Tanjina Kader 🎗️

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/cell-reports...

Thanks to funding bodies: National Breast Cancer Foundation, Australia (NBCF)

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....

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...

Immune Suppression in Fallopian Tube Precursors: Relevance for High-Grade Serous Ovarian Cancer A video from Tanjina Kader, posted on Oct 21, 2025.

Thanks for having me @vumedi to talk about the significance of our recent findings on HGSOC development!
www.vumedi.com/video/immune...

I can't thank Claude enough for teaching and fixing my errors in R in a daily basis! 🙏🏻 And it's very polite 🤭

dailyreporter.esmo.org/esmo-congres...

Even cells are smiling! 😊

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.

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.

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

13/n This was a dream postdoc project — the kind that kept me up late, but lit me up inside.
I grew immensely as a scientist, piecing together fragments of cancer evolution and immune microenvironment. Proud to share what we uncovered
#postdoclife #cancerevolution #GynOncol

12/n The dataset is available through cBioportal. cbioportal.org/study/summar...
Thanks to the cBioportal team!

11/n Incredibly grateful to be co-mentored by the brilliant (& genuinely kind) Sandro Santagata, MDPhD, collaborate with a true legend in the field @rdrapkin8-penn.bsky.social

Huge thanks to all co-authors - science is a team effort!

First for me: learning directly from developer
JiaRenLin

10/n All these coincide with a ⬇️ of total CD8+ T cells, especially in the epithelium. There were⬆️activated & exhausted CD8+ T during the later stages!
One culprit? Chronic IFN (IRDS= Interferon related DNA damage signature) is one of the factors contributing to exhaustion!

9/n
Then a shift towards reduced CD4+/CD8+ T cell-APC interactions!

8/n
👩‍🔬Function fades, but the story unfolds:

TIM3+ Antigen Presenting Cells (APC), reflecting their reduced function at later stages!

3D CyCIF helps us visualize the nearby immune cells!

7/n
As STIC progresses from early to advanced, we see a decline in the NK–cDC1 axis — key players in innate anti-tumor immunity.

Meanwhile, HLA-E expression increases: potential actionable immune evasion mechanism!

Both HLA-A & HLA-E are overexpressed in early STIC epithelium.

6/n
Why don’t most p53 signatures progress to cancer — even though they're common?

💡 Because the immune system is already at work. Innate immune players (NK–cDC1–CTL axis) and tissue-resident memory T cells help keep early lesions in check.

#ImmuneSurveillance matters!

5/n
Cancer doesn’t appear overnight — it builds gradually. Even before tumors form, hallmark pathways are already upregulated in advanced STICs! One standout? IFN signaling — it underpins early HGSOC development. A shift towards chronic IFN, driven by chromosomal instability 🧬

4/n⚡️Precancer evolution! 📷🔦
Incidental STICs might be the "early STICs" — with the potential to evolve into cancer-associated (advanced) STICs as disease progresses.

But what about their immune microenvironment? Almost nothing was known.

Time to map it. 🧬🔬#Pevention

3/n
We have developed a comprehensive resource of multiplexed tissue imaging (CyCIF) and spatial transcriptomic (GeoMx) data to study HGSOC development, from precancer lesions (incidental p53 signatures, incidental STICs and cancer-associated STICs) to invasive cancer.🔬

2/n Nearly 20 years ago, a pivotal discovery reshaped our understanding of HGSOC:

🔍 HGSOC originates in the fallopian tube — not the ovary.

It progresses through p53 signatures and STIC lesions, long before invasive disease appears.

A quiet beginning to a deadly cancer.

🚨🚨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
🧵👇

11/n Incredibly grateful to be co-mentored by the brilliant (& genuinely kind)
Sandro Santagata MDPhD, collaborate with a true legend in the field @rdrapkin8-penn.bsky.social

Huge thanks to all co-authors - science is a team effort!

First for me: learning directly from developer
JiaRenLin!

10/n All these coincide with a ⬇️ of total CD8+ T cells, especially in the epithelium. There were⬆️activated & exhausted CD8+ T during the later stages!

One culprit? Chronic IFN (IRDS= Interferon related DNA damage signature) is one of the factors contributing to exhaustion!

9/n
Then a shift towards reduced CD4+/CD8+ T cell-APC interactions!

8/n
👩‍🔬Function fades, but the story unfolds:

TIM3+ Antigen Presenting Cells (APC), reflecting their reduced function at later stages!

3D CyCIF helps us visualize the nearby immune cells!

7/n
As STIC progresses from early to advanced, we see a decline in the NK–cDC1 axis — key players in innate anti-tumor immunity.

Meanwhile, HLA-E expression increases: potential actionable immune evasion mechanism!

Both HLA-A & HLA-E are overexpressed in early STIC epithelium.

6/n
Why don’t most p53 signatures progress to cancer — even though they're common?

💡 Because the immune system is already at work. Innate immune players (NK–cDC1–CTL axis) and tissue-resident memory T cells help keep early lesions in check.

#ImmuneSurveillance matters!

5/n
Cancer doesn’t appear overnight — it builds gradually. Even before tumors form, hallmark pathways are already upregulated in advanced STICs!

One standout? IFN signaling — it underpins early HGSOC development. A shift towards chronic IFN, driven by chromosomal instability 🧬

4/n⚡️Precancer evolution! 📷🔦
Incidental STICs might be the "early STICs" — with the potential to evolve into cancer-associated (advanced) STICs as disease progresses.

But what about their immune microenvironment? Almost nothing was known.

Time to map it. 🧬🔬#Pevention