a subset of these “phenotypically normal” but mutated clones undergo clonal expansion and acquire additional mutations, ultimately developing into cancer. Early on, despite limited genomic instability, innate immune responses, including the NK-cDC1-CTL axis and tissue-resident memory T cells (TRM), help contain p53 signature cells. Increasing aneuploidy or extrinsic factors can enhance immune surveillance, potentially eliminating precancer clones before significant proliferation occurs. During early STIC expansion, there is pronounced IFN response activation, with activated cDC1 and APCs, and NK cell-secreted chemokines, further attracting cDC1. This environment suggests active immune surveillance and is accompanied by interactions among APCs, activated CD4+, and CD8+ T cells. However, immunosuppressive cells, such as M2-like macrophages and Tregs, also emerge, indicating a complex equilibrium where cytotoxic and suppressive forces coexist. As STIC lesions advance, there is a reduction in CD8+ T cells and the interactions between APCs and CD4 T cells, along with an increase in exhausted CD8+ CTL and CD4+ cells expressing LAG3, almost no NK and cDC1 cells, and more suppressive APCs. The transition from STIC to overt cancer involves hallmark mechanisms such as TGF-β signaling, which excludes CTLs, changes in cytokine and fibroblast profiles, and induction of EMT and migratory programs. Dotted arrows indicate the hypothetical timing of these events, suggesting a prolonged interval from p53 signature to early STIC, followed by a more rapid progression from early to late STIC.
December 24, 2024 at 5:40 PM
Reposted by Tanjina Kader 🎗️
kylie-gorringe.bsky.social
Beautiful work from my brilliant former PhD student/postdoc @tanjinakader.bsky.social and her colleagues
elizsmckenna.bsky.social Elizabeth McKenna @elizsmckenna.bsky.social · Dec 20
Now online in Cancer Discovery: Multimodal Spatial Profiling Reveals Immune Suppression and Microenvironment Remodeling in Fallopian Tube Precursors to High-Grade Serous Ovarian Carcinoma - by Tanjina Kader, Jia-Ren Lin, Clemens Hug, Ronny Drapkin, Sandro Santagata, et al. doi.org/10.1158/2159...
Schematic representation of HGSCO progression, emphasizing the temporal development of hallmark cancer features and the dynamic interplay and interactions between immune cells and precancer/cancer cells. Cancer often starts with oncogenic changes (mutations, aneuploidy, and other cancer hallmarks), under selective pressure. These cells may remain latent for decades. Only a subset of these “phenotypically normal” but mutated clones undergo clonal expansion and acquire additional mutations, ultimately developing into cancer. Early on, despite limited genomic instability, innate immune responses, including the NK-cDC1-CTL axis and tissue-resident memory T cells (TRM), help contain p53 signature cells. Increasing aneuploidy or extrinsic factors can enhance immune surveillance, potentially eliminating precancer clones before significant proliferation occurs. During early STIC expansion, there is pronounced IFN response activation, with activated cDC1 and APCs, and NK cell-secreted chemokines, further attracting cDC1. This environment suggests active immune surveillance and is accompanied by interactions among APCs, activated CD4+, and CD8+ T cells. However, immunosuppressive cells, such as M2-like macrophages and Tregs, also emerge, indicating a complex equilibrium where cytotoxic and suppressive forces coexist. As STIC lesions advance, there is a reduction in CD8+ T cells and the interactions between APCs and CD4 T cells, along with an increase in exhausted CD8+ CTL and CD4+ cells expressing LAG3, almost no NK and cDC1 cells, and more suppressive APCs. The transition from STIC to overt cancer involves hallmark mechanisms such as TGF-β signaling, which excludes CTLs, changes in cytokine and fibroblast profiles, and induction of EMT and migratory programs. Dotted arrows indicate the hypothetical timing of these events, suggesting a prolonged interval from p53 signature to early STIC, followed by a more rapid progression from early to late STIC.
December 21, 2024 at 1:30 AM