Tanjina Kader 🎗️
@tanjinakader.bsky.social
Cancer research | Post doctoral Fellow, Harvard Medical School | previously Peter MacCallum Cancer Centre, Melbourne.
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
I can't thank Claude enough for teaching and fixing my errors in R in a daily basis! 🙏🏻 And it's very polite 🤭
Even cells are smiling! 😊
September 25, 2025 at 10:40 PM
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.
September 23, 2025 at 12:22 PM
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.
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
I grew immensely as a scientist, piecing together fragments of cancer evolution and immune microenvironment. Proud to share what we uncovered
#postdoclife #cancerevolution #GynOncol
June 16, 2025 at 5:49 PM
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
I grew immensely as a scientist, piecing together fragments of cancer evolution and immune microenvironment. Proud to share what we uncovered
#postdoclife #cancerevolution #GynOncol
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!
One culprit? Chronic IFN (IRDS= Interferon related DNA damage signature) is one of the factors contributing to exhaustion!
June 16, 2025 at 5:49 PM
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!
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!
Then a shift towards reduced CD4+/CD8+ T cell-APC interactions!
June 16, 2025 at 5:49 PM
9/n
Then a shift towards reduced CD4+/CD8+ T cell-APC interactions!
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!
👩🔬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!
June 16, 2025 at 5:49 PM
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!
👩🔬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.
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.
June 16, 2025 at 5:49 PM
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.
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!
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!
June 16, 2025 at 5:49 PM
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!
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 🧬
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 🧬
June 16, 2025 at 5:49 PM
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 🧬
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 🧬
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.🔬
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.🔬
June 16, 2025 at 5:49 PM
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.🔬
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.
🔍 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.
June 16, 2025 at 5:49 PM
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.
🔍 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
🧵👇
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
🚨🚨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
🧵👇
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
🧵👇
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!
One culprit? Chronic IFN (IRDS= Interferon related DNA damage signature) is one of the factors contributing to exhaustion!
June 16, 2025 at 5:11 PM
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!
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!
Then a shift towards reduced CD4+/CD8+ T cell-APC interactions!
June 16, 2025 at 5:11 PM
9/n
Then a shift towards reduced CD4+/CD8+ T cell-APC interactions!
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!
👩🔬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!
June 16, 2025 at 5:11 PM
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!
👩🔬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.
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.
June 16, 2025 at 5:11 PM
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.
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!
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!
June 16, 2025 at 5:11 PM
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!
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 🧬
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 🧬
June 16, 2025 at 5:11 PM
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 🧬
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 🧬
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.🔬
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.🔬
June 16, 2025 at 5:11 PM
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.🔬
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.
🔍 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.
June 16, 2025 at 5:11 PM
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.
🔍 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.
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
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!